Heart Disease and Stroke Statistics—2012 Update: A Report From the American Heart Association
This article has been corrected.
VIEW CORRECTIONTable of Contents
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e3
1.
About These Statistics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e7
2.
American Heart Association's 2020 Impact Goals. . . . . . . . . . . . . . . . .e10
3.
Cardiovascular Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e21
4.
Subclinical Atherosclerosis . . . . . . . . . . . . . . . . . . . . .e45
5.
Coronary Heart Disease, Acute Coronary Syndrome, and Angina Pectoris . . . . . . . . .e54
6.
Stroke (Cerebrovascular Disease) . . . . . . . . . . . . . . . . . . . . . . . . . . . .e68
7.
High Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e88
8.
Congenital Cardiovascular Defects . . . . . . . . . . . . . . . . . . . . . . . . . . . .e97
9.
Cardiomyopathy and Heart Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . .e102
10.
Disorders of Heart Rhythm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e107
11.
Other Cardiovascular Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . .. . .e122
12.
Risk Factor: Family History and Genetics . . . . . . . . . . . . . . . . . . . . . . . .e130
13.
Risk Factor: Smoking/Tobacco Use . . . . . . . . . . . . . . . . . . . . . . . . . . .e134
14.
Risk Factor: High Blood Cholesterol and Other Lipids . . . . . . . . . . . . . . . . . . . .e139
15.
Risk Factor: Physical Inactivity . . . . . . . . . . . . . . . . . . . . . . . . . . . .e145
16.
Risk Factor: Overweight and Obesity . . . . . . . . . . . . . . . . . . . . . . . . . . .e152
17.
Risk Factor: Diabetes Mellitus . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e160
18.
End-Stage Renal Disease and Chronic Kidney Disease . . . . . . . . . . . . . . . . . . . .e170
19.
Metabolic Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e175
20.
Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e180
21.
Quality of Care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. .e193
22.
Medical Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e204
23.
Economic Cost of Cardiovascular Disease . . . . . . . . . . . . . . . . . . . . . .. . . . .e209
24.
At-a-Glance Summary Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e213
25.
Glossary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .e218
Summary
Each year, the American Heart Association (AHA), in conjunction with the Centers for Disease Control and Prevention, the National Institutes of Health, and other government agencies, brings together the most up-to-date statistics on heart disease, stroke, other vascular diseases, and their risk factors and presents them in its Heart Disease and Stroke Statistical Update. The Statistical Update is a valuable resource for researchers, clinicians, healthcare policy makers, media professionals, the lay public, and many others who seek the best national data available on disease morbidity and mortality and the risks, quality of care, medical procedures and operations, and costs associated with the management of these diseases in a single document. Indeed, since 1999, the Statistical Update has been cited more than 8700 times in the literature (including citations of all annual versions). In 2010 alone, the various Statistical Updates were cited ≈1600 times (data from ISI Web of Science). In recent years, the Statistical Update has undergone some major changes with the addition of new chapters and major updates across multiple areas. For this year's edition, the Statistics Committee, which produces the document for the AHA, updated all of the current chapters with the most recent nationally representative data and inclusion of relevant articles from the literature over the past year and added a new chapter detailing various disorders of heart rhythm. Also, the 2012 Statistical Update is a major source for monitoring both cardiovascular health and disease in the population, with a focus on progress toward achievement of the AHA's 2020 Impact Goals. Below are a few highlights from this year's Update.
Rates of Death Attributable to CVD Have Declined, Yet the Burden of Disease Remains High
•
The 2008 overall rate of death attributable to cardiovascular disease (CVD) (International Classification of Diseases, 10th Revision, codes I00–I99) was 244.8 per 100 000. The rates were 287.2 per 100 000 for white males, 390.4 per 100 000 for black males, 200.5 per 100 000 for white females, and 277.4 per 100 000 for black females.
•
From 1998 to 2008, the rate of death attributable to CVD declined 30.6%. Mortality data for 2008 show that CVD (I00–I99; Q20–Q28) accounted for 32.8% (811 940) of all 2 471 984 deaths in 2008, or 1 of every 3 deaths in the United States.
•
On the basis of 2008 mortality rate data, more than 2200 Americans die of CVD each day, an average of 1 death every 39 seconds. About 150 000 Americans killed by CVD (I00–I99) in 2008 were <65 years of age. In 2008, 33% of deaths due to CVD occurred before the age of 75 years, which is well before the average life expectancy of 77.9 years.
•
Coronary heart disease caused ≈1 of every 6 deaths in the United States in 2008. Coronary heart disease mortality in 2008 was 405 309. Each year, an estimated 785 000 Americans will have a new coronary attack, and ≈470 000 will have a recurrent attack. It is estimated that an additional 195 000 silent first myocardial infarctions occur each year. Approximately every 25 seconds, an American will have a coronary event, and approximately every minute, someone will die of one.
•
Each year, ≈795 000 people experience a new or recurrent stroke. Approximately 610 000 of these are first attacks, and 185 000 are recurrent attacks. Mortality data from 2008 indicate that stroke accounted for ≈1 of every 18 deaths in the United States. On average, every 40 seconds, someone in the United States has a stroke. From 1998 to 2008, the stroke death rate fell 34.8%, and the actual number of stroke deaths declined 19.4%.
•
In 2008, 1 in 9 death certificates (281 437 deaths) in the United States mentioned heart failure.
Prevalence and Control of Traditional Risk Factors Remains an Issue for Many Americans
•
Data from the National Health and Nutrition Examination Survey (NHANES) 2005–2008 indicate that 33.5% of US adults ≥20 years of age have hypertension (Table 7-1). This amounts to an estimated 76 400 000 US adults with hypertension. The prevalence of hypertension is nearly equal between men and women. African American adults have among the highest rates of hypertension in the world, at 44%.
•
Among hypertensive adults, ≈80% are aware of their condition, 71% are using antihypertensive medication, and only 48% of those aware that they have hypertension have their condition controlled.
•
Despite 4 decades of progress, in 2010, among Americans ≥18 years of age, 21.2% of men and 17.5% of women continued to be cigarette smokers. In 2009, 19.5% of students in grades 9 through 12 reported current cigarette use.
•
The percentage of the nonsmoking population with detectable serum cotinine (indicating exposure to secondhand smoke) declined from 52.5% in 1999 to 2000 to 40.1% in 2007 to 2008, with declines occurring, and was higher for those 3 to 11 years of age (53.6%) and those 12 to 19 years of age (46.5%) than for those 20 years of age and older (36.7%).
•
An estimated 33 600 000 adults ≥20 years of age have total serum cholesterol levels ≥240 mg/dL, with a prevalence of 15.0% (Table 14-1).
•
In 2008, an estimated 18 300 000 Americans had diagnosed diabetes mellitus, representing 8.0% of the adult population. An additional 7 100 000 had undiagnosed diabetes mellitus, and 36.8% had prediabetes, with abnormal fasting glucose levels. African Americans, Mexican Americans, Hispanic/Latino individuals, and other ethnic minorities bear a strikingly disproportionate burden of diabetes mellitus in the United States (Table 17-1).
The 2012 Update Expands Data Coverage of the Obesity Epidemic and Its Antecedents and Consequences
•
The estimated prevalence of overweight and obesity in US adults (≥20 years of age) is 149 300 000, which represents 67.3% of this group in 2008. Fully 33.7% of US adults are obese (body mass index ≥30 kg/m2). Men and women of all race/ethnic groups in the population are affected by the epidemic of overweight and obesity (Table 16-1).
•
Among children 2 to 19 years of age, 31.7% are overweight and obese (which represents 23.6 million children), and 16.9% are obese (12.6 million children). Mexican American boys and girls and African American girls are disproportionately affected. Over the past 3 decades, the prevalence of obesity in children 6 to 11 years of age has increased from ≈4% to >20%.
•
Obesity (body mass index ≥30 kg/m2) is associated with marked excess mortality in the US population. Even more notable is the excess morbidity associated with overweight and obesity in terms of risk factor development and incidence of diabetes mellitus, CVD end points (including coronary heart disease, stroke, and heart failure), and numerous other health conditions, including asthma, cancer, degenerative joint disease, and many others.
•
The prevalence of diabetes mellitus is increasing dramatically over time, in parallel with the increases in prevalence of overweight and obesity.
•
On the basis of NHANES 2003–2006 data, the age-adjusted prevalence of metabolic syndrome, a cluster of major cardiovascular risk factors related to overweight/obesity and insulin resistance, is ≈34% (35.1% among men and 32.6% among women).
•
The proportion of youth (≤18 years of age) who report engaging in no regular physical activity is high, and the proportion increases with age. In 2009, among adolescents in grades 9 through 12, 29.9% of girls and 17.0% of boys reported that they had not engaged in 60 minutes of moderate-to-vigorous physical activity, defined as any activity that increased heart rate or breathing rate, even once in the previous 7 days, despite recommendations that children engage in such activity ≥5 days per week.
•
Thirty-three percent of adults reported engaging in no aerobic leisure-time physical activity.
•
Data from NHANES indicate that between 1971 and 2004, average total energy consumption among US adults increased by 22% in women (from 1542 to 1886 kcal/d) and by 10% in men (from 2450 to 2693 kcal/d; see Chart 20-1).
•
The increases in calories consumed during this time period are attributable primarily to greater average carbohydrate intake, in particular, of starches, refined grains, and sugars. Other specific changes related to increased caloric intake in the United States include larger portion sizes, greater food quantity and calories per meal, and increased consumption of sugar-sweetened beverages, snacks, commercially prepared (especially fast food) meals, and higher energy-density foods.
The 2012 Update Provides Critical Data About Cardiovascular Quality of Care, Procedure Utilization, and Costs
In light of the current national focus on healthcare utilization, costs, and quality, it is critical to monitor and understand the magnitude of healthcare delivery and costs, as well as the quality of healthcare delivery, related to CVDs. The Statistical Update provides these critical data in several sections.
Quality-of-Care Metrics for CVDs
Chapter 21 reviews many metrics related to the quality of care delivered to patients with CVDs, as well as healthcare disparities. In particular, quality data are available from the AHA's “Get With The Guidelines” programs for coronary artery disease and heart failure and from the American Stroke Association/AHA's “Get With The Guidelines” program for acute stroke. Similar data from the Veterans Healthcare Administration, national Medicare and Medicaid data, and Acute Coronary Treatment and Intervention Outcomes Network–“Get With The Guidelines” Registry data are also reviewed. These data show impressive adherence with guideline recommendations for many, but not all, metrics of quality of care for these hospitalized patients. Data are also reviewed on screening for cardiovascular risk factor levels and control.
Cardiovascular Procedure Utilization and Costs
Chapter 22 provides data on trends and current usage of cardiovascular surgical and invasive procedures. For example, the total number of inpatient cardiovascular operations and procedures increased 22%, from 6 133 000 in 1999 to 7 453 000 in 2009 (National Heart, Lung, and Blood Institute computation based on National Center for Health Statistics annual data).
Chapter 23 reviews current estimates of direct and indirect healthcare costs related to CVDs, stroke, and related conditions using Medical Expenditure Panel Survey data. The total direct and indirect cost of CVD and stroke in the United States for 2008 is estimated to be $297.7 billion. This figure includes health expenditures (direct costs, which include the cost of physicians and other professionals, hospital services, prescribed medications, home health care, and other medical durables) and lost productivity resulting from mortality (indirect costs). By comparison, in 2008, the estimated cost of all cancer and benign neoplasms was $228 billion ($93 billion in direct costs, $19 billion in morbidity indirect costs, and $116 billion in mortality indirect costs). CVD costs more than any other diagnostic group.
The AHA, through its Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States to provide the most current data available in the Statistics Update.
Finally, it must be noted that this annual Statistical Update is the product of an entire year's worth of effort by dedicated professionals, volunteer physicians and scientists, and outstanding AHA staff members, without whom publication of this valuable resource would be impossible. Their contributions are gratefully acknowledged.
Véronique L. Roger, MD, MPH, FAHA
Melanie B. Turner, MPH
On behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee
Note: Population data used in the compilation of NHANES prevalence estimates is for the latest year of the NHANES survey being used. Extrapolations for NHANES prevalence estimates are based on the census resident population for 2008 because this is the most recent year of NHANES data used in the Statistical Update.
Acknowledgments
We wish to thank Thomas Thom, Michael Wolz, Dale Burwen, and Sean Coady for their valuable comments and contributions. We would like to acknowledge Karen Modesitt for her administrative assistance.
Disclosures
| Writing Group Member | Employment | Research Grant | Other Research Support | Speakers' Bureau/Honoraria | Expert Witness | Ownership Interest | Consultant/Advisory Board | Other |
|---|---|---|---|---|---|---|---|---|
| Véronique L. Roger | Mayo Clinic | None | None | None | None | None | None | None |
| Emelia J. Benjamin | Boston University School of Medicine | NIH† | None | None | None | None | NIH† | None |
| Jarett D. Berry | UT Southwestern Medical School | AHA†; NHLBI† | None | Merck† | None | None | None | None |
| William B. Borden | Weill Cornell Medical College | None | None | None | None | None | None | The Dr. Robert C. and Veronica Atkins Foundation provided an educational grant to develop a curriculum in Metabolic Diseases; Dr Borden receives salary support from that† |
| Dawn M. Bravata | University of Iowa | None | None | None | None | None | None | None |
| Shifan Dai | Centers for Disease Control and Prevention | None | None | None | None | None | None | None |
| Earl S. Ford | Centers for Disease Control and Prevention | None | None | None | None | None | None | None |
| Caroline S. Fox | NHLBI | None | None | None | None | None | None | None |
| Heather J. Fullerton | University of California, San Francisco | NIH/NINDS† | None | Cincinnati Children's Hospital*; Toronto Hospital for Sick Children* | None | None | DSMB for Berlin Heart* | None |
| Cathleen Gillespie | Centers for Disease Control and Prevention | None | None | None | None | None | None | None |
| Alan S. Go | The Permanente Medical Group | GlaxoSmithKline†; Johnson & Johnson† | None | None | None | None | None | None |
| Susan M. Hailpern | Independent Consultant | None | None | None | None | None | None | None |
| John A. Heit | Mayo Clinic | None | None | None | None | None | None | None |
| Virginia J. Howard | University of Alabama at Birmingham School of Public Health | NIH/NINDS† | None | None | None | None | None | None |
| Brett M. Kissela | University of Cincinnati | Nexstim* | None | Allergan* | Expert witness for defense in 1 stroke-related case in 2010† | None | Allergan* | None |
| Steven J. Kittner | University of Maryland School of Medicine | None | None | None | None | None | None | None |
| Daniel T. Lackland | Medical University of South Carolina | None | None | None | None | None | None | None |
| Judith H. Lichtman | Yale School of Medicine | None | None | None | None | None | None | None |
| Lynda D. Lisabeth | University of Michigan | NHLBI†; NINDS† | None | None | None | None | None | None |
| Donald M. Lloyd-Jones | Northwestern University | None | None | None | None | None | None | None |
| Diane M. Makuc | National Center for Health Statistics, CDC | None | None | None | None | None | None | None |
| Gregory M. Marcus | UCSF | Astellas*; Baylis Medical* | None | None | None | None | None | None |
| Ariane Marelli | McGill University Health Center | None | None | None | None | None | None | None |
| David B. Matchar | Duke-NUS Graduate Medical School | None | None | None | None | None | Boehringer Ingelheim* | None |
| Claudia S. Moy | National Institutes of Health | None | None | None | None | None | None | None |
| Dariush Mozaffarian | Division of Cardiovascular Medicine, Brigham and Women's Hospital/Harvard School of Public Health | NIH†; Genes and Environment Initiative at Harvard School of Public Health†; Gates Foundation/World Health Organization†; GlaxoSmithKline†; Pronova†; Searle Scholar Award from the Searle Funds at the Chicago Community Trust†; Sigma Tau† | None | Aramark*; the Chicago Council*; International Life Sciences Institute*; Norwegian Seafood Export Council*; Nutrition Impact*; SPRIM*; Unilever*; UN Food and Agricultural Organization*; US Food and Drug Administration*; World Health Organization* | None | Harvard has filed a provisional patent application that been assigned to Harvard, listing Dr Mozaffarian as a coinventor for use of trans-palmitoleic acid to prevent and treat insulin resistance, type 2 diabetes, and related conditions*; royalties from UpToDate for an online chapter* | FoodMinds* | None |
| Michael E. Mussolino | National Heart, Lung, and Blood Institute | None | None | None | None | None | None | None |
| Graham Nichol | University of Washington | Asmund S. Laerdal Foundation for Acute Medicine†; Medtronic Inc†; NHLBI†; NIH† | None | None | None | None | Gambro Renal Inc*; LIFEBRIDGE Medizintechnik AG*; Sotera Wireless* | None |
| Nina P. Paynter | Brigham and Women's Hospital | Celera Corp†; NIH/NHLBI† | None | None | None | None | None | None |
| Elsayed Z. Soliman | Wake Forest University School of Medicine | None | None | None | None | None | None | None |
| Paul D. Sorlie | National Heart, Lung and Blood Institute, NIH | None | None | None | None | None | None | None |
| Nona Sotoodehnia | University of Washington | None | None | None | None | None | None | None |
| Tanya N. Turan | Medical University of South Carolina | NIH/NINDS† | AstraZeneca supplied drug for SAMMPRIS study†; Stryker Co supplied stents for SAMMPRIS study† | None | None | None | Boehringer Ingelheim*; CardioNet*; WL Gore* | None |
| Melanie B. Turner | American Heart Association | None | None | None | None | None | None | None |
| Salim S. Virani | Department of Veterans Affairs | Merck†; NFL Charities†; NIH†; VA† | None | None | None | None | None | None |
| Nathan D. Wong | University of California, Irvine | Bristol-Myers Squibb†; Merck† | None | None | None | None | Abbott Pharmaceuticals* | None |
| Daniel Woo | University of Cincinnati | NIH† | None | None | None | None | None | None |
This table represents the relationships of writing group members that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure Questionnaire, which all members of the writing group are required to complete and submit. A relationship is considered to be “significant” if (a) the person receives $10 000 or more during any 12-month period, or 5% or more of the person's gross income; or (b) the person owns 5% or more of the voting stock or share of the entity, or owns $10 000 or more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant” under the preceding definition.
*
Modest.
†
Significant.
1. About These Statistics
The American Heart Association (AHA) works with the Centers for Disease Control and Prevention's (CDC's) National Center for Health Statistics (NCHS); the National Heart, Lung, and Blood Institute (NHLBI); the National Institute of Neurological Disorders and Stroke (NINDS); and other government agencies to derive the annual statistics in this Heart Disease and Stroke Statistical Update. This chapter describes the most important sources and the types of data we use from them. For more details, see Chapter 25 of this document, the Glossary.
The surveys used are:
•
Behavioral Risk Factor Surveillance System (BRFSS)—ongoing telephone health survey system
•
Greater Cincinnati/Northern Kentucky Stroke Study (GCNKSS)—stroke incidence rates and outcomes within a biracial population
•
Medical Expenditure Panel Survey (MEPS)—data on specific health services that Americans use, how frequently they use them, the cost of these services, and how the costs are paid
•
National Health and Nutrition Examination Survey (NHANES)—disease and risk factor prevalence and nutrition statistics
•
National Health Interview Survey (NHIS)—disease and risk factor prevalence
•
National Hospital Discharge Survey (NHDS)—hospital inpatient discharges and procedures (discharged alive, dead, or status unknown)
•
National Ambulatory Medical Care Survey (NAMCS)—physician office visits
•
National Home and Hospice Care Survey (NHHCS)—staff, services, and patients of home health and hospice agencies
•
National Hospital Ambulatory Medical Care Survey (NHAMCS)—hospital outpatient and emergency department (ED) visits
•
Nationwide Inpatient Sample of the Agency for Healthcare Research and Quality—hospital inpatient discharges, procedures, and charges
•
National Nursing Home Survey (NNHS)—nursing home residents
•
National Vital Statistics System—national and state mortality data
•
World Health Organization—mortality rates by country
•
Youth Risk Behavior Surveillance System (YRBSS)—health-risk behaviors in youth and young adults
| AHA | American Heart Association |
|---|---|
| AP | angina pectoris |
| ARIC | Atherosclerosis Risk in Communities Study |
| BP | blood pressure |
| BRFSS | Behavioral Risk Factor Surveillance System |
| CDC | Centers for Disease Control and Prevention |
| CHS | Cardiovascular Health Study |
| CVD | cardiovascular disease |
| DM | diabetes mellitus |
| ED | emergency department |
| FHS | Framingham Heart Study |
| GCNKSS | Greater Cincinnati/Northern Kentucky Stroke Study |
| HD | heart disease |
| HF | heart failure |
| ICD | International Classification of Diseases |
| ICD-9-CM | International Classification of Diseases, Clinical Modification, 9th Revision |
| ICD-10 | International Classification of Diseases, 10th Revision |
| MEPS | Medical Expenditure Panel Survey |
| MI | myocardial infarction |
| NAMCS | National Ambulatory Medical Care Survey |
| NCHS | National Center for Health Statistics |
| NHAMCS | National Hospital Ambulatory Medical Care Survey |
| NHANES | National Health and Nutrition Examination Survey |
| NHDS | National Hospital Discharge Survey |
| NHHCS | National Home and Hospice Care Survey |
| NHIS | National Health Interview Survey |
| NHLBI | National Heart, Lung, and Blood Institute |
| NINDS | National Institute of Neurological Disorders and Stroke |
| NNHS | National Nursing Home Survey |
| PAD | peripheral artery disease |
| YRBSS | Youth Risk Behavior Surveillance System |
See Glossary (Chapter 25) for explanation of terms.
Disease Prevalence
Prevalence is an estimate of how many people have a disease at a given point or period in time. The NCHS conducts health examination and health interview surveys that provide estimates of the prevalence of diseases and risk factors. In this Update, the health interview part of the NHANES is used for the prevalence of cardiovascular diseases (CVDs). NHANES is used more than the NHIS because in NHANES, angina pectoris (AP) is based on the Rose Questionnaire; estimates are made regularly for heart failure (HF); hypertension is based on blood pressure (BP) measurements and interviews; and an estimate can be made for total CVD, including myocardial infarction (MI), AP, HF, stroke, and hypertension.
A major emphasis of this Statistical Update is to present the latest estimates of the number of people in the United States who have specific conditions to provide a realistic estimate of burden. Most estimates based on NHANES prevalence rates are based on data collected from 2005 to 2008 (in most cases, these are the latest published figures). These are applied to census population estimates for 2008. Differences in population estimates based on extrapolations of rates beyond the data collection period by use of more recent census population estimates cannot be used to evaluate possible trends in prevalence. Trends can only be evaluated by comparing prevalence rates estimated from surveys conducted in different years.
Risk Factor Prevalence
The NHANES 2005–2008 data are used in this Update to present estimates of the percentage of people with high lipid values, diabetes mellitus (DM), overweight, and obesity. The NHIS is used for the prevalence of cigarette smoking and physical inactivity. Data for students in grades 9 through 12 are obtained from the YRBSS.
Incidence and Recurrent Attacks
An incidence rate refers to the number of new cases of a disease that develop in a population per unit of time. The unit of time for incidence is not necessarily 1 year, although we often discuss incidence in terms of 1 year. For some statistics, new and recurrent attacks or cases are combined. Our national incidence estimates for the various types of CVD are extrapolations to the US population from the Framingham Heart Study (FHS), the Atherosclerosis Risk in Communities (ARIC) study, and the Cardiovascular Health Study (CHS), all conducted by the NHLBI, as well as the GCNKSS, which is funded by the NINDS. The rates change only when new data are available; they are not computed annually. Do not compare the incidence or the rates with those in past editions of the Heart Disease and Stroke Statistics Update (also known as the Heart and Stroke Statistical Update for editions before 2005). Doing so can lead to serious misinterpretation of time trends.
Mortality
Mortality data are presented according to the underlying cause of death. “Any-mention” mortality means that the condition was nominally selected as the underlying cause or was otherwise mentioned on the death certificate. For many deaths classified as attributable to CVD, selection of the single most likely underlying cause can be difficult when several major comorbidities are present, as is often the case in the elderly population. It is useful, therefore, to know the extent of mortality attributable to a given cause regardless of whether it is the underlying cause or a contributing cause (ie, its “any-mention” status). The number of deaths in 2008 with any mention of specific causes of death was tabulated by the NHLBI from the NCHS public-use electronic files on mortality.
The first set of statistics for each disease in this Update includes the number of deaths for which the disease is the underlying cause. Two exceptions are Chapter 7 (High Blood Pressure) and Chapter 9 (Cardiomyopathy and Heart Failure). High BP, or hypertension, increases the mortality risks of CVD and other diseases, and HF should be selected as an underlying cause only when the true underlying cause is not known. In this Update, hypertension and HF death rates are presented in 2 ways: (1) as nominally classified as the underlying cause and (2) as any-mention mortality.
National and state mortality data presented according to the underlying cause of death were computed from the mortality tables of the NCHS World Wide Web site, the Health Data Interactive data system of the NCHS, or the CDC compressed mortality file. Any-mention numbers of deaths were tabulated from the electronic mortality files of the NCHS World Wide Web site and from Health Data Interactive.
Population Estimates
In this publication, we have used national population estimates from the US Census Bureau for 2008 in the computation of morbidity data. NCHS population estimates for 2008 were used in the computation of death rate data. The Census Bureau World Wide Web site1 contains these data, as well as information on the file layout.
Hospital Discharges and Ambulatory Care Visits
Estimates of the numbers of hospital discharges and numbers of procedures performed are for inpatients discharged from short-stay hospitals. Discharges include those discharged alive, dead, or with unknown status. Unless otherwise specified, discharges are listed according to the first-listed (primary) diagnosis, and procedures are listed according to all listed procedures (primary plus secondary). These estimates are from the NHDS of the NCHS unless otherwise noted. Ambulatory care visit data include patient visits to physician offices and hospital outpatient departments and EDs. Ambulatory care visit data reflect the first-listed (primary) diagnosis. These estimates are from NAMCS and NHAMCS of the NCHS.
International Classification of Diseases
Morbidity (illness) and mortality (death) data in the United States have a standard classification system: the International Classification of Diseases (ICD). Approximately every 10 to 20 years, the ICD codes are revised to reflect changes over time in medical technology, diagnosis, or terminology. Where necessary for comparability of mortality trends across the 9th and 10th ICD revisions, comparability ratios computed by the NCHS are applied as noted.2 Effective with mortality data for 1999, we are using the 10th revision (ICD-10). It will be a few more years before the 10th revision is used for hospital discharge data and ambulatory care visit data, which are based on the International Classification of Diseases, Clinical Modification, 9th Revision (ICD-9-CM).3
Age Adjustment
Prevalence and mortality estimates for the United States or individual states comparing demographic groups or estimates over time either are age specific or are age adjusted to the 2000 standard population by the direct method.4 International mortality data are age adjusted to the European standard.5 Unless otherwise stated, all death rates in this publication are age adjusted and are deaths per 100 000 population.
Data Years for National Estimates
In this Update, we estimate the annual number of new (incidence) and recurrent cases of a disease in the United States by extrapolating to the US population in 2008 from rates reported in a community- or hospital-based study or multiple studies. Age-adjusted incidence rates by sex and race are also given in this report as observed in the study or studies. For US mortality, most numbers and rates are for 2008. For disease and risk factor prevalence, most rates in this report are calculated from the 2005–2008 NHANES. Because NHANES is conducted only in the noninstitutionalized population, we extrapolated the rates to the total US population in 2008, recognizing that this probably underestimates the total prevalence, given the relatively high prevalence in the institutionalized population. The numbers and rates of hospital inpatient discharges for the United States are for 2009. Numbers of visits to physician offices, hospital EDs, and hospital outpatient departments are for 2009. Except as noted, economic cost estimates are for 2008.
Cardiovascular Disease
For data on hospitalizations, physician office visits, and mortality, CVD is defined according to ICD codes given in Chapter 25 of the present document. This definition includes all diseases of the circulatory system, as well as congenital CVD. Unless so specified, an estimate for total CVD does not include congenital CVD. Prevalence of CVD includes people with hypertension, heart disease (HD), stroke, peripheral artery disease (PAD), and diseases of the veins.
Race
Data published by governmental agencies for some racial groups are considered unreliable because of the small sample size in the studies. Because we try to provide data for as many racial groups as possible, we show these data for informational and comparative purposes.
Contacts
If you have questions about statistics or any points made in this Update, please contact the AHA National Center, Office of Science & Medicine at [email protected]. Direct all media inquiries to News Media Relations at [email protected] or 214-706-1173.
We do our utmost to ensure that this Update is error free. If we discover errors after publication, we will provide corrections at our World Wide Web site, http://www.heart.org/statistics, and in the journal Circulation.
References
1.
US Census Bureau population estimates. http://www.census.gov/popest/national/. Accessed October 30, 2011.
2.
National Center for Health Statistics. Health, United States, 2009, With Special Feature on Medical Technology. Hyattsville, MD: National Center for Health Statistics; 2010. http://www.cdc.gov/nchs/data/hus/hus09.pdf. Accessed July 30, 2010.
3.
National Center for Health Statistics, Centers for Medicare and Medicaid Services. International Classification of Diseases, Ninth Revision: Clinical Modification (ICD-9-CM). Hyattsville, MD: National Center for Health Statistics; 1978.
4.
Anderson RN, Rosenberg HM. Age standardization of death rates: implementation of the year 2000 standard. Natl Vital Stat Rep. 1998; 47: 1–16, 20.
5.
World Health Organization. World Health Statistics Annual. Geneva, Switzerland: World Health Organization; 1998.
2. American Heart Association's 2020 Impact Goals
| Level of Cardiovascular Health for Each Metric | |||
|---|---|---|---|
| Poor | Intermediate | Ideal | |
| Current smoking | |||
| Adults ≥20 y of age | Yes | Former ≤12 mo | Never or quit >12 mo |
| Children 12–19 y of age | Tried in prior 30 d | … | Never tried; never smoked whole cigarette |
| BMI | |||
| Adults ≥20 y of age | ≥30 kg/m2 | 25–29.9 kg/m2 | <25 kg/m2 |
| Children 2–19 y of age | >95th percentile | 85th–95th percentile | <85th percentile |
| Physical activity | |||
| Adults ≥20 y of age | None | 1–149 min/wk moderate or 1–74 min/wk vigorous or 1–149 min/wk moderate+2×vigorous | ≥150 min/wk moderate or ≥75 min/wk vigorous or ≥150 min/wk moderate+2×vigorous |
| Children 12–19 y of age | None | >0 and <60 min of moderate or vigorous every day | ≥60 min of moderate or vigorous every day |
| Healthy Diet Score, no. of components | |||
| Adults ≥20 y of age | 0–1 | 2–3 | 4–5 |
| Children 5–19 y of age | 0–1 | 2–3 | 4–5 |
| Total cholesterol, mg/dL | |||
| Adults ≥20 y of age | ≥240 | 200–239 or treated to goal | <200 |
| Children 6–19 y of age | ≥200 | 170–199 | <170 |
| Blood pressure | |||
| Adults ≥20 y of age | SBP ≥140 or DBP ≥90 mm Hg | SBP 120–139 or DBP 80–89 mm Hg or treated to goal | <120/<80 mm Hg |
| Children 8–19 y of age | >95th percentile | 90th–95th percentile or SBP ≥120 or DBP ≥80 mm Hg | <90th percentile |
| Fasting plasma glucose, mg/dL | |||
| Adults ≥20 y of age | ≥126 | 100–125 or treated to goal | <100 |
| Children 12–19 y of age | ≥126 | 100–125 | <100 |
AHA indicates American Heart Association; …, no definition for this stratum; BMI, body mass index; SBP, systolic blood pressure; and DBP, diastolic blood pressure.
| Ages 12–19 y | Ages ≥20 y* | Ages 20–39 y | Ages 40–59 y | Ages ≥60 y | |
|---|---|---|---|---|---|
| Ideal CV health profile (composite–all 7) | 0.0 | 0.0 | 0.0 | 0.0 | 0.0 |
| ≥6 Ideal CV health components | 9.1 | 3.8 | 7.2 | 2.1 | 0.1 |
| ≥5 Ideal CV health components | 41.2 | 16.2 | 29.4 | 9.7 | 2.5 |
| Ideal CV health factors (composite–all 4) | 37.9 | 14.4 | 27.5 | 7.3 | 1.0 |
| Individual components | |||||
| Total cholesterol <200 mg/dL (untreated) | 75.1 | 46.8 | 64.0 | 37.1 | 28.4 |
| SBP <120 mm Hg and DBP <80 mm Hg (untreated) | 82.3 | 43.8 | 63.8 | 36.9 | 14.6 |
| Not current smoker (never or quit ≥12 mo) | 83.7 | 72.9 | 66.4 | 72.9 | 86.1 |
| Fasting blood glucose <100 mg/dL | 76.2 | 52.0 | 67.4 | 45.6 | 31.9 |
| Ideal health behaviors (composite–all 4) | 0.0 | 0.1 | 0.1 | 0.0 | 0.0 |
| Individual components | |||||
| Physical activity at goal | 39.0 | 39.5 | 45.6 | 36.4 | 33.7 |
| Not current smoker (never or quit ≥12 mo) | 83.7 | 72.9 | 66.4 | 72.9 | 86.1 |
| BMI <25 kg/m2 | 62.5 | 31.9 | 39.1 | 28.0 | 25.3 |
| 4–5 Diet goals met† | 0.0 | 0.3 | 0.3 | 0.1 | 0.5 |
| Fruits and vegetables ≥4.5 cups/d | 7.9 | 12.3 | 11.7 | 11.4 | 15.8 |
| Fish ≥2 3.5-oz servings/wk (preferably oily fish) | 9.2 | 18.3 | 16.8 | 19.7 | 19.4 |
| Sodium <1500 mg/d | 0.0 | 0.6 | 0.6 | 0.8 | 0.3 |
| Sugar-sweetened beverages ≤450 kcal/wk | 32.0 | 51.9 | 41.0 | 54.6 | 71.2 |
| Whole grains (1.1 g fiber/10 g carbohydrates) ≥3 1-oz equivalents/d | 3.2 | 7.3 | 7.0 | 7.1 | 8.4 |
| Other dietary measures | |||||
| Nuts, legumes, seeds ≥4 servings/wk | 8.7 | 21.7 | 19.6 | 22.5 | 24.7 |
| Processed meats ≤2 servings/wk | 56.3 | 57.6 | 54.0 | 59.7 | 61.1 |
| Saturated fat <7% of total energy intake (kcal) | 4.5 | 8.7 | 9.3 | 8.0 | 9.0 |
NHANES indicates National Health and Nutrition Examination Survey; CV, cardiovascular; SBP, systolic blood pressure; DBP, diastolic blood pressure; and BMI, body mass index.
*
Standardized to the age distribution of the 2000 US standard population.
†
Scaled for 2000 kcal/d and in the context of intake with appropriate energy balance and a DASH (Dietary Approaches to Stop Hypertension)–like eating plan.
| In the Presence of CVD | In the Absence of CVD | |||||
|---|---|---|---|---|---|---|
| N* | %† | (SE) | N* | %† | (SE) | |
| Risk factor control | ||||||
| Smoking | 13 775 054 | 187 189 147 | ||||
| Current smoker or smokers who quit <12 mo ago | 3 482 092 | 40.64 | (5.20) | 44 333 396 | 23.35 | (1.42) |
| BP | 13 042 362 | 178 481 116 | ||||
| Prevalence of BP ≥140/90 mm Hg or taking medications | 8 790 237 | 44.58 | (3.71) | 47 737 172 | 27.18 | (0.63) |
| Awareness among those with hypertension | 8 277 582 | 95.80 | (1.50) | 36 832 906 | 70.63 | (3.84) |
| Treatment among those with hypertension | 7 739 839 | 88.72 | (2.48) | 32 685 394 | 57.25 | (2.14) |
| BP control to <140/<90 mm Hg among treated | 4 731 044 | 62.03 | (7.97) | 23 440 265 | 76.97 | (2.66) |
| Cholesterol | 12 935 387 | 177 322 590 | ||||
| Prevalence of total cholesterol ≥240 mg/dL or taking medications | 6 847 388 | 34.83 | (3.57) | 45 453 440 | 25.44 | (1.08) |
| Awareness among those with hypercholesterolemia | 6 218 269 | 83.43 | (6.43) | 33 326 995 | 62.57 | (2.36) |
| Treatment among those with hypercholesterolemia | 5 722 826 | 76.39 | (6.01) | 22 922 768 | 38.46 | (2.54) |
| Cholesterol control to <200 mg/dL among treated | 5 110 272 | 84.61 | (7.08) | 19 890 862 | 80.73 | (5.43) |
| Weight | 13 232 271 | 185 443 123 | ||||
| Overweight or obese BMI ≥25.0 kg/m2 | 10 401 572 | 70.65 | (4.93) | 125 175 950 | 67.69 | (0.97) |
| Obese BMI ≥30.0 kg/m2 | 6 221 362 | 43.73 | (6.12) | 61 956 664 | 33.42 | (1.11) |
| Diabetes mellitus | 14 292 850 | 188 058 669 | ||||
| Prevalence of fasting glucose ≥125 mg/dL or taking medications | 5 174 893 | 17.44 | (3.71) | 16 987 130 | 9.26 | (0.60) |
| Awareness among diabetics | 3 909 379 | 84.51 | (5.78) | 12 446 506 | 64.28 | (4.56) |
| Treatment among diabetics | 3 798 559 | 82.03 | (5.69) | 12 028 826 | 62.54 | (4.46) |
| Blood glucose control among treated | 1 460 295 | ‡ | 4 026 301 | 23.44 | (3.74) | |
| Physical activity | 13 775 054 | 187 296 417 | ||||
| Physical activity: intermediate or poor§ | 9 914 277 | 74.10 | (4.77) | 111 901 937 | 59.93 | (2.40) |
| Physical activity: none | 9 045 113 | 65.70 | (5.86) | 87 091 042 | 46.70 | (2.70) |
| Diet | 12 665 860 | 161 854 617 | ||||
| Total diet score 0–3 of 5 | 12 665 860 | 100.00 | (0.00) | 161 370 154 | 99.71 | (0.11) |
| Total diet score 0–1 of 5 | 9 540 532 | 70.06 | (4.69) | 127 156 293 | 78.84 | (1.42) |
NHANES indicates National Health and Nutrition Examination Survey; CVD, cardiovascular disease; SE, standard error; BP, blood pressure; and BMI, body mass index.
*
Weighted sample size.
†
Standardized to the age distribution of the 2000 US Standard population.
‡
Estimate suppressed because of instability by National Center for Health Statistics standards (relative SE >30%).
§
Moderate <150 min/wk AND Vigorous <75 min/wk AND Combined <150 min/wk.
| Percent BP ideal among adults, 2007–2008 | 43.82 |
| 20% Relative increase | 52.58 |
| Percent who would have ideal BP if population mean BP were lowered by* | |
| 2 mm Hg | 55.47 |
| 3 mm Hg | 59.79 |
| 4 mm Hg | 61.48 |
| 5 mm Hg | 65.49 |
NHANES indicates National Health and Nutrition Examination Survey; BP, blood pressure.
*
Reduction in BP=observed average systolic BP−X mm Hg AND observed average diastolic−X mm Hg.
Standardized to the age distribution of the 2000 US standard population.
After achieving its major Impact Goals for 2010, the AHA recently created a new set of Impact Goals for the current decade.1 Specifically, the AHA committed to the following organizational goals:
By 2020, to improve the cardiovascular health of all Americans by 20%, while reducing deaths from cardiovascular diseases and stroke by 20%.1
These goals include a novel concept, “cardiovascular health,” which encompasses 7 health behaviors and health factors (Table 2-1). “Ideal cardiovascular health” is defined by the absence of clinically manifest CVD and the simultaneous presence of optimal levels of all 7 health behaviors (lean body mass, avoidance of smoking, participation in physical activity [PA], and healthy dietary intake consistent with a Dietary Approaches to Stop Hypertension [DASH]–like eating pattern) and health factors (untreated total cholesterol <200 mg/dL, untreated BP <120/<80 mm Hg, and fasting blood glucose <100 mg/dL). Because the ideal cardiovascular health profile is known to be rare in the population, the entire spectrum of cardiovascular health can also be represented as being “ideal,” “intermediate,” or “poor” for each of the health behaviors and health factors, as shown in Table 2-1.1
Beginning in 2011, and recognizing the substantial time lag in the nationally representative data sets, the annual Statistical Update began to evaluate and publish metrics and information that gives the AHA directional insights into progress and/or areas critical for greater concentration, to meet their 2020 goals.
Cardiovascular Health
•
Table 2-1 provides the specific definitions for ideal, intermediate, and poor cardiovascular health for each of the 7 health behaviors and health factors, for adults ≥20 years of age and children of selected ages (depending on data availability).
•
The prevalences of ideal, intermediate, and poor levels of each of the 7 cardiovascular health metrics are shown in Chart 2-1 (for children ages 12–19 years) and Chart 2-2 (for adults ≥20 years of age).
—Among children (Chart 2-1), the prevalence (unadjusted) of ideal levels of cardiovascular health behaviors and factors currently varies from 0% for the healthy diet score (ie, essentially no children meet 4 or 5 of the 5 dietary components) to >80% for the smoking and BP metrics. More than 90% of US children meet 0 or only 1 of the 5 healthy dietary components.
—Among US adults (Chart 2-2), the age-standardized prevalence of ideal levels of cardiovascular health behaviors and factors currently varies from 0.1% for having 4 to 5 components of the healthy diet score up to 75% for the smoking metric (ie, 75% of US adults have never smoked or are current nonsmokers who have quit for >12 months).
—In general, the prevalence of ideal levels of health behaviors and health factors is higher in US children than in US adults.
•
Age-standardized and age-specific prevalence estimates for ideal cardiovascular health and for ideal levels of each of its components are shown in Table 2-2.
—The prevalence of ideal levels of all of the 7 health factors and health behaviors decreases dramatically from younger to older ages.
•
Chart 2-3 displays the prevalence estimates for the population of US children meeting different numbers of criteria for ideal cardiovascular health (out of 7 possible).
—Half of US children ages 12 to 19 years meet 4 or fewer criteria for ideal cardiovascular health.
—The distributions are similar overall in boys and girls.
•
Charts 2-4 and 2-5 display the age-standardized prevalence estimates for the population of US adults meeting different numbers of criteria for ideal cardiovascular health (out of 7 possible), overall and stratified by age groups, sex, and race.
—Approximately 2.5% of US adults have 0 of the 7 criteria at ideal levels, with 26% having 3 at ideal levels and 4% having 6 metrics at ideal levels (Chart 2-4).
—Compared with younger adults, older adults tend to have fewer of the 7 metrics at ideal levels; more than 60% of those >60 years of age have only 2 or fewer metrics at ideal levels (Chart 2-4).
—Women tend to have more metrics at ideal levels than do men (Chart 2-4).
—Approximately 63% of white adults and 71% of black and Mexican American adults have 3 or fewer metrics (out of 7) at ideal levels (Chart 2-5).
•
Chart 2-6 displays the age-standardized percentages of US adults and percentages of children who have 5 or more of the metrics (out of 7 possible) at ideal levels.
—Only ≈41% of US children aged 12 to 19 years have 5 or more metrics at ideal levels, including somewhat more girls than boys.
—However, only 16% of US adults have 5 or more metrics with ideal levels, including 12% of men and 21% of women.
—Whites have approximately twice the percentage of adults with 5 or more metrics with ideal levels as Mexican Americans.
•
Chart 2-7 displays the age-standardized percentages of US adults meeting different numbers of criteria for poor and ideal cardiovascular health. Meeting the AHA 2020 Strategic Impact Goals is predicated on reducing the relative percentage of those with poor levels while increasing the relative percentage of those with ideal levels for each of the 7 metrics.
—Approximately 94% of US adults have at least 1 metric at poor levels.
—Approximately 38% of US adults have at least 3 metrics at poor levels.
•
The prevalence of risk factors and their awareness, treatment, and control are displayed in Table 2-3 separately for those with and without self-reported CVD. Among those without CVD, NHANES 2007–2008 data indicate the following:
—Approximately 26% of US adults are current smokers or have recently quit for <12 months.
—Prevalence of hypertension is estimated to be 27%; 71% are aware of their hypertension, and 57% are treated. Among those with hypertension who are treated, control to goal BP levels of <140/<90 mm Hg is 77%.
—Prevalence of dyslipidemia (defined by total cholesterol ≥240 mg/dL or receiving medication) is 25%; 63% are aware of their dyslipidemia, and 38% are treated. Among those with dyslipidemia who are treated, 81% have total cholesterol <200 mg/dL.
—Prevalence of obesity is 33%, and prevalence of overweight or obesity is 68%.
—Prevalence of DM is 9%; 64% are aware of their DM, and 63% are treated. Among those with DM who are treated, 23% have controlled blood glucose levels.
—As measured by objective accelerometer data, 60% of adults have intermediate or poor levels of PA, with 47% having no moderate or vigorous activity at all.
—79% of US adults without CVD meet 0 or only 1 of the 5 healthy diet metrics.
| AHA | American Heart Association |
| ARIC | Atherosclerosis Risk in Communities Study |
| BMI | body mass index |
| BP | blood pressure |
| CVD | cardiovascular disease |
| DASH | Dietary Approaches to Stop Hypertension |
| DBP | diastolic blood pressure |
| DM | diabetes mellitus |
| HD | heart disease |
| HF | heart failure |
| HR | hazard ratio |
| MI | myocardial infarction |
| NHANES | National Health and Nutrition Examination Survey |
| PA | physical activity |
| SBP | systolic blood pressure |
| SE | standard error |
Cardiovascular Disease
•
In 2007, the age-standardized death rate attributable to all CVDs was 251.2 per 100 000 (Chart 2-8), down 4.3% from 262.5 in 2006 (baseline data for the 2020 Impact Goals on CVD and stroke mortality).
—Death rates attributable to stroke, heart diseases (HDs), and other cardiovascular causes were 42.2, 126.0, and 82.9 per 100 000, respectively.
•
Data from NHANES 2007–2008 reveal that overall, 6.6% of Americans self-reported having some type of CVD (Table 2-3).
—2.8% reported having coronary heart disease
—2.6% reported having a stroke
—2.0% reported having congestive heart failure
—2.7% reported having a heart attack
•
Among those with CVD, risk factor prevalence, awareness, treatment, and control in NHANES 2007 to 2008 were variable (Table 2-3).
—Nearly 48% were current smokers or had quit for <12 months.
—Prevalence of hypertension was estimated to be 45%; 96% were aware of their hypertension, and 89% were treated. Among those with hypertension who were treated, control to goal BP levels of <140/<90 mm Hg was 62%.
—Prevalence of dyslipidemia (defined by total cholesterol ≥240 mg/dL or receiving medication) was 35%; 83% were aware of their dyslipidemia, and 76% were treated. Among those with dyslipidemia who were treated, 85% had total cholesterol <200 mg/dL.
—Prevalence of obesity was 44%, and prevalence of overweight or obesity was 71%.
—Prevalence of DM was 17%; 85% were aware of their DM, and 82% were treated.
—As measured by objective accelerometer data, 74% of adults had intermediate or poor levels of PA; 66% had no moderate or vigorous activity at all.
—70% of US adults without CVD met 0 or only 1 of the 5 healthy dietary metrics.
Prognosis of Ideal Cardiovascular Health
•
Folsom et al2 recently published the first examination of the community prevalence of ideal cardiovascular health and its association with incident CVD events in 12 744 white and African American participants of the ARIC study aged 45 to 64 years at baseline who were followed up for up to 20 years.
—Overall, only 0.1% of participants, and fewer African Americans than whites, had all 7 metrics at ideal levels, consistent with national data.
—There was a stepwise decrease in the 20-year incidence of CVD events (defined as stroke, HF, MI, or fatal coronary disease) with greater numbers of health metrics at ideal levels. Age-, sex-, and race-adjusted CVD incidence rates per 1000 person-years were 32.1, 21.9, 16.0, 12.0, 8.6, 6.4, 3.9, and 0, respectively, for participants with 0, 1, 2, 3, 4, 5, 6, and 7 metrics at ideal levels.
—The corresponding age-, sex-, and race-adjusted hazard ratios (HRs) for incident CVD were 1.0 (reference), 0.65, 0.46, 0.34, 0.24, 0.18, 0.11, and 0 with increasing numbers of ideal health metrics. Thus, 20-year CVD incidence rates for those with 6 ideal health metrics were one-tenth those of participants with 0 ideal health metrics.
—The pattern of outcomes across number of ideal health metrics was similar for African-Americans and whites.
—Importantly, both ideal health behaviors and ideal health factors were associated in a stepwise fashion with lower CVD risk (Chart 2-9).
Implications
•
Taken together, these data continue to indicate the substantial progress that will need to occur for the AHA to achieve its 2020 Impact Goals over the next decade. If the goals can be met, there is evidence suggesting that CVD event rates could decrease significantly.
—To achieve improvements in cardiovascular health, all segments of the population will need to focus on improved cardiovascular health behaviors, in particular with regard to diet and weight, as well as on an increase in PA and further reduction of the prevalence of smoking.
—More children, adolescents, and young adults will need to learn how to preserve their ideal levels of cardiovascular health factors and health behaviors into older ages.
—With regard to reducing the burden of CVD and stroke morbidity and mortality, renewed emphasis will be needed on treatment of acute events and secondary and primary prevention through treatment and control of risk factors.
•
As shown in Table 2-4, relatively modest changes in population levels of health factors could result in important changes in the prevalence of overall and ideal cardiovascular health. For example, NHANES 2007–2008 data indicate that the current prevalence of ideal levels of BP among US adults is 43.8%. A 20% relative improvement by 2020 would mean the prevalence of ideal BP would need to increase to 52.6%. NHANES data indicate that a reduction in the population mean BP by just 2 mm Hg would result in 55.5% of US adults having ideal levels of BP. Further reductions in BP would mean even more people would achieve ideal levels. Such modest reductions could result from decreased salt intake at the population level of as little as 1 to 2 g per day, with significant projected decreases in CVD rates in US adults.3
•
Future issues of the Statistical Update will track progress toward the 2020 Strategic Impact Goals.
References
1.
Lloyd-Jones DM, Hong Y, Labarthe D, Mozaffarian D, Appel LJ, Van Horn L, Greenlund K, Daniels S, Nichol G, Tomaselli GF, Arnett DK, Fonarow GC, Ho PM, Lauer MS, Masoudi FA, Robertson RM, Roger V, Schwamm LH, Sorlie P, Yancy CW, Rosamond WD. Defining and setting national goals for cardiovascular health promotion and disease reduction: the American Heart Association's strategic Impact Goal through 2020 and beyond. Circulation. 2010; 121: 586–613.
2.
Folsom AR, Yatsuya H, Nettleton JA, Lutsey PL, Cushman M, Rosamond WD; ARIC Study Investigators. Community prevalence of ideal cardiovascular health, by the American Heart Association definition, and relationship with cardiovascular disease incidence. J Am Coll Cardiol. 2011; 57: 1690–1696.
3.
Bibbins-Domingo K, Chertow GM, Coxson PG, Moran A, Lightwood JM, Pletcher MJ, Goldman L. Projected effect of dietary salt reductions on future cardiovascular disease. N Engl J Med. 2010; 362: 590–599.
4.
Heron M, Hoyert DL, Murphy SL, Xu J, Kochanek KD, Tejada-Vera B. Deaths: final data for 2006. Natl Vital Stat Rep. 2009; 57: 1–134.
5.
Xu J, Kochanek K, Murphy S, Tejada-Vera B. Deaths: final data for 2007. Natl Vital Stat Rep. 2010; 58: 1–135.
3. Cardiovascular Diseases
ICD-9 390 to 459, 745 to 747, ICD-10 I00 to I99, Q20 to Q28; see Glossary (Chapter 25) for details and definitions. See Tables 3-1 through 3-4 and Charts 3-1 through 3-21.
| AHA | American Heart Association |
| AIDS | acquired immune deficiency syndrome |
| AMI | acute myocardial infarction |
| AP | angina pectoris |
| ARIC | Atherosclerosis Risk in Communities study |
| BMI | body mass index |
| BP | blood pressure |
| BRFSS | Behavioral Risk Factor Surveillance System |
| CABG | cardiac revascularization (coronary artery bypass graft) |
| CAD | coronary artery disease |
| CARDIA | Coronary Artery Risk Development in Young Adults |
| CDC | Centers for Disease Control and Prevention |
| CHD | coronary heart disease |
| CHF | congestive heart failure |
| CHS | Cardiovascular Health Study |
| CLRD | chronic lower respiratory disease |
| CVD | cardiovascular disease |
| DM | diabetes mellitus |
| ED | emergency department |
| FHS | Framingham Heart Study |
| HBP | high blood pressure |
| HD | heart disease |
| HF | heart failure |
| HIV | human immunodeficiency virus |
| ICD-9 | International Classification of Diseases, 9th Revision |
| ICD-10 | International Classification of Diseases, 10th Revision |
| LDL | low-density lipoprotein |
| MEPS | Medical Expenditure Panel Survey |
| MESA | Multi-Ethnic Study of Atherosclerosis |
| MI | myocardial infarction |
| MRFIT | Multiple Risk Factor Intervention Trial |
| NAMCS | National Ambulatory Medical Care Survey |
| NCHS | National Center for Health Statistics |
| NHAMCS | National Hospital Ambulatory Medical Care Survey |
| NHANES | National Health and Nutrition Examination Survey |
| NHDS | National Hospital Discharge Survey |
| NHES | National Health Examination Survey |
| NHIS | National Health Interview Survey |
| NHHCS | National Home and Hospice Care Survey |
| NHLBI | National Heart, Lung, and Blood Institute |
| NIS | National Inpatient Sample |
| NNHS | National Nursing Home Survey |
| PA | physical activity |
| PCI | percutaneous coronary intervention |
| RR | relative risk |
| SBP | systolic blood pressure |
| UA | unstable angina |
| Population Group | Prevalence, 2008—Age ≥20 y | Mortality, 2008—All Ages* | Hospital Discharges, 2009—All Ages | Cost, 2008 |
|---|---|---|---|---|
| Both sexes | 82 600 000 (36.2%) | 811 940 | 6 165 000 | $297.7 Billion |
| Males | 39 900 000 (37.4%) | 392 210 (48.3%)† | 3 230 000 | … |
| Females | 42 700 000 (35.0%) | 419 730 (51.7%)† | 2 935 000 | … |
| NH white males | 37.4% | 335 247 | … | … |
| NH white females | 33.8% | 360 441 | … | … |
| NH black males | 44.8% | 46 819 | … | … |
| NH black females | 47.3% | 49 819 | … | … |
| Mexican American males | 30.7% | … | … | … |
| Mexican American females | 30.9% | … | … | … |
Ellipses (…) indicate data not available; NH, non-Hispanic.
*
Mortality data are for whites and blacks and include Hispanics.
†
These percentages represent the portion of total cardiovascular disease mortality that is attributable to males vs females.
Sources: Prevalence: National Health and Nutrition Examination Survey (NHANES) 2005–2008, National Center for Health Statistics (NCHS) and National Heart, Lung, and Blood Institute (NHLBI). Percentages for racial/ethnic groups are age-adjusted for Americans ≥20 y of age. Age-specific percentages are extrapolated to the 2008 US population estimates. Mortality: NCHS. These data represent underlying cause of death only. Data include congenital cardiovascular disease mortality. Hospital discharges: National Hospital Discharge Survey, NCHS. Data include those inpatients discharged alive, dead, or of unknown status. Cost: NHLBI. Data include estimated direct and indirect costs for 2008.
| State | CVD* | CHD† | Stroke‡ | ||||||
|---|---|---|---|---|---|---|---|---|---|
| Rank§ | Death Rate | % Change 1999–2001 to 2005–2007 | Rank§ | Death Rate | % Change 1999–2001 to 2005–2007 | Rank§ | Death Rate | % Change 1999–2001 to 2005–2007 | |
| Alabama | 51 | 326.9 | −16.0 | 20 | 116.6 | −28.9 | 50 | 56.3 | −19.3 |
| Alaska | 6 | 221.6 | −22.3 | 4 | 87.9 | −31.7 | 35 | 48.1 | −26.1 |
| Arizona | 5 | 217.0 | −24.3 | 25 | 121.5 | −25.7 | 4 | 35.3 | −32.8 |
| Arkansas | 45 | 307.4 | −19.5 | 46 | 159.5 | −14.8 | 51 | 58.0 | −24.8 |
| California | 27 | 252.9 | −23.0 | 33 | 136.3 | −28.7 | 29 | 44.9 | −29.4 |
| Colorado | 4 | 216.1 | −21.8 | 7 | 98.2 | −23.9 | 11 | 40.1 | −29.6 |
| Connecticut | 14 | 229.6 | −23.4 | 14 | 110.1 | −31.4 | 5 | 35.7 | −29.4 |
| Delaware | 28 | 262.2 | −21.8 | 39 | 143.1 | −28.1 | 14 | 41.3 | −21.3 |
| District of Columbia | 50 | 325.6 | −13.4 | 52 | 187.6 | −7.2 | 18 | 42.5 | −11.5 |
| Florida | 12 | 227.7 | −26.4 | 27 | 128.5 | −32.1 | 6 | 35.7 | −27.7 |
| Georgia | 41 | 287.6 | −23.8 | 10 | 107.9 | −33.6 | 44 | 51.5 | −28.5 |
| Hawaii | 2 | 206.0 | −24.3 | 3 | 82.0 | −28.4 | 20 | 43.0 | −31.1 |
| Idaho | 19 | 234.4 | −21.2 | 11 | 108.9 | −26.3 | 38 | 48.9 | −24.8 |
| Illinois | 31 | 264.8 | −23.9 | 29 | 132.8 | −30.8 | 30 | 45.2 | −26.6 |
| Indiana | 39 | 284.7 | −21.6 | 32 | 136.2 | −27.4 | 37 | 48.6 | −28.9 |
| Iowa | 24 | 247.6 | −21.8 | 37 | 140.8 | −24.5 | 25 | 44.5 | −25.7 |
| Kansas | 25 | 252.7 | −20.9 | 15 | 112.4 | −27.4 | 34 | 46.8 | −23.4 |
| Kentucky | 44 | 304.5 | −22.3 | 42 | 149.6 | −25.5 | 42 | 49.6 | −26.7 |
| Louisiana | 47 | 311.0 | −17.9 | 36 | 139.6 | −26.0 | 45 | 52.6 | −19.8 |
| Maine | 18 | 234.2 | −24.3 | 16 | 113.5 | −30.9 | 16 | 41.8 | −27.7 |
| Maryland | 33 | 269.2 | −21.2 | 40 | 144.9 | −23.9 | 22 | 44.0 | −29.6 |
| Massachusetts | 9 | 224.1 | −22.6 | 9 | 106.9 | −27.2 | 10 | 37.9 | −24.7 |
| Michigan | 42 | 293.2 | −20.9 | 45 | 158.0 | −25.4 | 32 | 45.5 | −26.3 |
| Minnesota | 1 | 193.1 | −25.9 | 2 | 80.5 | −33.2 | 12 | 40.1 | −28.8 |
| Mississippi | 52 | 349.7 | −19.3 | 41 | 147.2 | −29.4 | 46 | 53.3 | −25.4 |
| Missouri | 43 | 293.9 | −21.0 | 44 | 154.2 | −25.1 | 43 | 50.4 | −21.6 |
| Montana | 11 | 226.6 | −20.9 | 6 | 97.6 | −21.5 | 19 | 42.7 | −29.2 |
| Nebraska | 17 | 232.8 | −23.0 | 5 | 94.4 | −29.2 | 28 | 44.8 | −22.8 |
| Nevada | 40 | 287.4 | −16.8 | 21 | 117.4 | −29.1 | 17 | 42.3 | −26.8 |
| New Hampshire | 13 | 229.1 | −26.9 | 24 | 120.9 | −33.9 | 2 | 35.2 | −36.8 |
| New Jersey | 25 | 252.2 | −23.7 | 38 | 141.1 | −29.0 | 7 | 35.9 | −23.8 |
| New Mexico | 7 | 222.1 | −19.8 | 17 | 114.7 | −25.0 | 9 | 37.7 | −26.2 |
| New York | 37 | 278.6 | −21.1 | 51 | 182.1 | −23.6 | 1 | 29.6 | −27.1 |
| North Carolina | 34 | 270.4 | −24.4 | 28 | 128.7 | −29.9 | 47 | 53.4 | −30.0 |
| North Dakota | 22 | 241.3 | −20.3 | 30 | 133.5 | −19.6 | 24 | 44.2 | −26.1 |
| Ohio | 38 | 283.2 | −22.0 | 43 | 151.4 | −25.3 | 33 | 46.5 | −23.3 |
| Oklahoma | 49 | 322.4 | −20.6 | 50 | 176.2 | −23.5 | 49 | 54.4 | −20.5 |
| Oregon | 15 | 230.6 | −22.1 | 8 | 98.7 | −26.8 | 40 | 49.3 | −33.1 |
| Pennsylvania | 35 | 271.4 | −22.1 | 34 | 137.9 | −28.0 | 26 | 44.6 | −22.6 |
| Puerto Rico¶ | 8 | 223.5 | −15.9 | 13 | 109.4 | −15.8 | 23 | 44.1 | −15.5 |
| Rhode Island | 29 | 260.4 | −16.8 | 48 | 170.6 | −19.0 | 3 | 35.2 | −26.7 |
| South Carolina | 36 | 274.1 | −25.2 | 23 | 119.8 | −32.3 | 48 | 53.7 | −33.1 |
| South Dakota | 20 | 238.1 | −21.2 | 35 | 137.9 | −17.5 | 31 | 45.4 | −21.9 |
| Tennessee | 48 | 315.3 | −19.4 | 49 | 171.1 | −22.3 | 52 | 58.1 | −23.7 |
| Texas | 32 | 266.9 | −24.0 | 31 | 134.9 | −30.5 | 41 | 49.3 | −25.1 |
| Utah | 3 | 213.2 | −21.3 | 1 | 78.6 | −30.8 | 13 | 40.4 | −34.0 |
| Vermont | 10 | 226.3 | −24.0 | 26 | 121.6 | −26.0 | 8 | 37.1 | −31.2 |
| Virginia | 28 | 254.7 | −23.1 | 19 | 114.8 | −27.4 | 36 | 48.3 | −28.4 |
| Washington | 16 | 232.4 | −22.6 | 22 | 117.5 | −26.0 | 21 | 43.7 | −36.8 |
| West Virginia | 46 | 309.1 | −22.0 | 47 | 160.7 | −27.1 | 39 | 49.2 | −19.9 |
| Wisconsin | 23 | 242.6 | −24.0 | 18 | 114.7 | −29.9 | 27 | 44.7 | −30.3 |
| Wyoming | 21 | 238.7 | −19.4 | 13 | 109.3 | −25.1 | 15 | 41.4 | −29.2 |
| Total United States | 262.7 | −22.6 | 135.1 | −27.7 | 44.1 | −26.9 | |||
CVD indicates cardiovascular disease; CHD, coronary heart disease.
*
CVD is defined here as International Classification of Diseases, 10th Revision (ICD-10) codes I00–I78.
†
CHD is defined here as ICD-10 I20–I25.
‡
Stroke is defined here as ICD-10 I60–I69.
§
Rank is lowest to highest.
¶
Percent changes for Puerto Rico are for 2000 to 2005–2007.
Source: Health Data Interactive, 2005–2007. Data provided by personal communication with the National Heart, Lung, and Blood Institute.
The Agency for Healthcare Research and Quality has released state-level data for heart disease for all 50 states and the District of Columbia. The data are taken from the congressionally mandated National Healthcare Quality Report (NHQR), available at http://statesnapshots.ahrq.gov/snaps07/index.jsp. In addition, the Women's Health and Mortality Chartbook of the National Center for Health Statistics has state-related data for women available at http://www.cdc.gov/nchs/data/healthywomen/womenschartbook_aug2004.pdf. Also, at http://apps.nccd.cdc.gov/brfss-smart/index.asp, Metropolitan/Micropolitan Area Risk (MMSA) data are available for 500 such areas nationwide. Behavioral Risk Factor Surveillance System data are also collected within each state (www.cdc.gov/brfss). The Centers for Disease Control and Prevention (CDC) has the Geographic Information Systems (GIS), which provides mortality rates down to the county level, by sex and ethnicity, available at http://www.cdc.gov/gis/. The 2008 Atlas of Stroke Hospitalizations Among Medicare Beneficiaries (CDC, 2008) is a new resource that provides data down to the county level, by sex and race (available at http://www.cdc.gov/dhdsp/atlas/2008_stroke_atlas/index.htm).
| CVD Deaths | CHD Deaths | Stroke Deaths | Total Deaths | |
|---|---|---|---|---|
| Men ages 35–74 y | ||||
| Russian Federation (2006) | 1299.2 | 706.0 | 351.4 | 2683.4 |
| Bulgaria (2008) | 803.7 | 219.4 | 218.2 | 1554.3 |
| Lithuania (2009) | 734.7 | 444.6 | 138.3 | 1842.3 |
| Romania (2009) | 677.9 | 276.4 | 200.2 | 1572.4 |
| Slovakia (2005) | 634.2 | 320.1 | 91.8 | 1528.3 |
| Hungary (2009) | 605.6 | 319.1 | 121.1 | 1652.3 |
| Poland (2008) | 495.2 | 180.0 | 100.8 | 1412.7 |
| Croatia (2009) | 419.3 | 202.2 | 113.6 | 1184.7 |
| Czech Republic (2009) | 386.6 | 198.6 | 64.4 | 1080.8 |
| Kuwait (2009) | 319.6 | 187.0 | 62.1 | 563.9 |
| Finland (2009) | 284.4 | 170.0 | 43.8 | 833.2 |
| United States (2008) | 256.0 | 149.2 | 30.0 | 862.7 |
| Greece (2009) | 251.6 | 136.7 | 50.8 | 721.6 |
| Germany (2006) | 242.1 | 125.3 | 34.5 | 788.5 |
| Ireland (2009) | 210.0 | 140.6 | 29.2 | 701.3 |
| Belgium (2005) | 209.6 | 99.5 | 35.9 | 821.7 |
| Denmark (2006) | 206.6 | 84.8 | 45.6 | 865.6 |
| New Zealand (2007) | 204.2 | 135.6 | 29.1 | 635.7 |
| United Kingdom (2009) | 202.0 | 125.8 | 29.9 | 687.6 |
| Canada (2004) | 198.3 | 130.8 | 24.2 | 705.3 |
| Austria (2009) | 189.3 | 110.2 | 26.3 | 736.3 |
| Sweden (2008) | 187.8 | 109.4 | 31.0 | 591.8 |
| Portugal (2009) | 168.7 | 61.3 | 62.1 | 825.3 |
| Spain (2008) | 168.2 | 77.6 | 33.7 | 714.0 |
| Italy (2007) | 160.6 | 75.6 | 29.9 | 625.8 |
| Netherlands (2009) | 157.9 | 64.6 | 24.6 | 649.4 |
| Israel (2007) | 156.3 | 86.3 | 32.5 | 655.9 |
| Norway (2009) | 154.4 | 84.6 | 29.0 | 607.0 |
| Switzerland (2007) | 150.4 | 78.2 | 16.6 | 587.5 |
| Japan (2009) | 145.2 | 46.5 | 52.2 | 605.0 |
| France (2007) | 145.0 | 57.1 | 26.5 | 774.6 |
| Australia (2006) | 141.3 | 88.9 | 22.0 | 553.4 |
| Korea, South (2009) | 138.4 | 41.0 | 65.9 | 783.6 |
| Women ages 35–74 y | ||||
| Russian Federation (2006) | 521.4 | 237.1 | 189.2 | 1001.8 |
| Bulgaria (2008) | 368.6 | 70.9 | 120.6 | 699.3 |
| Romania (2009) | 325.5 | 109.5 | 116.2 | 706.0 |
| Slovakia (2005) | 269.5 | 129.5 | 41.9 | 643.7 |
| Lithuania (2009) | 253.9 | 127.5 | 73.8 | 648.6 |
| Kuwait (2009) | 246.1 | 94.8 | 56.1 | 568.1 |
| Hungary (2009) | 239.2 | 113.7 | 56.0 | 719.4 |
| Croatia (2009) | 190.8 | 71.9 | 68.7 | 520.1 |
| Poland (2008) | 181.5 | 51.6 | 50.1 | 570.0 |
| Czech Republic (2009) | 164.3 | 69.9 | 34.8 | 506.6 |
| United States (2008) | 129.2 | 59.5 | 23.5 | 544.7 |
| Denmark (2006) | 100.0 | 32.4 | 32.1 | 557.8 |
| Germany (2006) | 97.8 | 38.2 | 20.1 | 402.4 |
| Greece (2009) | 97.1 | 33.3 | 29.3 | 319.0 |
| Belgium (2005) | 94.4 | 30.8 | 24.8 | 436.3 |
| New Zealand (2007) | 89.8 | 43.9 | 21.7 | 418.2 |
| United Kingdom (2009) | 88.1 | 38.5 | 22.5 | 438.5 |
| Ireland (2009) | 86.8 | 40.9 | 21.9 | 419.8 |
| Finland (2009) | 83.4 | 36.1 | 23.0 | 377.8 |
| Canada (2004) | 83.1 | 42.8 | 17.3 | 432.7 |
| Portugal (2009) | 76.5 | 20.0 | 33.5 | 377.6 |
| Austria (2009) | 75.5 | 33.7 | 16.4 | 368.2 |
| Sweden (2008) | 74.6 | 35.5 | 18.5 | 374.1 |
| Netherlands (2009) | 74.0 | 20.6 | 20.1 | 416.8 |
| Italy (2007) | 67.3 | 22.2 | 18.2 | 326.0 |
| Israel (2007) | 65.4 | 22.2 | 17.3 | 388.7 |
| Korea, South (2009) | 63.5 | 41.0 | 33.2 | 312.3 |
| Spain (2008) | 62.4 | 18.7 | 17.8 | 304.4 |
| Norway (2009) | 60.5 | 26.3 | 15.2 | 377.0 |
| Australia (2006) | 60.4 | 26.8 | 16.3 | 327.5 |
| Japan (2009) | 54.4 | 12.8 | 22.7 | 266.9 |
| Switzerland (2007) | 54.1 | 19.4 | 12.4 | 327.6 |
| France (2007) | 51.3 | 12.1 | 13.9 | 346.0 |
CVD indicates cardiovascular disease; CHD, coronary heart disease.
Rates are adjusted to the European Standard population. International Classification of Diseases, 10th Revision (ICD-10) codes are used for all countries except Greece, for which International Classification of Diseases, 9th Revision (ICD-9) codes are used. For countries using ICD-9, the ICD-9 codes are 390–459 for CVD, 410–414 for CHD, and 430–438 for stroke. ICD-10 codes are I00–I99 for CVD, I20–I25 for CHD, and I60–I69 for stroke.
The following countries have been dropped from the table because data on number of deaths or population are no longer furnished to the World Health Organization: Argentina, China, Colombia, and Mexico.
Sources: The World Health Organization, National Center for Health Statistics, and National Heart, Lung, and Blood Institute.
| Diseases | Remaining Lifetime Risk at Age 40 y | Remaining Lifetime Risk at Age 70 y | ||
|---|---|---|---|---|
| Men | Women | Men | Women | |
| Any CVD* | 2 in 3 | 1 in 2 | 1 in 2 | 1 in 2 |
| CHD6 | 1 in 2 | 1 in 3 | 1 in 3 | 1 in 4 |
| AF23 | 1 in 4 | 1 in 4 | 1 in 4 | 1 in 4 |
| CHF24 | 1 in 5 | 1 in 5 | 1 in 5 | 1 in 5 |
| Stroke25 | 1 in 6† | 1 in 5† | 1 in 6 | 1 in 5 |
| Dementia25 | … | … | 1 in 7 | 1 in 5 |
| Hip fracture38 | 1 in 20 | 1 in 6 | … | … |
| Breast cancer39,42 | 1 in 1000 | 1 in 8 | … | 1 in 14 |
| Prostate cancer39 | 1 in 6 | … | … | … |
| Lung cancer39 | 1 in 12 | 1 in 17 | … | … |
| Colon cancer39 | 1 in 16 | 1 in 17 | … | … |
| Diabetes43 | 1 in 3 | 1 in 3 | 1 in 9 | 1 in 7 |
| Hypertension44 | 9 in 10† | 9 in 10† | 9 in 10‡ | 9 in 10‡ |
| Obesity45 | 1 in 3 | 1 in 3 | … | … |
CVD indicates cardiovascular disease; ellipses (…), not estimated; CHD, coronary heart disease; AF, atrial fibrillation; and CHF, congestive heart failure.
*
Personal communication from Donald Lloyd-Jones, based on Framingham Heart Study data.
†
Age 55 y.
‡
Age 65 y.
Prevalence
An estimated 82 600 000 American adults (>1 in 3) have 1 or more types of CVD. Of these, 40 400 000 are estimated to be ≥60 years of age. Total CVD includes diseases listed in the bullet points below, with the exception of congenital CVD. Because of overlap across conditions, it is not possible to add these conditions to arrive at a total.
•
High BP (HBP)—76 400 000 (defined as systolic pressure ≥140 mm Hg and/or diastolic pressure ≥90 mm Hg, use of antihypertensive medication, or being told at least twice by a physician or other health professional that one has HBP).
•
Coronary heart disease (CHD)—16 300 000
—MI (heart attack)—7 900 000
—AP (chest pain)—9 000 000
—HF—5 700 000
—Stroke (all types)—7 000 000
—Congenital cardiovascular defects—650 000 to 1 300 000
•
The following age-adjusted prevalence estimates from the NHIS, NCHS are for diagnosed conditions for people ≥18 years of age in 20101:
—Among whites only, 11.7% have HD, 6.4% have CHD, 23.6% have hypertension, and 2.5% have had a stroke.
—Among blacks or African Americans, 10.9% have HD, 6.3% have CHD, 33.8% have hypertension, and 3.9% have had a stroke.
—Among Hispanics or Latinos, 8.1% have HD, 5.2% have CHD, 22.5% have hypertension, and 2.6% have had a stroke.
—Among Asians, 7.2% have HD, 4.9% have CHD, 20.5% have hypertension, and 2.0% have had a stroke.
—Among American Indians or Alaska Natives, 12.5% have HD, 5.9% have CHD, 30.0% have hypertension, and 5.9% have had a stroke (estimate considered unreliable). Among Native Hawaiians or other Pacific Islanders, 20.2% have HD, 19.7% have CHD, 40.8% have hypertension, and 10.6% have had a stroke.
•
Asian Indian adults (9%) are ≈2-fold more likely than Korean adults (4%) to have ever been told they have HD, based on data for 2004 to 2006.2
•
By 2030, 40.5% of the US population is projected to have some form of CVD.3
Incidence
•
On the basis of the NHLBI's FHS original and offspring cohort data from 1980 to 20034:
—The average annual rates of first cardiovascular events rise from 3 per 1000 men at 35 to 44 years of age to 74 per 1000 men at 85 to 94 years of age. For women, comparable rates occur 10 years later in life. The gap narrows with advancing age.
—Before 75 years of age, a higher proportion of CVD events attributable to CHD occur in men than in women, and a higher proportion of events attributable to stroke occur in women than in men.
•
Among American Indian men 45 to 74 years of age, the incidence of CVD ranges from 15 to 28 per 1000 population. Among women, it ranges from 9 to 15 per 1000.5
•
Data from the FHS indicate that the subsequent lifetime risk for all CVD in recipients starting free of known disease is 2 in 3 for men and >1 in 2 for women at 40 years of age (personal communication, Donald Lloyd-Jones, MD, Northwestern University, Chicago, IL; Table 3-4).
•
Analysis of FHS data among participants free of CVD at 50 years of age showed the lifetime risk for developing CVD was 51.7% for men and 39.2% for women. Median overall survival was 30 years for men and 36 years for women.6
Mortality
ICD-10 I00 to I99, Q20 to Q28 for CVD (CVD mortality includes congenital cardiovascular defects); C00 to C97 for cancer; C33 to C34 for lung cancer; C50 for breast cancer; J40 to J47 for chronic lower respiratory disease (CLRD); G30 for Alzheimer disease; E10 to E14 for DM; and V01 to X59, Y85 to Y86 for accidents.
•
Mortality data show that CVD (I00–I99, Q20–Q28) as the listed underlying cause of death (including congenital cardiovascular defects) accounted for 32.8% (811 940) of all 2 471 984 deaths in 2008, or 1 of every 3 deaths in the United States. CVD any-mentions (1 354 527 deaths in 2008) constituted 55.0% of all deaths that year (NHLBI; NCHS public-use data files).7
•
•
On average, >2200 Americans die of CVD each day, an average of 1 death every 39 seconds. CVD currently claims more lives each year than cancer, CLRD, and accidents combined.7
•
The 2008 death rate attributable to CVD (I00–I99) was 244.8 (excluding congenital cardiovascular defects) (NCHS).7 The rates were 287.2 for white males, 390.4 for black males, 200.5 for white females, and 277.4 for black females. From 1998 to 2008, death rates attributable to CVD (ICD-10 I00–I99) declined 30.6%. In the same 10-year period, the actual number of CVD deaths per year declined 14.1% (NHLBI tabulation).7 (Appropriate comparability ratios were applied.)
•
Among other causes of death in 2008, cancer caused 565 469 deaths; CLRD, 141 090; accidents, 121 902; and Alzheimer disease, 82 435.7
•
The 2008 CVD (I00–I99) death rates were 292.6 for males and 206.1 for females. There were 40 589 deaths due to breast cancer in females in 2008; lung cancer claimed 70 070 in females. Death rates for females were 22.5 for breast cancer and 39.0 for lung cancer. One in 31 deaths in females was attributable to breast cancer, whereas 1 in 6.6 was attributable to CHD. For comparison, 1 in 4.6 females died of cancer, whereas 1 in 3.0 died of CVD (I00–I99, Q20–Q28). On the basis of 2008 mortality data, CVD caused ≈1 death per minute among females, or 419 730 deaths in females in 2008. That represents more female lives than were claimed by cancer, CLRD, and Alzheimer disease combined (unpublished NHLBI tabulation).7
•
About 150 000 Americans died of CVD (I00–I99) in 2008 who were <65 years of age, and 33% of deaths attributed to CVD occurred before the age of 75 years, which is well below the average life expectancy of 77.9 years.7
•
According to the NCHS, if all forms of major CVD were eliminated, life expectancy could rise by almost 7 years. If all forms of cancer were eliminated, the estimated gain could be 3 years. According to the same study, the probability at birth of eventually dying of major CVD (I00–I78) is 47%, and the chance of dying of cancer is 22%. Additional probabilities are 3% for accidents, 2% for DM (unrelated to CVD), and 0.7% for HIV.10
•
In 2008, the leading causes of death in women ≥65 years of age were diseases of the heart (No. 1), cancer (No. 2), stroke (No. 3), and CLRD (No. 4). In older men, they were diseases of the heart (No. 1), cancer (No. 2), CLRD (No. 3), and stroke (No. 4).7
•
A study of the decrease in US deaths attributable to CHD from 1980 to 2000 suggests that ≈47% of the decrease was attributable to increased use of evidence-based medical therapies and 44% to changes in risk factors in the population attributable to lifestyle and environmental changes.11
•
Analysis of data from NCHS was used to determine the number of disease-specific deaths attributable to all nonoptimal levels of each risk factor exposure, by age and sex. In 2005, tobacco smoking and HBP were estimated to be responsible for 467 000 deaths, accounting for ≈1 in 5 or 6 deaths among US adults. Overweight/obesity and physical inactivity were each estimated to be responsible for nearly 1 in 10 deaths. High dietary salt, low dietary omega-3 fatty acids, and high dietary trans fatty acids were the dietary risks with the largest estimated excess mortality effects.12
Aftermath
•
Among an estimated 45 million people with functional disabilities in the United States, HD, stroke, and hypertension are among the 15 leading conditions that caused those disabilities. Disabilities were defined as difficulty with activities of daily living or instrumental activities of daily living, specific functional limitations (except vision, hearing, or speech), and limitation in ability to do housework or work at a job or business.13
Awareness of Warning Signs and Risk Factors for CVD
•
Surveys conducted by the AHA in 1997, 2000, 2003, and 2006 to evaluate trends in women's awareness, knowledge, and perceptions related to CVD found that in 2006, awareness of HD as the leading cause of death among women was 57%, significantly higher than in prior surveys. Awareness was lower among black and Hispanic women than among white women, and the racial/ethnic difference has not changed appreciably over time. In 2006, more than twice as many women felt uninformed about stroke compared with HD. Hispanic women were more likely than white women to report that there is nothing they can do to keep themselves from getting CVD. The majority of respondents reported confusion related to basic CVD prevention strategies.14
•
A nationally representative sample of women responded to a questionnaire about history of CVD risk factors, self-reported actions taken to reduce risk, and barriers to heart health. According to the study, published in 2006, the rate of awareness of CVD as the leading cause of death had nearly doubled since 1997, was significantly greater for whites than for blacks and Hispanics, and was independently correlated with increased PA and weight loss in the previous year. Fewer than half of the respondents were aware of healthy levels of risk factors. Awareness that their personal level was not healthy was positively associated with preventive action. Most women took steps to lower risk in family members and themselves.15
•
A total of 875 students in 4 Michigan high schools were given a survey to obtain data on the perception of risk factors and other knowledge-based assessment questions about CVD. Accidents were rated as the greatest perceived lifetime health risk (39%). Nearly 17% selected CVD as the greatest lifetime risk, which made it the third most popular choice after accidents and cancer. When asked to identify the greatest cause of death for each sex, 42% correctly recognized CVD for men, and 14% correctly recognized CVD for women; 40% incorrectly chose abuse/use behavior with a substance other than cigarettes as the most important CVD risk behavior.16
Awareness of Cardiopulmonary Resuscitation
•
Seventy-nine percent of the lay public are confident that they know what actions to take in a medical emergency; 98% recognize an automated external defibrillator as something that administers an electric shock to restore a normal heart beat among victims of sudden cardiac arrest; and 60% are familiar with cardiopulmonary resuscitation (Harris Interactive survey conducted on behalf of the AHA among 1132 US residents ≥18 years of age, January 8, 2008, through January 21, 2008).
Risk Factors
•
Data from the 2003 CDC BRFSS survey of adults ≥18 years of age showed the prevalence of respondents who reported having ≥2 risk factors for HD and stroke was successively higher at higher age groups. The prevalence of having ≥2 risk factors was highest among blacks (48.7%) and American Indian/Alaska Natives (46.7%) and lowest among Asians (25.9%); prevalence was similar in women (36.4%) and men (37.8%). The prevalence of multiple risk factors ranged from 25.9% among college graduates to 52.5% among those with less than a high school diploma (or its equivalent). People reporting household income of ≥$50 000 had the lowest prevalence (28.8%), and those reporting household income of <$10 000 had the highest prevalence (52.5%). Adults who reported being unable to work had the highest prevalence (69.3%) of ≥2 risk factors, followed by retired people (45.1%), unemployed adults (43.4%), homemakers (34.3%), and employed people (34.0%). Prevalence of ≥2 risk factors varied by state/territory and ranged from 27.0% (Hawaii) to 46.2% (Kentucky). Twelve states and 2 territories had a multiple risk factor prevalence of ≥40%: Alabama, Arkansas, Georgia, Indiana, Kentucky, Louisiana, Mississippi, North Carolina, Ohio, Oklahoma, Tennessee, West Virginia, Guam, and Puerto Rico.17
•
Data from the Chicago Heart Association Detection Project (1967–1973, with an average follow-up of 31 years) showed that in younger women (18–39 years of age) with favorable levels for all 5 major risk factors (BP, serum cholesterol, body mass index [BMI], DM, and smoking), future incidence of CHD and CVD is rare, and long-term and all-cause mortality are much lower than for those who have unfavorable or elevated risk factor levels at young ages. Similar findings applied to men in this study.18,19
•
Analysis of several data sets by the CDC showed that in adults ≥18 years of age, disparities were common in all risk factors examined. In men, the highest prevalence of obesity (29.7%) was found in Mexican Americans who had completed a high school education. Black women with or without a high school education had a high prevalence of obesity (48.4%). Hypertension prevalence was high among blacks (41.2%) regardless of sex or educational status. Hypercholesterolemia was high among white and Mexican American men and white women regardless of educational status. CHD and stroke were inversely related to education, income, and poverty status. Hospitalization for total HD and acute MI (AMI) was greater among men, but hospitalization for congestive heart failure (CHF) and stroke was greater among women. Among Medicare enrollees, CHF hospitalization was higher among blacks, Hispanics, and American Indian/Alaska Natives than among whites, and stroke hospitalization was highest among blacks. Hospitalizations for CHF and stroke were highest in the southeastern United States. Life expectancy remains higher in women than in men and in whites than in blacks by ≈5 years. CVD mortality at all ages tended to be highest in blacks.20
•
Analysis of 5 cross-sectional, nationally representative surveys from the National Health Examination Survey (NHES) 1960 to 1962 to the NHANES 1999 to 2000 showed that the prevalence of key risk factors (ie, high cholesterol, HBP, current smoking, and total DM) decreased over time across all BMI groups, with the greatest reductions observed among overweight and obese groups. Total DM prevalence was stable within BMI groups over time; however, the trend has leveled off or been reversed for some of the risk factors in more recent years.21
•
Data from BRFSS 2006 to 2008 demonstrated that during this 3-year period, 25.6% of non-Hispanic blacks, non-Hispanic whites, and Hispanics were obese, but prevalent obesity varied across groups: 35.7% for non-Hispanic blacks, 28.7% for Hispanics, and 23.7% for non-Hispanic whites.
•
Data from NHANES 2005 to 2006 showed that 90.4% of US adults exceeded their recommended target limit of daily dietary sodium intake.22
•
Analysis of >14 000 middle-aged subjects in the ARIC study sponsored by the NHLBI showed that >90% of CVD events in black subjects, compared with ≈70% in white subjects, appeared to be explained by elevated or borderline risk factors. Furthermore, the prevalence of participants with elevated risk factors was higher in black subjects; after accounting for education and known CVD risk factors, the incidence of CVD was identical in black and white subjects. Thus, the observed higher CVD incidence rate in black subjects appears to be largely attributable to a greater prevalence of elevated risk factors. These results suggest that the primary prevention of elevated risk factors might substantially impact the future incidence of CVD, and these beneficial effects would likely be applicable not only for white but also for black subjects.23
•
Data from the MEPS 2004 Full-Year Data File showed that nearly 26 million US adults ≥18 years of age were told by a doctor that they had HD, stroke, or any other heart-related disease24:
—38.6% maintained a healthy weight. Among those told that they had HD, 33.9% had a healthy weight compared with 39.3% who had never been told they had HD.
—78.8% did not currently smoke. Among those ever told that they had indicators of HD, 18.3% continued to smoke.
—More than 93% engaged in at least 1 recommended behavior for prevention of HD: 75.5% engaged in 1 or 2; 18% engaged in all 3; and 6.5% did not engage in any of the recommended behaviors.
—Age-based variations:
○Moderate to vigorous PA ≥3 times per week varied according to age. Younger people (18–44 years of age) were more likely (59.9%) than those who were older (45–64 and ≥65 years of age, 55.3% and 48.5%, respectively) to engage in regular PA.
○A greater percentage of those 18 to 44 years of age had a healthy weight (43.7%) than did those 45 to 64 years of age and ≥65 years of age (31.4% and 37.3%, respectively).
○People ≥65 years of age were more likely to be current nonsmokers (89.7%) than were people 18 to 44 years of age and 45 to 64 years of age (76.1% and 77.7%, respectively).
—Race/ethnicity-based variations:
○Non-Hispanic whites were more likely than Hispanics or non-Hispanic blacks to engage in moderate-to-vigorous PA (58.5% versus 51.4% and 52.5%, respectively).
○Non-Hispanic whites were more likely to have maintained a healthy weight than were Hispanics or non-Hispanic blacks (39.8% versus 32.1% and 29.7%, respectively).
○Hispanics were more likely to be nonsmokers (84.2%) than were non-Hispanic whites and non-Hispanic blacks (77.8% and 76.3%, respectively).
—Sex-based variations:
○Men were more likely to have engaged in moderate-to-vigorous PA ≥3 times per week than women (60.3% versus 53.1%, respectively).
○Women were more likely than men to have maintained a healthy weight (45.1% versus 31.7%, respectively).
○81.7% of women did not currently smoke, compared with 75.7% of men.
—Variations based on education level:
○A greater percentage of adults with at least some college education engaged in moderate-to-vigorous PA ≥3 times per week (60.8%) than did those with a high school education or less than a high school education (55.3% and 48.3%, respectively).
○A greater percentage of adults with at least some college education had a healthy weight (41.2%) than did those with a high school or less than high school education (36.2% and 36.1%, respectively).
○There was a greater percentage of nonsmokers among those with a college education (85.5%) than among those with a high school or less than high school education (73.8% and 69.9%, respectively).
•
Participants (18–64 years of age at baseline) in the Chicago Heart Association Detection Project in Industry without a history of MI were investigated to determine whether traditional CVD risk factors were similarly associated with CVD mortality in black and white men and women. In general, the magnitude and direction of associations were similar by race. Most traditional risk factors demonstrated similar associations with mortality in black and white adults of the same sex. Small differences were primarily in the strength and not the direction of the association.25
•
A study of nearly 1500 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) study found that Hispanics with hypertension, hypercholesterolemia, and/or DM who speak Spanish at home and/or have spent less than half a year in the United States have higher systolic BP (SBP), low-density lipoprotein (LDL) cholesterol, and fasting blood glucose, respectively, than Hispanics who speak English and who have lived a longer period of time in the United States.26
Family History of CVD
•
A family history of CVD increases risk of CVD, with the largest increase in risk if the family member's CVD was premature.27
•
There is consistent evidence from multiple large-scale prospective epidemiology studies for a strong and significant association of a reported family history of premature parental CHD with incident MI or CHD in offspring. In the FHS, the occurrence of a validated premature atherosclerotic CVD event in either a parent28 or a sibling29 was associated with an ≈2-fold elevated risk for CVD, independent of other traditional risk factors.
•
Addition of family history of premature CVD to a model that contained traditional risk factors provided modestly improved prognostic value in the FHS.28 Family history of premature MI is also an independent risk factor in other multivariable risk models that contain traditional risk factors in large cohorts of women30 and men.31
•
•
In the FHS, a parental history of validated HF is associated with a 1.7-fold higher risk of HF in offspring, after multivariable adjustment.34
•
A family history of early-onset sudden cardiac death in a first-degree relative is associated with a >2-fold higher risk for sudden cardiac death in offspring on the basis of available case-control studies.35
•
The 2004 HealthStyles survey of 4345 people in the United States indicated that most respondents believe that knowing their family history is important for their own health, but few are aware of the specific health information from relatives necessary to develop a family history.36
•
An accurate and complete family history may identify rare mendelian conditions such as hypertrophic cardiomyopathy (HCM), long-QT syndrome, or familial hypercholesterolemia. However, in the majority of people with a family history of a CVD event, a known rare mendelian condition is not identified.
•
Studies are under way to determine genetic variants that may help identify individuals at increased risk of CVD.
Impact of Healthy Lifestyle and Low Risk Factor Levels
Much of the literature on CVD has focused on factors associated with increasing risk for CVD and on factors associated with poorer outcomes in the presence of CVD; however, in recent years, a number of studies have defined the potential beneficial effects of healthy lifestyle factors and lower CVD risk factor burden on CVD outcomes and longevity. These studies suggest that prevention of risk factor development at younger ages may be the key to “successful aging,” and they highlight the need for evaluating the potential benefits of intensive prevention efforts at younger and middle ages once risk factors develop to increase the likelihood of healthy longevity.
•
The lifetime risk for CVD and median survival were highly associated with risk factor presence and burden at 50 years of age among >7900 men and women from the FHS followed up for 111 000 person-years. In this study, optimal risk factor burden at 50 years of age was defined as BP <120/80 mm Hg, total cholesterol <180 mg/dL, absence of DM, and absence of smoking. Elevated risk factors were defined as stage 1 hypertension or borderline high cholesterol (200–239 mg/dL). Major risk factors were defined as stage 2 hypertension, elevated cholesterol (≥240 mg/dL), current smoking, and DM. Remaining lifetime risks for atherosclerotic CVD events were only 5.2% in men and 8.2% in women with optimal risk factors at 50 years of age compared with 68.9% in men and 50.2% in women with ≥2 major risk factors at age 50. In addition, men and women with optimal risk factors had a median life expectancy ≥10 years longer than those with ≥2 major risk factors at age 50 years.6
•
A recent study examined the association between low lifetime predicted risk for CVD (ie, having all optimal or near-optimal risk factor levels) and burden of subclinical atherosclerosis in younger adults in the Coronary Artery Risk Development in Young Adults (CARDIA) and MESA studies of the NHLBI. Among participants <50 years of age, nearly half had low and half had high predicted lifetime risks for CVD. Those with low predicted lifetime risk had lower prevalence and less severe amounts of coronary calcification and less carotid intima-media thickening, even at these younger ages, than those with high predicted lifetime risk. During follow-up, those with low predicted lifetime risk also had less progression of coronary calcium.37
•
In another study, FHS investigators followed up 2531 men and women who were examined between the ages of 40 and 50 years and observed their overall rates of survival and survival free of CVD to 85 years of age and beyond. Low levels of the major risk factors in middle age were associated with overall survival and morbidity-free survival to ≥85 years of age.38
—Overall, 35.7% survived to the age of 85 years, and 22% survived to that age free of major morbidities.
—Factors associated with survival to the age of 85 years included female sex, lower SBP, lower total cholesterol, better glucose tolerance, absence of current smoking, and higher level of education attained. Factors associated with survival to the age of 85 years free of MI, unstable angina (UA), HF, stroke, dementia, and cancer were nearly identical.
—When adverse levels of 4 of these factors were present in middle age, <5% of men and ≈15% of women survived to 85 years of age.
•
A study of 366 000 men and women from the Multiple Risk Factor Intervention Trial (MRFIT) and Chicago Heart Association Detection Project in Industry defined low-risk status as follows: Serum cholesterol level <200 mg/dL, untreated BP 120/80 mm Hg, absence of current smoking, absence of DM, and absence of major electrocardiographic abnormalities. Compared with those who did not have low risk factor burden, those with low risk factor burden had between 73% and 85% lower relative risk (RR) for CVD mortality, 40% to 60% lower relative total mortality rates, and 6 to 10 years' longer life expectancy.19
•
A study of 84 129 women enrolled in the Nurses' Health Study identified 5 healthy lifestyle factors, including absence of current smoking, drinking half a glass or more of wine per day (or equivalent alcohol consumption), half an hour or more per day of moderate or vigorous PA, BMI <25 kg/m2, and dietary score in the top 40% (which included diets with lower amounts of trans fats, lower glycemic load, higher cereal fiber, higher marine omega-3 fatty acids, higher folate, and higher polyunsaturated-to-saturated fat ratio). When 3 of the 5 healthy lifestyle factors were present, the RR for CHD over a 14-year period was 57% lower; when 4 were present, RR was 66% lower; and when all 5 factors were present, RR was 83% lower.39 However, data from NHANES 1999 to 2002 showed that only about one third of adults complied with ≥6 of the recommended heart-healthy behaviors. Dietary recommendations, in general, and daily fruit intake recommendations, in particular, were least likely to be followed.40
•
In the Chicago Heart Association Detection Project in Industry, remaining lifetime risks for CVD death were noted to increase substantially and in a graded fashion according to the number of risk factors present in middle age (40–59 years of age). However, remaining lifetime risks for non-CVD death also increased dramatically with increasing CVD risk factor burden. These data help to explain the markedly greater longevity experienced by those who reach middle age free of major CVD risk factors.41
•
Among individuals 70 to 90 years of age, adherence to a Mediterranean-style diet and greater PA are associated with 65% to 73% relatively lower rates of all-cause mortality, as well as lower mortality rates attributable to CHD, CVD, and cancer.42
•
Seventeen-year mortality data from the NHANES II Mortality Follow-Up Study indicated that the RR for fatal CHD was 51% lower for men and 71% lower for women with none of 3 major risk factors (hypertension, current smoking, and elevated total cholesterol [≥ 240 mg/dL]) than for those with ≥1 risk factors. Had all 3 major risk factors not occurred, it is hypothesized that 64% of all CHD deaths among women and 45% of CHD deaths in men could theoretically have been avoided.43
•
Investigators from the Chicago Heart Association Detection Project in Industry have also observed that risk factor burden in middle age is associated with better quality of life at follow-up in older age (≈25 years later) and lower average annual Medicare costs at older ages.
•
The presence of a greater number of risk factors in middle age is associated with lower scores at older ages on assessment of social functioning, mental health, walking, and health perception in women, with similar findings in men.44
•
Similarly, the existence of a greater number of risk factors in middle age is associated with higher average annual CVD-related and total Medicare costs (once Medicare eligibility is attained).45
Hospital Discharges, Ambulatory Care Visits, and Nursing Home Residents
•
From 1999 to 2009, the number of inpatient discharges from short-stay hospitals with CVD as the first-listed diagnosis decreased from 6 344 000 to 6 165 000 (NHDS, NCHS, and NHLBI). In 2009, CVD ranked highest among all disease categories in hospital discharges (NHDS, NCHS, and NHLBI).
•
In 2009, there were 94 871 000 physician office visits with a primary diagnosis of CVD (NCHS, NAMCS, NHLBI tabulation). In 2009, there were 4 761 000 ED visits and 7 261 000 hospital outpatient department visits with a primary diagnosis of CVD (NCHS, NHAMCS, NHLBI tabulation).
•
In 2005, ≈1 of every 6 hospital stays, or almost 6 million, resulted from CVD (Agency for Healthcare Research and Quality, NIS). The total inpatient hospital cost for CVD was $71.2 billion, approximately one fourth of the total cost of inpatient hospital care in the United States. The average cost per hospitalization was ≈41% higher than the average cost for all stays. Hospital admissions that originated in the ED accounted for 60.7% of all hospital stays for CVD. This was 41% higher than the rate of 43.1% for all types of hospital stays; 3.3% of patients admitted to the hospital for CVD died in the hospital, which was significantly higher than the average in-hospital death rate of 2.1% for all hospitalized patients.46
•
In 2004, coronary artery disease (CAD) was estimated to be responsible for 1.2 million hospital stays and was the most expensive condition treated. This condition resulted in >$44 billion in expenses. More than half of the hospital stays for CAD were among patients who also received percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) during their stay. AMI resulted in $31 billion of inpatient hospital charges for 695 000 hospital stays. The 1.1 million hospitalizations for CHF amounted to nearly $29 billion in hospital charges.47
•
In 2003, ≈48.3% of inpatient hospital stays for CVD were for women, who accounted for 42.8% of the national cost ($187 billion) associated with these conditions. Although only 40% of hospital stays for AMI and CAD were for women, more than half of all stays for nonspecific chest pain, CHF, and stroke were for women. There was no difference between men and women in hospitalizations for cardiac dysrhythmias.48
•
Circulatory disorders were the most frequent reason for admission to the hospital through the ED, accounting for 26.3% of all admissions through the ED. After pneumonia, the most common heart-related conditions (in descending order) were CHF, chest pain, hardening of the arteries, and heart attack, which together accounted for >15% of all admissions through the ED. Stroke and irregular heart beat ranked seventh and eighth, respectively.49
•
In 2004, 23.7% of nursing home residents had a primary diagnosis of CVD at admission, and 25% had CVD as the primary diagnosis at the time of interview. This was the leading primary diagnosis for these residents (NCHS, NNHS).49
•
Among current home healthcare patients in 2007, 18.3% had a primary diagnosis of CVD at admission and 62.9% had any diagnosis of CVD at the time of interview (NCHS, NHHCS unpublished data).
•
Among patients discharged from hospice in 2007, 15.8% had a primary diagnosis of CVD at admission (NCHS, NHHCS unpublished data).
Operations and Procedures
•
In 2009, an estimated 7 453 000 inpatient cardiovascular operations and procedures were performed in the United States; 4.2 million were performed on males, and 3.3 million were performed on females (NHLBI tabulation of NHDS, NCHS).
Cost
•
The estimated direct and indirect cost of CVD for 2008 is $297.7 billion (MEPS, Agency for Healthcare Research and Quality, and NHLBI).
•
In 2006, $32.7 billion in program payments were made to Medicare beneficiaries discharged from short-stay hospitals with a principal diagnosis of CVD. That was an average of $10 201 per discharge.50
•
Between 2010 and 2030, real (2008$) total direct medical costs of CVD are projected to triple, from $273 billion to $818 billion.3
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4. Subclinical Atherosclerosis
| ABI | ankle-brachial index |
| ARIC | Atherosclerosis Risk in Communities study |
| BMI | body mass index |
| BP | blood pressure |
| CAC | coronary artery calcification |
| CAD | coronary artery disease |
| CARDIA | Coronary Artery Risk Development in Young Adults |
| CHD | coronary heart disease |
| CHS | Cardiovascular Health Study |
| CT | computed tomography |
| CVD | cardiovascular disease |
| DBP | diastolic blood pressure |
| DM | diabetes mellitus |
| FHS | Framingham Heart Study |
| FMD | flow-mediated dilation |
| FRS | Framingham Risk Score |
| HDL | high-density lipoprotein |
| HD | heart disease |
| HR | hazard ratio |
| IMT | intima-media thickness |
| LDL | low-density lipoprotein |
| MESA | Multi-Ethnic Study of Atherosclerosis |
| NHLBI | National Heart, Lung, and Blood Institute |
| RR | relative risk |
| SBP | systolic blood pressure |
| Age, y | 75th Percentile CAC Scores* | |||
|---|---|---|---|---|
| Black | Chinese | Hispanic | White | |
| Women | ||||
| 45 | 0 | 0 | 0 | 0 |
| 55 | 0 | 2 | 0 | 1 |
| 65 | 26 | 45 | 19 | 54 |
| 75 | 138 | 103 | 116 | 237 |
| Men | ||||
| 45 | 0 | 3 | 0 | 0 |
| 55 | 15 | 34 | 27 | 68 |
| 65 | 95 | 121 | 141 | 307 |
| 75 | 331 | 229 | 358 | 820 |
CAC indicates coronary artery calcification.
*
The 75th percentile CAC score is the score at which 75% of people of the same age, sex, and race have a score at or below this level, and 25% of people of the same age, sex, and race have a higher score. (Source: Multi-Ethnic Study of Atherosclerosis CAC Tools Web site: http://www.mesa-nhlbi.org/Calcium/input.aspx.)
Atherosclerosis, a systemic disease process in which fatty deposits, inflammation, cells, and scar tissue build up within the walls of arteries, is the underlying cause of the majority of clinical cardiovascular events. Individuals who develop atherosclerosis tend to develop it in a number of different types of arteries (large and small arteries and those feeding the heart, brain, kidneys, and extremities), although they may have much more in some parts of the body than others. In recent decades, advances in imaging technology have allowed for improved ability to detect and quantify atherosclerosis at all stages and in multiple different vascular beds. Two modalities, computed tomography (CT) of the chest for evaluation of coronary artery calcification (CAC) and B-mode ultrasound of the neck for evaluation of carotid artery intima-media thickness (IMT), have been used in large studies with outcomes data and may help define the burden of atherosclerosis in individuals before they develop clinical events such as heart attack or stroke. Another commonly used method for detecting and quantifying atherosclerosis in the peripheral arteries is the ankle-brachial index (ABI), which is discussed in Chapter 11. Data on cardiovascular outcomes are starting to emerge for additional modalities that measure anatomic and functional measures of subclinical disease, including brachial artery reactivity testing, aortic and carotid magnetic resonance imaging, and tonometric methods of measuring vascular compliance or microvascular reactivity. Further research may help to define the role of these techniques in cardiovascular risk assessment. Some guidelines have recommended screening for subclinical atherosclerosis, especially by CAC, or IMT may be appropriate in people at intermediate risk for HD (eg, 10-year estimated risk of 10% to 20%) but not for lower-risk general population screening or for people with preexisting HD or most other high-risk conditions.1,2 However, a recent guideline notes those with DM who are ≥40 years of age may be suitable for screening of risk by coronary calcium. There are still limited data demonstrating whether screening with these and other imaging modalities can improve patient outcomes or whether it only increases downstream medical care costs. A recently published report in a large cohort randomly assigned to coronary calcium screening or not showed such screening to result in an improved risk factor profile without increasing downstream medical costs.3
Coronary Artery Calcification
Background
•
CAC is a measure of the burden of atherosclerosis in the heart arteries and is measured by CT. Other components of the atherosclerotic plaque, including fatty (eg, cholesterol-rich components) and fibrotic components, often accompany CAC and may be present even in the absence of CAC.
•
The presence of any CAC, which indicates that at least some atherosclerotic plaque is present, is defined by an Agatston score >0. Clinically significant plaque, frequently an indication for more aggressive risk factor management, is often defined by an Agatston score ≥100 or a score ≥75th percentile for one's age and sex. An Agatston score ≥400 has been noted to be an indication for further diagnostic evaluation (eg, exercise testing or myocardial perfusion imaging) for CAD.
Prevalence
•
The NHLBI's FHS reported CAC measured in 3238 white adults in age groups ranging from <45 years of age to ≥75 years of age.4
—Overall, 32.0% of women and 52.9% of men had prevalent CAC.
—Among participants at intermediate risk according to Framingham Risk Score (FRS), 58% of women and 67% of men had prevalent CAC.
•
The NHLBI's CARDIA study measured CAC in 3043 black and white adults 33 to 45 years of age (at the CARDIA year 15 examination).5
—Overall, 15.0% of men and 5.1% of women, 5.5% of those 33 to 39 years of age and 13.3% of those 40 to 45 years of age, had prevalent CAC. Overall, 1.6% of participants had an Agatston score that exceeded 100.
—Chart 4-1 shows the prevalence of CAC by ethnicity and sex. The prevalence of CAC was lower in black men than in white men but was similar in black and white women at these ages.
•
The NHLBI's MESA study measured CAC in 6814 participants 45 to 84 years of age, including white (n=2619), black (n=1898), Hispanic (n=1494), and Chinese (n=803) men and women.6
—Chart 4-2 shows the prevalence of CAC by sex and ethnicity.
—The prevalence and 75th percentile levels of CAC were highest in white men and lowest in black and Hispanic women. Significant ethnic differences persisted after adjustment for risk factors, with the RR of coronary calcium being 22% less in blacks, 15% less in Hispanics, and 8% less in Chinese than in whites.
—Table 4-1 shows the 75th percentile levels of CAC by sex and race at selected ages. These might be considered cut points above which more aggressive efforts to control risk factors (eg, elevated cholesterol or BP) could be implemented and/or at which treatment goals might be more aggressive (eg, LDL cholesterol <100 mg/dL instead of <130 mg/dL).
•
The prevalence of CAC varies widely according to FRS. In a report from the MESA study,7 the prevalence of CAC among individuals with very low FRS (10-year risk <5%) was low. These findings may have important implications for population screening for subclinical atherosclerosis.
•
Investigators from the NHLBI's CARDIA study examined the association between neighborhood attributes and subclinical atherosclerosis in younger adult populations. Using 2000 US Census block-group-level data, among women, higher odds of CAC were associated with higher neighborhood deprivation and lower neighborhood cohesion. Among all men, neither neighborhood deprivation nor neighborhood cohesion was associated with CAC, whereas among men in deprived neighborhoods, low cohesion was associated with higher odds of CAC.8
CAC and Incidence of Coronary Events
•
The NHLBI's MESA study recently reported on the association of CAC scores with first CHD events over a median follow-up of 3.9 years among a population-based sample of 6722 men and women (39% white, 27% black, 22% Hispanic, and 12% Chinese).9
—Chart 4-3 shows the HRs associated with CAC scores of 1 to 100, 101 to 300, and >300 compared with those without CAC (score=0), after adjustment for standard risk factors. People with CAC scores of 1 to 100 had ≈4 times greater risk and those with CAC scores >100 were 7 to 10 times more likely to experience a coronary event than those without CAC.
—CAC provided similar predictive value for coronary events in whites, Chinese, blacks, and Hispanics (HRs ranging from 1.15–1.39 for each doubling of coronary calcium).
•
In another report of a community-based sample, not referred for clinical reasons, the South Bay Heart Watch examined CAC in 1461 adults (average age 66 years) with coronary risk factors, with a median of 7.0 years of follow-up.10
—Chart 4-4 shows the HRs associated with increasing CAC scores (relative to CAC=0 and <10% risk category) in low-risk (<10%), intermediate-risk (10% to 15% and 16% to 20%), and high-risk (>20%) FRS categories of estimated risk for CHD in 10 years. Increasing CAC scores further predicted risk in intermediate- and high-risk groups.
•
In a study of healthy adults 60 to 72 years of age who were free of clinical CAD, predictors of the progression of CAC were assessed. Predictors tested included age, sex, race/ethnicity, smoking status, BMI, family history of CAD, C-reactive protein, several measures of DM, insulin levels, BP, and lipids. Insulin resistance, in addition to the traditional cardiac risk factors, independently predicts progression of CAC.11 Clinically, however, it is not yet recommended to conduct serial scanning of CAC to measure effects of therapeutic interventions.
•
A recent publication from MESA also used CAC, in particular, and carotid IMT to stratify CHD and CVD event risk in people with metabolic syndrome and DM; those with low levels of CAC or carotid IMT have CHD and CVD event rates as low as many people without metabolic syndrome and DM. Those with DM who have CAC scores <100 have annual CHD event rates of <1%.12
•
It is noteworthy, as recently demonstrated in MESA in 5878 participants with a median of 5.8 years of follow-up, that the addition of CAC to standard risk factors resulted in significant improvement of classification of risk for incident CHD events, placing 77% of people in the highest or lowest risk categories compared with 69% based on risk factors alone. An additional 23% of those who experienced events were reclassified as high risk, and 13% with events were reclassified as low risk.13
CAC Progression and Risk
A recent report in 4609 individuals who had baseline and repeat cardiac CT found that progression of CAC in predicting future all-cause mortality provided only incremental information over baseline score, demographics, and cardiovascular risk factors.16
Carotid IMT
Background
•
Carotid IMT measures the thickness of 2 layers (the intima and media) of the wall of the carotid arteries, the largest conduits of blood going to the brain. Carotid IMT is thought to be an even earlier manifestation of atherosclerosis than CAC, because thickening precedes the development of frank atherosclerotic plaque. Carotid IMT methods are still being refined, so it is important to know which part of the artery was measured (common carotid, internal carotid, or bulb) and whether near and far walls were both measured. This information can affect the average-thickness measurement that is usually reported.
•
Unlike CAC, everyone has some thickness to the layers of their arteries, but people who develop atherosclerosis have greater thickness. Ultrasound of the carotid arteries can also detect plaques and determine the degree of narrowing of the artery they may cause. Epidemiological data, including the data discussed below, have indicated that high-risk levels of thickening might be considered as those in the highest quartile or quintile for one's age and sex, or ≥1 mm.
•
Although ultrasound is commonly used to diagnose plaque in the carotid arteries in people who have had strokes or who have bruits (sounds of turbulence in the artery), guidelines are limited as to screening of asymptomatic people with carotid IMT to quantify atherosclerosis or predict risk. However, some organizations have recognized that carotid IMT measurement by B-mode ultrasonography may provide an independent assessment of coronary risk.17
Prevalence and Association With Incident Cardiovascular Events
•
The Bogalusa Heart Study measured carotid IMT in 518 black and white men and women at a mean age of 32±3 years. These men and women were healthy but overweight.18
—The mean values of carotid IMT for the different segments are shown in Chart 4-5 by sex and race. Men had significantly higher carotid IMT in all segments than women, and blacks had higher common carotid and carotid bulb IMTs than whites.
—Even at this young age, after adjustment for age, race, and sex, carotid IMT was associated significantly and positively with waist circumference, SBP, diastolic BP (DBP), and LDL cholesterol. Carotid IMT was inversely correlated with high-density lipoprotein (HDL) cholesterol levels. Participants with greater numbers of adverse risk factors (0, 1, 2, 3, or more) had stepwise increases in mean carotid IMT levels.
•
In a subsequent analysis, the Bogalusa investigators examined the association of risk factors measured since childhood with carotid IMT measured in these young adults.19 Higher BMI and LDL cholesterol levels measured at 4 to 7 years of age were associated with increased risk for being >75th percentile for carotid IMT in young adulthood. Higher SBP and LDL cholesterol and lower HDL cholesterol in young adulthood were also associated with having high carotid IMT. These data highlight the importance of adverse risk factor levels in early childhood and young adulthood in the early development of atherosclerosis.
•
Among both women and men in MESA, blacks had the highest common carotid IMT, but they were similar to whites and Hispanics in internal carotid IMT. Chinese participants had the lowest carotid IMT, in particular in the internal carotid, of the 4 ethnic groups (Chart 4-6).
•
The NHLBI's CHS reported follow-up of 4476 men and women ≥65 years of age (mean age 72 years) who were free of CVD at baseline.20
—Mean maximal common carotid IMT was 1.03±0.20 mm, and mean internal carotid IMT was 1.37±0.55 mm.
—After a mean follow-up of 6.2 years, those with maximal combined carotid IMT in the highest quintile had a 4- to 5-fold greater risk for incident heart attack or stroke than those in the bottom quintile. After adjustment for other risk factors, there was still a 2- to 3-fold greater risk for the top versus the bottom quintile.
•
A study of 441 individuals ≤65 years of age without a history of CAD, DM, or hyperlipidemia who were examined for carotid IMT found 42% had high-risk carotid ultrasound findings (carotid IMT ≥75th percentile adjusted for age, sex, and race or presence of plaque). Among those with an FRS ≤5%, 38% had high-risk carotid ultrasound findings.21
•
Conflicting data have been reported on the contribution of carotid IMT to risk prediction. In 13 145 participants in the NHLBI's ARIC study, the addition of carotid IMT combined with identification of plaque presence or absence to traditional risk factors reclassified risk in 23% of individuals overall, with a net reclassification improvement of 9.9%. There was a modest but statistically significant improvement in the area under the receiver operating characteristic curve, from 0.742 to 0.755.22 In contrast, data reported recently from the Carotid Atherosclerosis Progression Study observed a net reclassification improvement of −1.4% that was not statistically significant.23
CAC and Carotid IMT
•
In the NHLBI's MESA study of white, black, Chinese, and Hispanic adults 45 to 84 years of age, carotid IMT and CAC were found to be commonly associated, but patterns of association differed somewhat by sex and race.24
—Common and internal carotid IMT were greater in women and men who had CAC than in those who did not, regardless of ethnicity.
—Overall, CAC prevalence and scores were associated with carotid IMT, but associations were somewhat weaker in blacks than in other ethnic groups.
—In general, blacks had the thickest carotid IMT of all 4 ethnic groups, regardless of the presence of CAC.
—Common carotid IMT differed little by race/ethnicity in women with any CAC, but among women with no CAC, IMT was higher among blacks (0.86 mm) than in the other 3 groups (0.76–0.80 mm).
•
In a more recent analysis from the NHLBI's MESA study, the investigators reported on follow-up of 6698 men and women in 4 ethnic groups over 5.3 years and compared the predictive utility of carotid IMT and CAC.25
—CAC was associated more strongly than carotid IMT with the risk of incident CVD.
—After adjustment for each other (CAC score and IMT) and for traditional CVD risk factors, the HR for CVD increased 2.1-fold for each 1-standard deviation increment of log-transformed CAC score versus 1.3-fold for each 1-standard deviation increment of the maximum carotid IMT.
—For CHD events, the HRs per 1-standard deviation increment increased 2.5-fold for CAC score and 1.2-fold for IMT.
—A receiver operating characteristic curve analysis also suggested that CAC score was a better predictor of incident CVD than was IMT, with areas under the curve of 0.81 versus 0.78, respectively.
—Investigators from the NHLBI's CARDIA and MESA studies examined the burden and progression of subclinical atherosclerosis among adults <50 years of age. Ten-year and lifetime risks for CVD were estimated for each participant, and the participants were stratified into 3 groups: (1) those with low 10-year (<10%) and low lifetime (<39%) predicted risk for CVD; (2) those with low 10-year (<10%) but high lifetime (≥39%) predicted risk; and (3) those with high 10-year risk (>10%). The latter group had the highest burden and greatest progression of subclinical atherosclerosis. Given the young age of those studied, ≈90% of participants were at low 10-year risk, but of these, half had high predicted lifetime risk. Compared with those with low short-term/low lifetime predicted risks, those with low short-term/high lifetime predicted risk had significantly greater burden and progression of CAC and significantly greater burden of carotid IMT, even at these younger ages. These data confirm the importance of early exposure to risk factors for the onset and progression of subclinical atherosclerosis.26
CT Angiography
CT angiography is widely used by cardiologists to aid in the diagnosis of CAD, particularly when other test results may be equivocal. It is also of interest because of its ability to detect and possibly quantitate overall plaque burden and certain characteristics of plaques that may make them prone to rupture, such as positive remodeling or low attenuation. However, because of the limited outcome data in asymptomatic people, as well as the associated expense and risk of CT angiography (including generally higher radiation levels than CT scanning to detect CAC), current guidelines do not recommend its use as a screening tool for assessment of cardiovascular risk in asymptomatic people.2
Measures of Vascular Function and Incident CVD Events
Background
•
Measures of arterial tonometry (stiffness) are based on the concept that pulse pressure has been shown to be an important risk factor for CVD. Arterial tonometry offers the ability to directly and noninvasively measure central pulse wave velocity in the thoracic and abdominal aorta.
•
Brachial flow-mediated dilation (FMD) is a marker for nitric oxide release from the endothelium that can be measured by ultrasound. Impaired FMD is an early marker of CVD.
•
Recommendations have not been specific, however, as to which, if any, measures of vascular function may be useful for CVD risk stratification in selected patient subgroups. Because of the absence of significant prospective data relating these measures to outcomes, latest guidelines do not currently recommend measuring either FMD or arterial stiffness for cardiovascular risk assessment in asymptomatic adults.2
Arterial Tonometry and CVD
•
The Rotterdam Study measured arterial stiffness in 2835 elderly participants (mean age 71 years27). They found that as aortic pulse wave velocity increased, the risk of CHD was 1.72 (second versus first tertile) and 2.45 (third versus first tertile). Results remained robust even after accounting for carotid IMT, ankle-brachial index (ABI), and pulse pressure.
•
A study from Denmark measured 1678 individuals 40 to 70 years of age and found that aortic pulse wave velocity increased CVD risk by 16% to 20%.28
•
The FHS measured several indices of arterial stiffness, including pulse wave velocity, wave reflection, and central pulse pressure.29 They found that not only was higher pulse wave velocity associated with a 48% increased risk of incident CVD events, but pulse wave velocity additionally improved CVD risk prediction (integrated discrimination improvement of 0.7%, P<0.05).
FMD and CVD
•
The MESA study measured FMD in 3026 participants (mean age 61 years) who were free of CVD. As FMD increased (ie, improved brachial function), the risk of CVD was 16% lower.30 FMD also improved CVD risk prediction compared with the FRS by improving net reclassification by 29%.
References
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Greenland P, Alpert JS, Beller GA, Benjamin EJ, Budoff MJ, Fayad ZA, Foster E, Hlatky MA, Hodgson JM, Kushner FG, Lauer MS, Shaw LJ, Smith SC, Taylor AJ, Weintraub WS, Wenger NK. 2010 ACCF/AHA guideline for assessment of cardiovascular risk in asymptomatic adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2010; 122: e584–e636.
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Rozanski A, Gransar H, Shaw LJ, Kim J, Miranda-Peats L, Wong ND, Rana JS, Orakzai R, Hayes SW, Friedman JD, Thomson LE, Polk D, Min J, Budoff MJ, Berman DS. Impact of coronary artery calcium scanning on coronary risk factors and downstream testing: the EISNER (Early Identification of Subclinical Atherosclerosis by Noninvasive Imaging Research) prospective randomized trial. J Am Coll Cardiol. 2011; 57: 1622–1632.
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Loria CM, Liu K, Lewis CE, Hulley SB, Sidney S, Schreiner PJ, Williams OD, Bild DE, Detrano R. Early adult risk factor levels and subsequent coronary artery calcification: the CARDIA Study. J Am Coll Cardiol. 2007; 49: 2013–2020.
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Bild DE, Detrano R, Peterson D, Guerci A, Liu K, Shahar E, Ouyang P, Jackson S, Saad MF. Ethnic differences in coronary calcification: the Multi-Ethnic Study of Atherosclerosis (MESA). Circulation. 2005; 111: 1313–1320.
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Okwuosa TM, Greenland P, Ning H, Liu K, Bild DE, Burke GL, Eng J, Lloyd-Jones DM. Distribution of coronary artery calcium scores by Framingham 10-year risk strata in the MESA (Multi-Ethnic Study of Atherosclerosis): potential implications for coronary risk assessment. J Am Coll Cardiol. 2011; 57: 1838–1845.
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Kim D, Diez Roux AV, Kiefe CI, Kawachi I, Liu K. Do neighborhood socioeconomic deprivation and low social cohesion predict coronary calcification? The CARDIA study. Am J Epidemiol. 2010; 172: 288–298.
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Detrano R, Guerci AD, Carr JJ, Bild DE, Burke G, Folsom AR, Liu K, Shea S, Szklo M, Bluemke DA, O'Leary DH, Tracy R, Watson K, Wong ND, Kronmal RA. Coronary calcium as a predictor of coronary events in four racial or ethnic groups. N Engl J Med. 2008; 358: 1336–1345.
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Greenland P, LaBree L, Azen SP, Doherty TM, Detrano RC. Coronary artery calcium score combined with Framingham score for risk prediction in asymptomatic individuals [published correction appears in JAMA. 2004;291:563]. JAMA. 2004; 291: 210–215.
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Lee KK, Fortmann SP, Fair JM, Iribarren C, Rubin GD, Varady A, Go AS, Quertermous T, Hlatky MA. Insulin resistance independently predicts the progression of coronary artery calcification. Am Heart J. 2009; 157: 939–945.
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Malik S, Budoff MJ, Katz R, Blumenthal RS, Bertoni AG, Nasir K, Szklo M, Barr RG, Wong ND. Impact of subclinical atherosclerosis on cardiovascular disease events in individuals with metabolic syndrome and diabetes: the Multi-Ethnic Study of Atherosclerosis. Diabetes Care. 2011; 34: 2285–2290.
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Polonsky TS, McClelland RL, Jorgensen NW, Bild DE, Burke GL, Guerci AD, Greenland P. Coronary artery calcium score and risk classification for coronary heart disease prediction. JAMA. 2010; 303: 1610–1616.
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Erbel R, Möhlenkamp S, Moebus S, Schmermund A, Lehmann N, Stang A, Dragano N, Grönemeyer D, Seibel R, Kälsch H, Bröcker-Preuss M, Mann K, Siegrist J, Jöckel KH; Heinz Nixdorf Recall Study Investigative Group. Coronary risk stratification, discrimination, and reclassification improvement based on quantification of subclinical coronary atherosclerosis: the Heinz Nixdorf Recall study. J Am Coll Cardiol. 2010; 56: 1397–1406.
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Elias-Smale SE, Proenca RV, Koller MT, Kavousi M, van Rooij FJ, Hunink MG, Steyerberg EW, Hofman A, Oudkerk M, Witteman JC. Coronary calcium score improves classification of coronary heart disease risk in the elderly: the Rotterdam study. J Am Coll Cardiol. 2010; 56: 1407–1414.
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Budoff MJ, Hokanson JE, Nasir K, Shaw LJ, Kinney GL, Chow D, Demoss D, Nuguri V, Nabavi V, Ratakonda R, Berman DS, Raggi P. Progression of coronary artery calcium predicts all-cause mortality. JACC Cardiovasc Imaging. 2010; 3: 1229–1236.
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Smith SC, Greenland P, Grundy SM. AHA conference proceedings: Prevention Conference V: beyond secondary prevention: identifying the high-risk patient for primary prevention: executive summary. Circulation. 2000; 101: 111–116.
18.
Urbina EM, Srinivasan SR, Tang R, Bond M, Kieltyka L, Berenson GS; Bogalusa Heart Study. Impact of multiple coronary risk factors on the intima-media thickness of different segments of carotid artery in healthy young adults (the Bogalusa Heart Study). Am J Cardiol. 2002; 90: 953–958.
19.
Li S, Chen W, Srinivasan SR, Bond MG, Tang R, Urbina EM, Berenson GS. Childhood cardiovascular risk factors and carotid vascular changes in adulthood: the Bogalusa Heart Study [published correction appears in JAMA. 2003;290:2943]. JAMA. 2003; 290: 2271–2276.
20.
O'Leary DH, Polak JF, Kronmal RA, Manolio TA, Burke GL, Wolfson SK; Cardiovascular Health Study Collaborative Research Group. Carotid-artery intima and media thickness as a risk factor for myocardial infarction and stroke in older adults. N Engl J Med. 1999; 340: 14–22.
21.
Eleid MF, Lester SJ, Wiedenbeck TL, Patel SD, Appleton CP, Nelson MR, Humphries J, Hurst RT. Carotid ultrasound identifies high risk subclinical atherosclerosis in adults with low Framingham risk scores. J Am Soc Echocardiogr. 2010; 23: 802–808.
22.
Nambi V, Chambless L, Folsom AR, He M, Hu Y, Mosley T, Volcik K, Boerwinkle E, Ballantyne CM. Carotid intima-media thickness and presence or absence of plaque improves prediction of coronary heart disease risk: the ARIC (Atherosclerosis Risk In Communities) study. J Am Coll Cardiol. 2010; 55: 1600–1607.
23.
Lorenz MW, Schaefer C, Steinmetz H, Sitzer M. Is carotid intima media thickness useful for individual prediction of cardiovascular risk? Ten-year results from the Carotid Atherosclerosis Progression Study (CAPS). Eur Heart J. 2010; 31: 2041–2048.
24.
Manolio TA, Arnold AM, Post W, Bertoni AG, Schreiner PJ, Sacco RL, Saad MF, Detrano RL, Szklo M. Ethnic differences in the relationship of carotid atherosclerosis to coronary calcification: the Multi-Ethnic Study of Atherosclerosis. Atherosclerosis. 2008; 197: 132–138.
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Folsom AR, Kronmal RA, Detrano RC, O'Leary DH, Bild DE, Bluemke DA, Budoff MJ, Liu K, Shea S, Szklo M, Tracy RP, Watson KE, Burke GL. Coronary artery calcification compared with carotid intima-media thickness in the prediction of cardiovascular disease incidence: the Multi-Ethnic Study of Atherosclerosis (MESA) [published correction appears in Arch Intern Med. 2008;168:1782]. Arch Intern Med. 2008; 168: 1333–1339.
26.
Berry JD, Liu K, Folsom AR, Lewis CE, Carr JJ, Polak JF, Shea S, Sidney S, O'Leary DH, Chan C;, Lloyd-Jones DM. Prevalence and progression of subclinical atherosclerosis in younger adults with low short-term but high lifetime estimated risk for cardiovascular disease: the Coronary Artery Risk Development in Young Adults Study and Multi-Ethnic Study of Atherosclerosis. Circulation. 2009; 119: 382–389.
27.
Mattace-Raso FU, van der Cammen TJ, Hofman A, van Popele NM, Bos ML, Schalekamp MA, Asmar R, Reneman RS, Hoeks AP, Breteler M;, Witteman JC. Arterial stiffness and risk of coronary heart disease and stroke: the Rotterdam Study. Circulation. 2006; 113: 657–663.
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Willum Hansen T, Staessen JA, Torp-Pedersen C, Rasmussen S, Thijs L, Ibsen H, Jeppesen J. Prognostic value of aortic pulse wave velocity as index of arterial stiffness in the general population. Circulation. 2006; 113: 664–670.
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Mitchell GF, Hwang SJ, Vasan RS, Larson MG, Pencina MJ, Hamburg NM, Vita JA, Levy D, Benjamin EJ. Arterial stiffness and cardiovascular events: the Framingham Heart Study. Circulation. 2010; 121: 505–511.
30.
Yeboah J, Folsom AR, Burke GL, Johnson C, Polak JF, Post W, Lima JA, Crouse JR, Herrington DM. Predictive value of brachial flow-mediated dilation for incident cardiovascular events in a population-based study: the Multi-Ethnic Study of Atherosclerosis. Circulation. 2009; 120: 502–509.
5. Coronary Heart Disease, Acute Coronary Syndrome, and Angina Pectoris
Coronary Heart Disease
ICD-9 410 to 414, 429.2; ICD-10 I20 to I25; see Glossary (Chapter 25) for details and definitions. See Tables 5-1 and 5-2. See Charts 5-1 through 5-8.
| Population Group | Prevalence, CHD, 2008 Age ≥20 y | Prevalence, MI, 2008 Age ≥20 y | New and Recurrent MI and Fatal CHD, Age ≥35 y | New and Recurrent MI, Age ≥35 y | Mortality,* CHD, 2008, All Ages | Mortality,* MI, 2008, All Ages | Hospital Discharges, CHD, 2009, All Ages |
|---|---|---|---|---|---|---|---|
| Both sexes | 16 300 000 (7.0%) | 7 900 000 (3.1%) | 1 255 000 | 935 000 | 405 309 | 133 958 | 1 537 000 |
| Males | 8 800 000 (8.3%) | 4 800 000 (4.3%) | 740 000 | 565 000 | 216 248 (53.4%)† | 72 447 (54.1%)† | 933 000 |
| Females | 7 500 000 (6.1%) | 3 100 000 (2.2%) | 515 000 | 370 000 | 189 061 (46.6%)† | 61 511 (45.9%)† | 604 000 |
| NH white males | 8.5% | 4.3% | 675 000‡ | … | 189 354 | 63 842 | … |
| NH white females | 5.8% | 2.1% | 445 000‡ | … | 164 485 | 53 276 | … |
| NH black males | 7.9% | 4.3% | 70 000‡ | … | 21 407 | 6883 | … |
| NH black females | 7.6% | 2.2% | 65 000‡ | … | 20 491 | 6908 | … |
| Mexican American males | 6.3% | 3.0% | … | … | … | … | … |
| Mexican American females | 5.6% | 1.1% | … | … | … | … | … |
| Hispanic or Latino§ | 5.2% | … | … | … | … | … | … |
| Asian§ | 4.9% | … | … | … | 7414 | 2448 | … |
| American Indian/ Alaska Native§ | 5.9% | … | … | … | 1777 | 601 | … |
CHD indicates coronary heart disease; MI, myocardial infarction; and NH, non-Hispanic.
CHD includes people who responded “yes” to at least 1 of the questions in “Has a doctor or other health professional ever told you had coronary heart disease, angina or angina pectoris, heart attack, or myocardial infarction?” Those who answered “no” but were diagnosed with Rose angina are also included (the Rose questionnaire is only administered to survey participants >40 years of age). Ellipses indicate data not available. Sources: Prevalence: National Health and Nutrition Examination Survey 2005–2008 (National Center for Health Statistics) and National Heart, Lung, and Blood Institute. Percentages for racial/ethnic groups are age-adjusted for Americans ≥20 years of age. Age-specific percentages are extrapolated to the 2008 US population estimates. These data are based on self-reports. Incidence: Atherosclerosis Risk in Communities study (1987–2004), National Heart, Lung, and Blood Institute. Mortality: National Center for Health Statistics (these data represent underlying cause of death only). Hospital discharges: National Hospital Discharge Survey, National Center for Health Statistics (data include those inpatients discharged alive, dead, or status unknown).
*
Mortality data for the white, black, Asian or Pacific Islander, and American Indian/Alaska Native populations include deaths of persons of Hispanic and non-Hispanic origin. Numbers of deaths for the American Indian/Alaska Native and Asian or Pacific Islander populations are known to be underestimated.
†
These percentages represent the portion of total CHD mortality that is for males vs females.
‡
Estimates include Hispanics and non-Hispanics. Estimates for whites include other nonblack races.
§
National Health Interview Survey, National Center for Health Statistics 2010; data are weighted percentages for Americans ≥18 years of age.1
| Population Group | Prevalence, 2008 Age ≥20 y | Incidence of Stable AP, Age ≥45 y | Hospital Discharges, 2009,* All Ages |
|---|---|---|---|
| Both sexes | 9 000 000 (3.9%) | 500 000 | 34 000 |
| Males | 4 000 000 (3.8%) | 320 000 | 19 000 |
| Females | 5 000 000 (4.0%) | 180 000 | 15 000 |
| NH white males | 3.8% | … | … |
| NH white females | 3.7% | … | … |
| NH black males | 3.3% | … | … |
| NH black females | 5.6% | … | … |
| Mexican American males | 3.6% | … | … |
| Mexican American females | 3.7% | … | … |
AP indicates angina pectoris; NH, non-Hispanic; and ellipses, data not available.
AP is chest pain or discomfort that results from insufficient blood flow to the heart muscle. Stable AP is predictable chest pain on exertion or under mental or emotional stress. The incidence estimate is for AP without myocardial infarction.
Sources: Prevalence: National Health and Nutrition Examination Survey 2005–2008 (National Center for Health Statistics) and National Heart, Lung, and Blood Institute; percentages for racial/ethnic groups are age adjusted for US adults ≥20 years of age. AP includes persons who either answered “yes” to the question of ever having angina or AP or who were diagnosed with Rose angina (the Rose questionnaire is only administered to survey participants >40 years of age). Estimates from National Health and Nutrition Examination Survey 2005–2008 (National Center for Health Statistics) were applied to 2008 population estimates (≥20 years of age). Incidence: AP uncomplicated by a myocardial infarction or with no myocardial infarction (Framingham Heart Study 1980 to 2001–2003 of the original cohort and 1980 to 1998–2001 of the Offspring Cohort, National Heart, Lung, and Blood Institute). Hospital discharges: National Hospital Discharge Survey, National Center for Health Statistics; data include those inpatients discharged alive, dead, or status unknown.
*
There were 166 000 days of care for discharges of patients with AP from short-stay hospitals in 2009.
| ACC | American College of Cardiology |
| ACS | acute coronary syndrome |
| AHA | American Heart Association |
| AMI | acute myocardial infarction |
| AP | angina pectoris |
| ARIC | Atherosclerosis Risk in Communities study |
| BMI | body mass index |
| BP | blood pressure |
| BRFSS | Behavioral Risk Factor Surveillance System |
| CABG | coronary artery bypass graft |
| CAD | coronary artery disease |
| CDC | Centers for Disease Control and Prevention |
| CHD | coronary heart disease |
| CHS | Cardiovascular Health Study |
| CI | confidence interval |
| CRUSADE | Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the ACC/AHA Guidelines |
| CVD | cardiovascular disease |
| DM | diabetes mellitus |
| ECG | electrocardiogram/electrocardiographic |
| ED | emergency department |
| EMS | emergency medical services |
| FHS | Framingham Heart Study |
| GRACE | Global Registry of Acute Coronary Events |
| GWTG | Get With The Guidelines |
| HD | heart disease |
| HDL | high-density lipoprotein |
| HF | heart failure |
| ICD-9 | International Classification of Diseases, 9th Revision |
| ICD-10 | International Classification of Diseases, 10th Revision |
| LDL | low-density lipoprotein |
| MEPS | Medical Expenditure Panel Survey |
| MI | myocardial infarction |
| NAMCS | National Ambulatory Medical Care Survey |
| NCHS | National Center for Health Statistics |
| NH | non-Hispanic |
| NHAMCS | National Hospital Ambulatory Medical Care Survey |
| NHANES | National Health and Nutrition Examination Survey |
| NHDS | National Hospital Discharge Survey |
| NHIS | National Health Interview Study |
| NHLBI | National Heart, Lung, and Blood Institute |
| NRMI | National Registry of Myocardial Infarction |
| NSTEMI | non–ST-segment–elevation myocardial infarction |
| OR | odds ratio |
| PA | physical activity |
| PCI | percutaneous coronary intervention |
| PREMIER | Prospective Registry Evaluating Myocardial Infarction: Events and Recovery |
| SBP | systolic blood pressure |
| STEMI | ST-segment–elevation myocardial infarction |
| UA | unstable angina |
Prevalence
•
On the basis of data from NHANES 2005–2008 (NCHS; unpublished NHLBI tabulation;Table 5-1; Chart 5-1), an estimated 16.3 million Americans ≥20 years of age have CHD:
— Total CHD prevalence is 7.0% in US adults ≥20 years of age. CHD prevalence is 8.3% for men and 6.1% for women.
— Among non-Hispanic whites, CHD prevalence is 8.5% for men and 5.8% for women.
— Among non-Hispanic blacks, CHD prevalence is 7.9% for men and 7.6% for women.
— Among Mexican Americans, CHD prevalence is 6.3% for men and 5.6% for women.
•
On the basis of data from the 2010 NHIS:
•
According to data from NHANES 2005–2008 (NCHS; unpublished NHLBI tabulation), the overall prevalence for MI is 3.1% in US adults ≥20 years of age. MI prevalence is 4.3% for men and 2.2% for women.
— Among non-Hispanic whites, MI prevalence is 4.3% for men and 2.1% for women.
— Among non-Hispanic blacks, MI prevalence is 4.3% for men and 2.2% for women.
— Among Mexican Americans, MI prevalence is 3.0% for men and 1.1% for women.
•
Data from the BRFSS 2010 survey indicated that 4.2% of respondents had been told that they had an MI. The highest prevalence was in Arizona (6.7%) and West Virginia (6.3%). The lowest prevalence was in Alaska (2.6%) and Utah (2.8%). In the same survey, 4.1% of respondents were told that they had angina or CHD. The highest prevalence was in Arizona (6.8%), and the lowest was in Hawaii (2.3%).2
•
Projections show that by 2030 an additional 8 million people could have CHD, a 16.6% increase in prevalence from 2010.3
Incidence
•
On the basis of unpublished data from the ARIC and CHS studies of the NHLBI:
— The estimated annual incidence of MI is 610 000 new attacks and 325 000 recurrent attacks.
— Average age at first MI is 64.5 years for men and 70.3 years for women.
•
On the basis of the NHLBI-sponsored FHS:
— CHD makes up more than half of all cardiovascular events in men and women <75 years of age.4
— The lifetime risk of developing CHD after 40 years of age is 49% for men and 32% for women.6
— The incidence of CHD in women lags behind men by 10 years for total CHD and by 20 years for more serious clinical events such as MI and sudden death.4
•
In the NHLBI-sponsored ARIC study, in participants 45 to 64 years of age, the average age-adjusted CHD incidence rates per 1000 person-years were as follows: white men, 12.5; black men, 10.6; white women, 4.0; and black women, 5.1. Incidence rates excluding revascularization procedures were as follows: white men, 7.9; black men, 9.2; white women, 2.9; and black women, 4.9.7
•
Incidence rates for MI in the NHLBI-sponsored ARIC study are displayed in Charts 5-3 and 5-4, stratified by age, race, and sex. The annual age-adjusted rates per 1000 population of first MI (1987–2001) in ARIC Surveillance (NHLBI) were 4.2 in black men, 3.9 in white men, 2.8 in black women, and 1.7 in white women.8
•
Analysis of more than 40 years of physician-validated AMI data in the FHS study of the NHLBI found that AMI rates diagnosed by electrocardiographic (ECG) criteria declined ≈50%, with a concomitant 2-fold increase in rates of AMI diagnosed by blood markers. These findings may explain the paradoxical stability of AMI rates in the United States despite concomitant improvements in CHD risk factors.9
•
Among American Indians 65 to 74 years of age, the annual rates per 1000 population of new and recurrent MIs were 7.6 for men and 4.9 for women.10 Analysis of data from NHANES III (1988–1994) and NHANES 1999–2002 (NCHS) showed that in adults 20 to 74 years of age, the overall distribution of 10-year risk of developing CHD changed little during this time. Among the 3 racial/ethnic groups, blacks had the highest proportion of participants in the high-risk group.11
•
On the basis of data from the NHDS, since the mid-1990s, the rate of hospitalization for MI and in-hospital case fatality rates have decreased.12
•
From 2002 to 2007, the rates of hospitalization for MI decreased among Medicare beneficiaries; however, the degree of reduction was more significant in whites than African Americans.13
Mortality
•
CHD caused ≈1 of every 6 deaths in the United States in 2008. CHD mortality was 405 309.14
•
CHD any-mention mortality was 571 366. MI mortality was 133 958. MI any-mention mortality was 172 733 (NHLBI tabulation; NCHS public-use data files).14
•
In 2008, the overall CHD death rate was 122.7. From 1998 to 2008, the annual death rate due to CHD declined 28.7% and actual number of deaths declined 11.9%. The death rates were 161.7 for white males and 183.7 for black males; for white females, the rate was 91.9 and for black females it was 115.6 (NHLBI tabulation; NCHS public-use data files).14
•
Approximately every 25 seconds, an American will experience a coronary event, and approximately every minute, someone will die of one.
•
Approximately 34% of the people who experience a coronary attack in a given year will die of it, and ≈15% who experience a heart attack (MI) will die of it (AHA computation).
•
Approximately every 34 seconds, an American will have an MI.
•
The percentage of CHD deaths that occurred out of the hospital in 2008 was 70%. According to NCHS mortality data, 287 000 CHD deaths occur out of the hospital or in hospital EDs annually (2008, ICD-10 codes I20 to I25) (NHLBI tabulation of NCHS mortality data).
•
A study of 1275 health maintenance organization enrollees 50 to 79 years of age who had cardiac arrest showed that the incidence of out-of-hospital cardiac arrest was 6.0/1000 subject-years in subjects with any clinically recognized HD compared with 0.8/1000 subject-years in subjects without HD. In subgroups with HD, incidence was 13.6/1000 subject-years in subjects with prior MI and 21.9/1000 subject-years in subjects with HF.15
•
Approximately 81% of people who die of CHD are ≥65 years of age (NCHS; AHA computation).
•
The estimated average number of years of life lost because of an MI is 16.6 (NHLBI tabulation of NCHS mortality data).
•
On the basis of data from the FHS of the NHLBI4:
— Fifty percent of men and 64% of women who die suddenly of CHD have no previous symptoms of this disease. Between 70% and 89% of sudden cardiac deaths occur in men, and the annual incidence is 3 to 4 times higher in men than in women; however, this disparity decreases with advancing age.
— People who have had an MI have a sudden death rate 4 to 6 times that of the general population.
•
Researchers investigating variation in hospital-specific 30-day risk-stratified mortality rates for patients with AMI found teaching status, number of hospital beds, AMI volume, cardiac facilities available, urban/rural location, geographic region, hospital ownership type, and socioeconomic status profile of the patients were all significantly associated with mortality rates. However, a substantial proportion of variation in outcomes for patients with AMI between hospitals remains unexplained by measures of hospital characteristics.16
Temporal Trends in CHD Mortality
•
An analysis of FHS data (NHLBI) from 1950 to 1999 showed that overall CHD death rates decreased by 59%. Nonsudden CHD death decreased by 64%, and sudden cardiac death fell by 49%. These trends were seen in men and women, in subjects with and without a prior history of CHD, and in smokers and nonsmokers.17
•
The decline in CHD mortality rates in part reflects the shift in the pattern of clinical presentations of AMI. In the past decade, there has been a marked decline in ST-segment–elevation myocardial infarction (STEMI; from 133 to 50 cases per 100 000 person-years).18
•
From 1997 to 2007, the annual death rate attributable to CHD declined 26.3%, and the actual number of deaths declined 12.9%. (Appropriate comparability ratios were applied.) In 2007, the overall CHD death rate was 126.0 per 100 000 population. The death rates were 165.6 for white males and 191.6 for black males; for white females, the rate was 94.2, and for black females, it was 121.5.14 Age-adjusted death rates attributable to CHD were 122.3 for Hispanic or Latino males and 77.8 for females, 112.2 for American Indian or Alaska Native males and 65.6 for females, and 91.7 for Asian or Pacific Islander males and 55.0 for females.14
•
According to data from the National Registry of Myocardial Infarction19:
— From 1990 to 1999, in-hospital AMI mortality declined from 11.2% to 9.4%.
— Mortality rate increases for every 30 minutes that elapse before a patient with ST-segment elevation is recognized and treated.
•
Other studies also reported declining case fatality rates after MI:
— In Olmsted County, Minnesota, the age- and sex-adjusted 30-day case fatality rate decreased by 56% from 1987 to 2006.20
— In Worcester, MA, the hospital case fatality rates, 30-day postadmission case fatality rates, and 1-year postdischarge case fatality rates for STEMI were 11.1%, 13.2%, and 10.6%, respectively, in 1997 and 9.7%, 11.4%, and 8.4%, respectively, in 2005. The hospital case fatality rates, 30-day postadmission case fatality rates, and 1-year postdischarge case fatality rates for non–ST-segment MI (NSTEMI) were 12.9%, 16.0%, and 23.1%, respectively, in 1997 and 9.5%, 14.0%, and 18.7%, respectively, in 2005.21
— Among enrollees of the Kaiser Permanente Northern California healthcare delivery system, the age- and sex-adjusted 30-day mortality rate for MI dropped from 10.5% in 1999 to 7.8% in 2008, and the 30-day mortality rate for NSTEMI dropped from 10.0% in 1999 to 7.6% in 2008.18
•
CHD death rates have fallen from 1968 to the present. Analysis of NHANES (NCHS) data compared CHD death rates between 1980 and 2000 to determine how much of the decline in deaths attributable to CHD over that period could be explained by the use of medical and surgical treatments versus changes in CVD risk factors (resulting from lifestyle/behavior). After 1980 and 2000 data were compared, it was estimated that ≈47% of the decrease in CHD deaths was attributable to treatments, including the following22:
— Secondary preventive therapies after MI or revascularization (11%).
— Initial treatments for AMI or UA (10%).
— Treatments for HF (9%).
— Revascularization for chronic angina (5%).
— Other therapies (12%), including antihypertensive and lipid-lowering primary prevention therapies.
•
It was also estimated that a similar amount of the reduction in CHD deaths, ≈44%, was attributable to changes in risk factors, including the following22:
— Lower total cholesterol (24%).
— Lower SBP (20%).
— Lower smoking prevalence (12%).
— Decreased physical inactivity (5%).
— Nevertheless, these favorable improvements in risk factors were offset in part by increases in BMI and in DM prevalence, which accounted for an increased number of deaths (8% and 10%, respectively).
•
Between 1980 and 2002, death rates attributable to CHD among men and women ≥65 years of age fell by 52% in men and 49% in women. Among men, the death rate declined on average by 2.9% per year in the 1980s, 2.6% per year during the 1990s, and 4.4% per year from 2000 to 2002. Among women, death rates fell by 2.6%, 2.4%, and 4.4%, respectively. However, when stratified by age, among men 35 to 54 years of age, the average annual rate of death fell by 6.2%, 2.3%, and 0.5%, respectively. Among women 35 to 54 years of age, the average annual rate of death fell by 5.4% and 1.2% and then increased by 1.5%, respectively. This increase was not statistically significant; however, in even younger women (35–44 years of age), the rate of death has been increasing by an average of 1.3% annually between 1997 and 2002, which is statistically significant.23
•
An analysis of 28 studies published from 1977 to 2007 found that revascularization by coronary bypass surgery or percutaneous intervention in conjunction with medical therapy in patients with nonacute CAD is associated with significantly improved survival compared with medical therapy alone.24
•
A recent analysis of Centers for Medicare & Medicaid Services data suggests that between 1995 and 2006, the 30-day mortality rate attributable to MI decreased, as did hospital variation in mortality attributable to MI.25
•
Data from the Nationwide Inpatient Sample database suggest that mortality attributable to MI has decreased since 1988.26
Risk Factors
•
Risk factors for CHD act synergistically to increase CHD risk, as shown in the example in Chart 5-6.
•
A study of men and women in 3 prospective cohort studies found that antecedent major CHD risk factor exposures were common among those who developed CHD. Approximately 90% of patients with CHD have prior exposure to at least 1 of these major risk factors, which include high total blood cholesterol levels or current medication with cholesterol-lowering drugs, hypertension or current medication with BP-lowering drugs, current cigarette use, and clinical report of DM.27
•
According to a case-control study of 52 countries (INTERHEART), optimization of 9 easily measured and potentially modifiable risk factors could result in a 90% reduction in the risk of an initial AMI. The effect of these risk factors is consistent in men and women across different geographic regions and by ethnic group, which makes the study applicable worldwide. These 9 risk factors include cigarette smoking, abnormal blood lipid levels, hypertension, DM, abdominal obesity, a lack of PA, low daily fruit and vegetable consumption, alcohol overconsumption, and psychosocial index.28
•
A study of >3000 members of the FHS (NHLBI) Offspring Cohort without CHD showed that among men with 10-year predicted risk for CHD of 20%, both failure to reach target heart rate and ST-segment depression more than doubled the risk of an event, and each metabolic equivalent increment in exercise capacity reduced risk by 13%.29
•
An analysis of data from non-Hispanic white adults 35 to 74 years of age who participated in NHANES III (NCHS) showed that 26% of men and 41% of women had at least 1 borderline risk factor (smoking, blood pressure, LDL cholesterol, HDL cholesterol, or glucose intolerance). Additional analyses using data from the FHS (NHLBI) indicated that >90% of hard CHD events over a 10-year period were projected to occur in non-Hispanic white adults 35 to 74 years of age with at least 1 elevated risk factor and ≈8% in adults with only borderline levels of risk factors.30
•
A recent analysis examined the number and combination of risk factors necessary to exceed Adult Treatment Panel III treatment thresholds. In this analysis, relatively high risk factor levels were required to exceed Adult Treatment Panel III treatment thresholds in men <45 years of age and women <65 years of age, which suggests that alternative means of risk prediction that focus on a longer time horizon than the 10 years captured by the traditional Framingham CHD risk score may be necessary to estimate risk in these individuals.31
•
Analysis of data from the CHS study (NHLBI) among participants ≥65 years of age at entry into the study showed that subclinical CVD is prevalent among older individuals, is independently associated with risk of CHD (even over a 10-year follow-up period), and substantially increases the risk of CHD among participants with hypertension or DM.32
•
On the basis of data from the CDC/BRFSS, it was found that patients with CHD are less likely to comply with PA recommendations than are subjects without CHD. Only 32% of CHD patients met moderate PA recommendations, 22% met vigorous PA recommendations, and 40% met total PA recommendations. In contrast, the percentage of subjects without CHD who met PA recommendations was significantly higher, and this percentage almost achieved the Healthy People 2010 objectives for PA.33
•
Analysis of data from the PREMIER trial (Prospective Registry Evaluating Myocardial Infarction: Events and Recovery), sponsored by the NHLBI, found that in people with prehypertension or stage 1 hypertension, 2 multicomponent behavioral interventions significantly reduced estimated 10-year CHD risk by 12% and 14%, respectively, compared with advice only.34
Awareness of Warning Signs and Risk Factors for HD
•
Data from the Women Veterans Cohort showed that 42% of women ≥35 years of age were concerned about HD. Only 8% to 20% were aware that CAD is the major cause of death for women.35
•
Among people in 14 states and Washington, DC, participating in the 2005 BRFSS, only 27% were aware of 5 heart attack warning signs and symptoms (1, pain in jaw, neck, or back; 2, weak, lightheaded, or faint; 3, chest pain or discomfort; 4, pain or discomfort in arms or shoulder; and 5, shortness of breath) and indicated that they would first call 911 if they thought someone was having a heart attack or stroke. Awareness of all 5 heart attack warning signs and symptoms and the need to call 911 was higher among non-Hispanic whites (30.2%), women (30.8%), and those with a college education or more (33.4%) than among non-Hispanic blacks and Hispanics (16.2% and 14.3%, respectively), men (22.5%), and those with less than a high school education (15.7%), respectively. By state, awareness was highest in West Virginia (35.5%) and lowest in Washington, DC (16.0%).36
•
•
A recent community surveillance study in 4 US communities reported that in 2000, the overall proportion of people with delays of ≥4 hours from onset of AMI symptoms to hospital arrival was 49.5%. The study also reported that from 1987 to 2000, there was no statistically significant change in the proportion of patients whose delays were ≥4 hours, which indicates that there has been little improvement in the speed at which patients with MI symptoms arrive at the hospital after symptom onset. Although the proportion of patients with MI who arrived at the hospital by emergency medical services (EMS) increased over this period, from 37% in 1987 to 55% in 2000, the total time between onset and hospital arrival did not change appreciably.39
•
According to 2003 data from the BRFSS (CDC), 36.5% of all women surveyed had multiple risk factors for HD and stroke. The age-standardized prevalence of multiple risk factors was lowest in whites and Asians. After adjustment for age, income, education, and health coverage, the odds for multiple risk factors were greater in black and Native American women and lower for Hispanic women than for white women. Prevalence estimates and odds of multiple risk factors increased with age; decreased with education, income, and employment; and were lower in those with no health coverage. Smoking was more common in younger women, whereas older women were more likely to have medical conditions and to be physically inactive.40
•
Individuals with documented CHD have 5 to 7 times the risk of having a heart attack or dying as the general population. Survival rates improve after a heart attack if treatment begins within 1 hour; however, most patients are admitted to the hospital 2.5 to 3 hours after symptoms begin. More than 3500 patients surveyed with a history of CHD were asked to identify possible symptoms of heart attack. Despite their history of CHD, 44% had low knowledge levels. In this group, who were all at high risk of future AMI, 43% assessed their risk as less than or the same as others their age. More men than women perceived themselves as being at low risk, at 47% versus 36%, respectively.41
•
Data from Worcester, MA, indicate that the average time from symptom onset to hospital arrival has not improved and that delays in hospital arrival are associated with less receipt of guidelines-based care. Mean and median prehospital delay times from symptom onset to arrival at the hospital were 4.1 and 2.0 hours in 1986 and 4.6 and 2.0 hours in 2005, respectively. Compared with those arriving within 2 hours of symptom onset, those with prolonged prehospital delay were less likely to receive thrombolytic therapy and PCI within 90 minutes of hospital arrival.42
•
In an analysis from ARIC, low neighborhood household income (odds ratio [OR] 1.46, 95% confidence interval [CI] 1.09–1.96) and being a Medicaid recipient (OR 1.87, 95% CI 1.10–3.19) were associated with increased odds of having prolonged prehospital delays from symptom onset to hospital arrival for AMI compared with individuals with higher neighborhood household income and other insurance providers, respectively.43
Aftermath
•
Depending on their sex and clinical outcome, people who survive the acute stage of an MI have a chance of illness and death 1.5 to 15 times higher than that of the general population. Among these people, the risk of another MI, sudden death, AP, HF, and stroke—for both men and women—is substantial (FHS, NHLBI).4
•
On the basis of pooled data from the FHS, ARIC, and CHS studies of the NHLBI, within 1 year after a first MI:
— At ≥45 years of age, 19% of men and 26% of women will die.
— At 45 to 64 years of age, 5% of white men, 9% of white women, 14% of black men, and 8% of black women will die.
— At ≥65 years of age, 25% of white men, 30% of white women, 25% of black men, and 30% of black women will die.
— In part because women have MIs at older ages than men, they are more likely to die of MIs within a few weeks.
•
Within 5 years after a first MI:
— At ≥45 years of age, 36% of men and 47% of women will die.
— At 45 to 64 years of age, 11% of white men, 18% of white women, 22% of black men, and 28% of black women will die.
— At ≥65 years of age, 46% of white men, 53% of white women, 54% of black men, and 58% of black women will die.
•
Of those who have a first MI, the percentage with a recurrent MI or fatal CHD within 5 years is:
— At 45 to 64 years of age, 15% of men and 22 of women.
— At ≥65 years of age, 22% of men and women.
— At 45 to 64 years of age, 14% of white men, 18% of white women, 22% of black men, and 28% of black women.
— At ≥65 years of age, 21% of white men and women, 33% of black men, and 26% of black women.
•
The percentage of people with a first MI who will have HF in 5 years is:
— At 45 to 64 years of age, 8% of men and 18% of women.
— At ≥65 years of age, 20% of men and 23% of women.
— At 45 to 64 years of age, 7% of white men, 15% of white women, 13% of black men, and 25% of black women.
— At ≥65 years of age, 19% of white men, 23% of white women, 31% of black men, and 24% of black women.
•
The percentage of people with a first MI who will have a stroke within 5 years is:
— At 45 to 64 years of age, 2% of men and 6% of women.
— At ≥65 years of age, 5% of men and 8% of women.
— At 45 to 64 years of age, 2% of white men, 4% of white women, 3% of black men, and 10% of black women.
— At ≥65 years of age, 5% of white men, 8% of white women, 9% of black men, and 10% of black women.
•
The median survival time (in years) after a first MI is:
— At 55 to 64 years of age, 17.0 for men and 13.3 for women.
— At 65 to 74 years of age, 9.3 for men and 8.8 for women.
— At ≥75 years of age, 3.2 for men and 3.2 for women.
•
A Mayo Clinic study found that cardiac rehabilitation after an MI is underused, particularly in women and the elderly. Women were 55% less likely than men to participate in cardiac rehabilitation, and older study patients were less likely to participate than younger participants. Only 32% of men and women ≥70 years of age participated in cardiac rehabilitation compared with 66% of those 60 to 69 years of age and 81% of those <60 years of age.44
•
Among survivors of an MI, in 2005, 34.7% of BRFSS respondents participated in outpatient cardiac rehabilitation. The prevalence of cardiac rehabilitation was higher among older age groups (≥50 years of age), among men versus women, among Hispanics, among those who were married, among those with higher education, and among those with higher levels of household income.45
•
A recent analysis of Medicare claims data revealed that only 13.9% of Medicare beneficiaries enroll in cardiac rehabilitation after an AMI, and only 31% enroll after CABG. Older people, women, nonwhites, and individuals with comorbidities were less likely to enroll in cardiac rehabilitation programs.46
Hospital Discharges and Ambulatory Care Visits
•
From 1999 to 2009, the number of inpatient discharges from short-stay hospitals with CHD as the first-listed diagnosis decreased from 2 270 000 to 1 537 000 (NHLBI tabulation of NHDS, NCHS).
•
In 2009, there were 14 044 000 ambulatory care visits with CHD as the first-listed diagnosis (NCHS, NAMCS, NHAMCS). There were 12 816 000 physician office visits, 639 000 ED visits, and 589 000 outpatient department visits with a primary diagnosis of CHD (unpublished data, NCHS, NHAMCS, NHLBI tabulation). The majority of these visits (77.7%) were for coronary atherosclerosis.47
•
Age-adjusted hospitalization rate for MI was 215 per 100 000 people in 1979 to 1981, increased to 342 in 1985 to 1987, stabilized for the next decade, and then declined after 1996 to 242 during the period from 2003 to 2005. Rates for men were almost twice those of women. Trends were similar for men and women. Hospitalization rates increased with age and were the highest among those ≥85 years of age.12
•
Most hospitalized patients >65 years of age are women. For MI, 28.4% of hospital stays for people 45 to 64 years of age were for women, but 63.7% of stays for those ≥85 years of age were for women. Similarly, for coronary atherosclerosis, 32.7% of stays among people 45 to 64 years of age were for women; this figure increased to 60.7% of stays among those ≥85 years of age. For nonspecific chest pain, women were more numerous than men among patients <65 years of age. Approximately 54.4% of hospital stays among people 45 to 64 years of age were for women. Women constituted 73.9% of hospital stays for nonspecific chest pain among patients ≥85 years of age, higher than for any other condition examined. For AMI, one third more women than men died in the hospital: 9.3% of women died in the hospital compared with 6.2% of men.48
Operations and Procedures
•
In 2009, an estimated 1 133 000 inpatient PCI procedures, 416 000 inpatient bypass procedures, 1 072 000 inpatient diagnostic cardiac catheterizations, 116 000 inpatient implantable defibrillator procedures, and 397 000 pacemaker procedures were performed for inpatients in the United States. (NHLBI, NCHS, unpublished tabulation).
Cost
•
The estimated direct and indirect cost of heart disease in 2008 is $190.3 billion (MEPS, NHLBI tabulation).
•
•
Over the next 20 years, medical costs of CHD (real 2008$) are projected to increase by ≈200%:
— Indirect costs for all CVD (real 2008$) are projected to increase 61% (from $171.7 billion to $275.8 billion) between 2010 and 2030. Of these indirect costs, CHD is projected to account for ≈40% and has the largest indirect costs.3
Acute Coronary Syndrome
ICD-9 codes 410, 411; ICD-10 I20.0, I21, I22
The term acute coronary syndrome (ACS) is increasingly used to describe patients who present with either AMI or UA. (UA is chest pain or discomfort that is accelerating in frequency or severity and may occur while at rest but does not result in myocardial necrosis.) The discomfort may be more severe and prolonged than typical AP or may be the first time a person has AP. UA, NSTEMI, and STEMI share common pathophysiological origins related to coronary plaque progression, instability, or rupture with or without luminal thrombosis and vasospasm.
•
A conservative estimate for the number of discharges with ACS from hospitals in 2009 is 683 000. Of these, an estimated 399 000 are males and 284 000 are females. This estimate is derived by adding the first-listed inpatient hospital discharges for MI (634 000) to those for UA (49 000; NHDS, NHLBI).
•
When secondary discharge diagnoses in 2009 were included, the corresponding number of inpatient hospital discharges was 1 190 000 unique hospitalizations for ACS; 694 000 were males, and 496 000 were females. Of the total, 829 000 were for MI alone, 357 000 were for UA alone, and 4000 hospitalizations received both diagnoses (NHDS, NHLBI).
Decisions about medical and interventional treatments are based on specific findings noted when a patient presents with ACS. Such patients are classified clinically into 1 of 3 categories according to the presence or absence of ST-segment elevation on the presenting ECG and abnormal (“positive”) elevations of myocardial biomarkers, such as troponins, as follows:
•
STEMI
•
NSTEMI
•
UA
The percentage of ACS or MI cases with ST-segment elevation varies in different registries/databases and depends heavily on the age of patients included and the type of surveillance used. According to the National Registry of Myocardial Infarction 4 (NRMI-4), ≈29% of patients with MI are patients with STEMI.50 The AHA Get With The Guidelines (GWTG) project found that 32% of the patients with MI in the CAD module are patients with STEMI (personal communication from AHA GWTG staff, October 1, 2007). The Global Registry of Acute Coronary Events (GRACE) study, which includes US patient populations, found that 38% of ACS patients have STEMI, whereas the second Euro Heart Survey on ACS (EHS-ACS-II) reported that ≈47% of patients with ACS have STEMI.51
In addition, the percentage of ACS or MI cases with ST-segment elevation appears to be declining. In an analysis of 46 086 hospitalizations for ACS in the Kaiser Permanente Northern California study, the percentage of MI cases with ST-segment elevation decreased from 48.5% to 24% between 1999 and 2008.18
•
Analysis of data from the GRACE multinational observational cohort study of patients with ACS found evidence of a change in practice for both pharmacological and interventional treatments in patients with either STEMI or non–ST-segment–elevation ACS. These changes have been accompanied by significant decreases in the rates of in-hospital death, cardiogenic shock, and new MI among patients with non–ST-segment–elevation ACS. The use of evidence-based therapies and PCI interventions increased in the STEMI population. This increase was matched with a statistically significant decrease in the rates of death, cardiogenic shock, and HF or pulmonary edema.52
•
A study of patients with non–ST-segment–elevation ACS treated at 350 US hospitals found that up to 25% of opportunities to provide American College of Cardiology (ACC)/AHA guideline–recommended care were missed in current practice. The composite guideline adherence rate was significantly associated with in-hospital mortality.52
•
A study of hospital process performance in 350 centers of nearly 65 000 patients enrolled in the CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the ACC/AHA Guidelines) National Quality Improvement Initiative found that ACC/AHA guideline–recommended treatments were adhered to in 74% of eligible instances.53
•
After adjustment for clinical differences and the severity of CAD by angiogram, 30-day mortality after ACS is similar in men and women.54
Angina Pectoris
Prevalence
•
A study of 4 national cross-sectional health examination studies found that among Americans 40 to 74 years of age, the age-adjusted prevalence of AP was higher among women than men. Increases in the prevalence of AP occurred for Mexican American men and women and African American women but were not statistically significant for the latter.55
Incidence
•
Only 18% of coronary attacks are preceded by long-standing AP (NHLBI computation of FHS follow-up since 1986).
•
The annual rates per 1000 population of new episodes of AP for nonblack men are 28.3 for those 65 to 74 years of age, 36.3 for those 75 to 84 years of age, and 33.0 for those ≥85 years of age. For nonblack women in the same age groups, the rates are 14.1, 20.0, and 22.9, respectively. For black men, the rates are 22.4, 33.8, and 39.5, and for black women, the rates are 15.3, 23.6, and 35.9, respectively (CHS, NHLBI).8
•
On the basis of 1987 to 2001 data from the ARIC study of the NHLBI, the annual rates per 1000 population of new episodes of AP for nonblack men are 8.5 for those 45 to 54 years of age, 11.9 for those 55 to 64 years of age, and 13.7 for those 65 to 74 years of age. For nonblack women in the same age groups, the rates are 10.6, 11.2, and 13.1, respectively. For black men, the rates are 11.8, 10.6, and 8.8, and for black women, the rates are 20.8, 19.3, and 10.0, respectively.8
Mortality
A small number of deaths resulting from CHD are coded as being attributable to AP. These are included as a portion of total deaths attributable to CHD.
Cost
For women with nonobstructive CHD enrolled in the Women's Ischemia Syndrome Evaluation (WISE) study of the NHLBI, the average lifetime cost estimate was ≈$770 000 and ranged from $1.0 to $1.1 million for women with 1-vessel to 3-vessel CHD.56
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Rogers WJ, Canto JG, Lambrew CT, Tiefenbrunn AJ, Kinkaid B, Shoultz DA, Frederick PD, Every N. for the Investigators in the National Registry of Myocardial Infarction 1, 2 and 3. Temporal Trends in the Treatment of Over 1.5 Million Patients With Myocardial Infarction in the U.S. from 1990 Through 1999: The National Registry of Myocardial Infarction 1, 2 and 3. J Am Coll Cardiol. 2000;36:2056–2063.
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Roger VL, Weston SA, Gerber Y, Killian JM, Dunlay SM, Jaffe AS, Bell MR, Kors J, Yawn BP, Jacobsen SJ. Trends in incidence, severity, and outcome of hospitalized myocardial infarction. Circulation. 2010;121:863–869.
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McManus DD, Gore J, Yarzebski J, Spencer F, Lessard D, Goldberg RJ. Recent trends in the incidence, treatment, and outcomes of patients with STEMI and NSTEMI. Am J Med. 2011;124:40–47.
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Ford ES, Ajani UA, Croft JB, Critchley JA, Labarthe DR, Kottke TE, Giles WH, Capewell S. Explaining the decrease in U.S. deaths from coronary disease, 1980–2000. N Engl J Med. 2007;356:2388–2398.
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Ford ES, Capewell S. Coronary heart disease mortality among young adults in the U.S. from 1980 through 2002: concealed leveling of mortality rates. J Am Coll Cardiol. 2007;50:2128–2132.
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Krumholz HM, Wang Y, Chen J, Drye EE, Spertus JA, Ross JS, Curtis JP, Nallamothu BK, Lichtman JH, Havranek EP, Masoudi FA, Radford MJ, Han LF, Rapp MT, Straube BM, Normand S-LT. Reduction in acute myocardial infarction mortality in the United States: risk-standardized mortality rates from 1995–2006. JAMA.2009;302:767–773.
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Movahed M-R, John J, Hashemzadeh M, Jamal MM, Hashemzadeh M. Trends in the age adjusted mortality from acute ST segment elevation myocardial infarction in the United States (1988–2004) based on race, gender, infarct location and comorbidities. Am J Cardiol. 2009;104:1030–1034.
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Greenland P, Knoll MD, Stamler J, Neaton JD, Dyer AR, Garside DB, Wilson PW. Major risk factors as antecedents of fatal and nonfatal coronary heart disease events. JAMA. 2003;290:891–897.
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Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L; INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet. 2004;364:937–952.
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Balady GJ, Larson MG, Vasan RS, Leip EP, O'Donnell CJ, Levy D. Usefulness of exercise testing in the prediction of coronary disease risk among asymptomatic persons as a function of the Framingham risk score. Circulation. 2004;110:1920–1925.
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Vasan RS, Sullivan LM, Wilson PW, Sempos CT, Sundström J, Kannel WB, Levy D, D'Agostino RB. Relative importance of borderline and elevated levels of coronary heart disease risk factors [published correction appears in Ann Intern Med. 2005;142:681]. Ann Intern Med. 2005;142:393–402.
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Cavanaugh-Hussey MW, Berry JD, Lloyd-Jones DM. Who exceeds ATP-III risk thresholds? Systematic examination of the effect of varying age and risk factor levels in the ATP-III risk assessment tool. Prev Med. 2008;47:619–623.
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Kuller LH, Arnold AM, Psaty BM, Robbins JA, O'Leary DH, Tracy RP, Burke GL, Manolio TA, Chaves PH. 10-Year follow-up of subclinical cardiovascular disease and risk of coronary heart disease in the Cardiovascular Health Study. Arch Intern Med. 2006;166:71–78.
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Zhao G, Ford ES, Li C, Mokdad AH. Are United States adults with coronary heart disease meeting physical activity recommendations? Am J Cardiol. 2008;101:557–561.
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Maruthur NM, Wang NY, Appel LJ. Lifestyle interventions reduce coronary heart disease risk: results from the PREMIER Trial. Circulation. 2009;119:2026–2031.
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Biswas MS, Calhoun PS, Bosworth HB, Bastian LA. Are women worrying about heart disease? Womens Health Issues. 2002;12:204–211.
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Mosca L, Linfante AH, Benjamin EJ, Berra K, Hayes SN, Walsh BW, Fabunmi RP, Kwan J, Mills T, Simpson SL. National study of physician awareness and adherence to cardiovascular disease prevention guidelines. Circulation. 2005;111:499–510.
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Mosca L, Mochari-Greenberger H, Dolor RJ, Newby LK, Robb KJ. Twelve-year follow-up of American women's awareness of cardiovascular disease risk and barriers to heart health. Circ Cardiovasc Qual Outcomes. 2010;3:120–127.
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McGinn AP, Rosamond WD, Goff DC, Taylor HA, Miles JS, Chambless L. Trends in prehospital delay time and use of emergency medical services for acute myocardial infarction: experience in 4 US communities from 1987–2000. Am Heart J. 2005;150:392–400.
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Hayes DK, Denny CH, Keenan NL, Croft JB, Sundaram AA, Greenlund KJ. Racial/ethnic and socioeconomic differences in multiple risk factors for heart disease and stroke in women: Behavioral Risk Factor Surveillance System, 2003. J Womens Health (Larchmt). 2006;15:1000–1008.
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Dracup K, McKinley S, Doering LV, Riegel B, Meischke H, Moser DK, Pelter M, Carlson B, Aitken L, Marshall A, Cross R, Paul SM. Acute coronary syndrome: what do patients know? Arch Intern Med. 2008;168:1049–1054.
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Saczynski JS, Yarzebski J, Lessard D, Spencer FA, Gurwitz JH, Gore JM, Goldberg RJ. Trends in prehospital delay in patients with acute myocardial infarction (from the Worcester Heart Attack Study). Am J Cardiol. 2008;102:1589–1594.
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Foraker RE, Rose KM, McGinn AP, Suchindran CM, Goff DC, Whitsel EA, Wood JL, Rosamond WD. Neighborhood income, health insurance, and prehospital delay for myocardial infarction: the Atherosclerosis Risk in Communities Study. Arch Intern Med. 2008;168:1874–1879.
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Witt BJ, Jacobsen SJ, Weston SA, Killian JM, Meverden RA, Allison TG, Reeder GS, Roger VL. Cardiac rehabilitation after myocardial infarction in the community. J Am Coll Cardiol. 2004;44:988–996.
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Centers for Disease Control and Prevention (CDC). Receipt of outpatient cardiac rehabilitation among heart attack survivors–United States, 2005. MMWR Morb Mortal Wkly Rep. 2008;57:89–94.
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Suaya JA, Shepard DS, Normand SL, Ades PA, Prottas J, Stason WB. Use of cardiac rehabilitation by Medicare beneficiaries after myocardial infarction or coronary bypass surgery. Circulation. 2007;116:1653–1662.
47.
Deleted in proof.
48.
Elixhauser A, Jiang HJ. Hospitalizations for Women With Circulatory Disease, 2003. HCUP Statistical Brief No. 5. Rockville, MD: Agency for Healthcare Research and Quality; May 2006. http://www.hcupus.ahrq.gov/reports/statbriefs/sb5.pdf. Accessed August 3, 2011.
49.
Centers for Medicare & Medicaid Services. Medicare & Medicaid Statistical Supplement. Table 5.5: Discharges, total days of care, and program payments for Medicare beneficiaries discharged from short-stay hospitals, by principal diagnoses within major diagnostic classifications (MDCs): calendar year 2006. Baltimore, MD: Centers for Medicare & Medicaid Services; 2007. http://www.cms.hhs.gov/MedicareMedicaidStatSupp/downloads/2007Table5.5b.pdf. Accessed July 25, 2011.
50.
Roe MT, Parsons LS, Pollack CV, Canto JG, Barron HV, Every NR, Rogers WJ, Peterson ED; National Registry of Myocardial Infarction Investigators. Quality of care by classification of myocardial infarction: treatment patterns for ST-segment elevation vs non-ST-segment elevation myocardial infarction. Arch Intern Med. 2005;165:1630–1636.
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Mandelzweig L, Battler A, Boyko V, Bueno H, Danchin N, Filippatos G, Gitt A, Hasdai D, Hasin Y, Marrugat J, Van de Werf F, Wallentin L, Behar S; Euro Heart Survey Investigators. The second Euro Heart Survey on acute coronary syndromes: characteristics, treatment, and outcome of patients with ACS in Europe and the Mediterranean Basin in 2004. Eur Heart J. 2006;27:2285–2293.
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Fox KA, Steg PG, Eagle KA, Goodman SG, Anderson FA, Granger CB, Flather MD, Budaj A, Quill A, Gore JM; GRACE Investigators. Decline in rates of death and heart failure in acute coronary syndromes, 1999–2006. JAMA. 2007;297:1892–1900.
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Peterson ED, Roe MT, Mulgund J, DeLong ER, Lytle BL, Brindis RG, Smith SC, Pollack CV, Newby LK, Harrington RA, Gibler WB, Ohman EM. Association between hospital process performance and outcomes among patients with acute coronary syndromes. JAMA. 2006;295:1912–1920.
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Berger JS, Elliott L, Gallup D, Roe M, Granger CB, Armstrong PW, Simes RJ, White HD, Van de Werf F, Topol EJ, Hochman JS, Newby LK, Harrington RA, Califf RM, Becker RC, Douglas PS. Sex differences in mortality following acute coronary syndromes. JAMA. 2009;302:874–882.
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Ford ES, Giles WH. Changes in prevalence of nonfatal coronary heart disease in the United States from 1971–1994. Ethn Dis. 2003;13:85–93.
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Shaw LJ, Merz CN, Pepine CJ, Reis SE, Bittner V, Kip KE, Kelsey SF, Olson M, Johnson BD, Mankad S, Sharaf BL, Rogers WJ, Pohost GM, Sopko G; Women's Ischemia Syndrome Evaluation Investigators. The economic burden of angina in women with suspected ischemic heart disease: results from the National Institutes of Health–National Heart, Lung, and Blood Institute–sponsored Women's Ischemia Syndrome Evaluation. Circulation. 2006;114:894–904.
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Wilson PW, D'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. Prediction of coronary heart disease using risk factor categories. Circulation. 1998;97:1837–1847.
6. Stroke (Cerebrovascular Disease)
| Population Group | Prevalence, 2008: Age ≥20 y | New and Recurrent Attacks All Ages | Mortality, 2008: All Ages* | Hospital Discharges, 2009: All Ages | Cost, 2008 |
|---|---|---|---|---|---|
| Both sexes | 7 000 000 (3.0%) | 795 000 | 134 148 | 971 000 | $34.3 billion |
| Males | 2 800 000 (2.7%) | 370 000 (46.5%)† | 53 525 (39.9%)† | 467 000 | |
| Females | 4 200 000 (3.3%) | 425 000 (53.5%)† | 80 623 (60.1%)† | 504 000 | |
| NH white males | 2.4% | 325 000‡ | 44 457 | ||
| NH white females | 3.3% | 365 000‡ | 68 787 | ||
| NH black males | 4.5% | 45 000‡ | 7222 | ||
| NH black females | 4.4% | 60 000‡ | 9488 | ||
| Mexican-American males | 2.0% | ||||
| Mexican-American females | 2.7% | ||||
| Hispanic or Latino | 2.6%§ | ||||
| Asian | 2.0%§ | ||||
| Hawaiian and other Pacific Islander | 10.6%§ | ||||
| American Indian/Alaska Native | 5.9% §‖ |
NH indicates non-Hispanic; ellipses (…) indicate data not available.
*
Mortality data for the white, black, Asian or Pacific Islander, and American Indian/Alaska Native populations include deaths of persons of Hispanic and non-Hispanic origin. Numbers of deaths for the American Indian/Alaska Native and Asian or Pacific Islander populations are known to be underestimated.
†
These percentages represent the portion of total stroke incidence or mortality that applies to males vs females.
‡
Estimates include Hispanics and non-Hispanics. Estimates for whites include other nonblack races.
§
National Health Interview Survey (2010), National Center for Health Statistics (NCHS); data are weighted percentages for Americans >18 years of age.146
‖
This estimate has a relative standard error of >30% but <50%.
Sources: Prevalence: National Health and Nutrition Examination Survey 2005 to 2008, NCHS and National Heart, Lung, and Blood Institute (NHLBI). Percentages for racial/ethnic groups are age adjusted for Americans ≥20 years of age. Age-specific percentages are extrapolated to the 2008 US population.
Incidence: Greater Cincinnati/Northern Kentucky Stroke Study/National Institutes of Neurological Disorders and Stroke data for 1999 provided on August 1, 2007. US estimates compiled by NHLBI. Data include children. Mortality: NCHS. These data represent underlying cause of death only. Mortality data for white and black males and females include Hispanics. Hospital discharges: National Hospital Discharge Survey, NCHS. Data include those inpatients discharged alive, dead, or status unknown. Cost: NHLBI. Data include estimated direct and indirect costs for 2008.
RR indicates relative risk; SAH, subarachnoid hemorrhage; CI, confidence interval; HDL, high-density lipoprotein; and CHD, coronary heart disease.
*
Population attributable risk is the proportion of ischemic stroke in the population that can be attributed to a particular risk factor (see Goldstein et al78 for formula).
†
Population attributable risk is for stroke deaths, not ischemic stroke incidence.
‡
Population attributable risk percent=100[(prevalence)(RR−1)/((prevalence)(RR−1)+1)].
§
Calculated on the basis of point estimates of referenced data provided in the table. For peripheral arterial disease, calculation was based on average relative risk for men and women.
‖
Calculated based on referenced data provided in the table or text.
¶
Relative to stroke risk in children without sickle cell disease.
Adapted from Goldstein et al.78
| AF | atrial fibrillation |
| AHA | American Heart Association |
| ARIC | Atherosclerosis Risk in Communities study |
| BASIC | Brain Attack Surveillance in Corpus Christi |
| BP | blood pressure |
| BRFSS | Behavioral Risk Factor Surveillance System |
| CDC | Centers for Disease Control and Prevention |
| CHD | coronary heart disease |
| CHS | Cardiovascular Health Study |
| CI | confidence interval |
| CLRD | chronic lower respiratory disease |
| CREST | Carotid Revascularization Endarterectomy versus Stenting Trial |
| CVD | cardiovascular disease |
| DM | diabetes mellitus |
| ED | emergency department |
| EMS | emergency medical services |
| FHS | Framingham Heart Study |
| FRS | Framingham Risk Score |
| GCNKSS | Greater Cincinnati/Northern Kentucky Stroke Study |
| HD | heart disease |
| HDL | high-density lipoprotein |
| HERS | Heart and Estrogen/Progestin Replacement Study |
| HR | hazard ratio |
| ICD-9 | International Classification of Diseases, 9th Revision |
| ICD-10 | International Classification of Diseases, 10th Revision |
| MEPS | Medical Expenditure Panel Survey |
| MI | myocardial infarction |
| NCHS | National Center for Health Statistics |
| NH | Non-Hispanic |
| NHANES | National Health and Nutrition Examination Survey |
| NHDS | National Hospital Discharge Survey |
| NHIS | National Health Interview Survey |
| NHLBI | National Heart, Lung, and Blood Institute |
| NIHSS | National Institutes of Health Stroke Scale |
| NINDS | National Institutes of Neurological Disorders and Stroke |
| NOMAS | Northern Manhattan Study |
| OR | odds ratio |
| PA | physical activity |
| REGARDS | Reasons for Geographic and Racial Differences in Stroke study |
| RR | relative risk |
| TIA | transient ischemic attack |
| WEST | Women's Estrogen for Stroke Trial |
| WHI | Women's Health Initiative |
Stroke Prevalence
•
An estimated 7 000 000 Americans ≥20 years of age have had a stroke (extrapolated to 2008 using NCHS/NHANES 2005–2008 data). Overall stroke prevalence during this period is an estimated 3.0% (Table 6-1).
•
According to data from the 2010 BRFSS (CDC), 2.6% of men and 2.6% of women ≥18 years of age had a history of stroke; 2.4% of non-Hispanic whites, 4.0% of non-Hispanic blacks, 1.4% of Asian/Pacific Islanders, 2.5% of Hispanics (of any race), 5.8% of American Indian/Alaska Natives, and 4.1% of other races or multiracial people had a history of stroke (NHLBI tabulation of BRFSS).
•
The prevalence of silent cerebral infarction is estimated to range from 6% to 28%, with higher prevalence with increasing age.1–3 The prevalence estimates also vary depending on the population studied (eg, ethnicity, sex, risk factor profile), definition of silent cerebral infarction, and imaging technique. It has been estimated that 13 million people had prevalent silent stroke in the 1998 US population.4,5
•
The prevalence of stroke-related symptoms was found to be relatively high in a general population free of a prior diagnosis of stroke or transient ischemic attack (TIA). On the basis of data from 18 462 participants enrolled in a national cohort study, 17.8% of the population >45 years of age reported at least 1 symptom. Stroke symptoms were more likely among blacks than whites, among those with lower income and lower educational attainment, and among those with fair to poor perceived health status. Symptoms also were more likely in participants with higher Framingham stroke risk score (Reasons for Geographic and Racial Differences in Stroke study [REGARDS], NINDS).6
•
Projections show that by 2030, an additional 4 million people will have had a stroke, a 24.9% increase in prevalence from 2010.7
Stroke Incidence
•
Each year, ≈795 000 people experience a new or recurrent stroke. Approximately 610 000 of these are first attacks, and 185 000 are recurrent attacks (GCNKSS, NINDS, and NHLBI; GCNKSS and NINDS data for 1999 provided July 9, 2008; estimates compiled by NHLBI). Of all strokes, 87% are ischemic and 10% are intracerebral hemorrhagic strokes, whereas 3% are subarachnoid hemorrhage strokes (GCNKSS, NINDS, 1999).
•
On average, every 40 seconds, someone in the United States has a stroke (AHA computation based on the latest available data).
•
Each year, ≈55 000 more women than men have a stroke (GCNKSS, NINDS).8
•
Women have a higher lifetime risk of stroke than men. In the FHS, lifetime risk of stroke among those 55 to75 years of age was 1 in 5 for women (20% to 21%) and approximately 1 in 6 for men (14% to 17%).9
•
Women have lower age-adjusted stroke incidence than men; however, sex differences in stroke risk may be modified by age.10 Data from FHS demonstrate that compared with white men, white women 45 to 84 years of age have lower stroke risk than men, but this association is reversed in older ages such that women >85 years of age have elevated risk compared with men.11 Similarly, a population-based study in Sweden found stroke incidence to be lower for women than men at ages 55 to 64 years, but at 75 to 85 years of age, this association reversed, and women had a higher incidence than men.12 Other studies report an excess risk of stroke in men compared with women that persists throughout the life course or diminishes but does not reverse with age.13–15
•
On average, women are older at stroke onset than men (≈75 years compared with 71 years).11
•
Blacks have a risk of first-ever stroke that is almost twice that of whites.16
•
In the national REGARDS cohort, in 27 744 participants followed up over 4.4 years (2003–2010), the overall age- and sex-adjusted black/white incidence rate ratio was 1.51, but for ages 45 to 54 years, it was 4.02, whereas for those ≥85 years of age, it was 0.86.17 Similar trends for decreasing incidence rate ratio were seen in the GCNKSS.18
•
Analysis of data from the FHS suggests that stroke incidence is declining over time in this largely white cohort. Data from 1950 to 1977, 1978 to 1989, and 1990 to 2004 showed that the age-adjusted incidence of first stroke per 1000 person-years in each of the 3 periods was 7.6, 6.2, and 5.3 in men and 6.2, 5.8, and 5.1 in women, respectively. Lifetime risk for incident stroke at 65 years of age decreased significantly in the latest data period compared with the first, from 19.5% to 14.5% in men and from 18.0% to 16.1% in women.19
•
In a similar fashion, data from the most recent GCNKSS show that compared with the 1990s, when incidence rates of stroke were stable, stroke incidence in 2005 was decreased for whites. Unfortunately, a similar decline was not seen in blacks. These changes for whites were driven by a decline in ischemic strokes for whites. There were no changes in incidence of ischemic stroke for blacks or for hemorrhagic strokes in blacks or whites.8
•
The BASIC (Brain Attack Surveillance in Corpus Christi) project (NINDS) demonstrated an increased incidence of stroke among Mexican Americans compared with non-Hispanic whites in a community in southeast Texas. The crude 3-year cumulative incidence (2000–2002) was 16.8 per 1000 in Mexican Americans and 13.6 per 1000 in non-Hispanic whites. Specifically, Mexican Americans had a higher cumulative incidence for ischemic stroke at younger ages (45–59 years of age: RR 2.04, 95% CI 1.55–2.69; 60–74 years of age: RR 1.58, 95% CI 1.31–1.91) but not at older ages (≥75 years of age: RR 1.12, 95% CI 0.94–1.32). Mexican Americans also had a higher incidence of intracerebral hemorrhage and subarachnoid hemorrhage than non-Hispanic whites, adjusted for age.20
•
The age-adjusted incidence of first ischemic stroke per 1000 was 0.88 in whites, 1.91 in blacks, and 1.49 in Hispanics according to data from the Northern Manhattan Study (NOMAS; NINDS) for 1993 to 1997. Among blacks, compared with whites, the relative rate of intracranial atherosclerotic stroke was 5.85; of extracranial atherosclerotic stroke, 3.18; of lacunar stroke, 3.09; and of cardioembolic stroke, 1.58. Among Hispanics (primarily Cuban and Puerto Rican), compared with whites, the relative rate of intracranial atherosclerotic stroke was 5.00; of extracranial atherosclerotic stroke, 1.71; of lacunar stroke, 2.32; and of cardioembolic stroke, 1.42.21
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Among 4507 American Indian participants without a prior stroke in the Strong Heart Study in 1989 to 1992, the age- and sex-adjusted incidence of stroke through 2004 was 6.79 per 100 person-years, with 86% of incident strokes being ischemic.22
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A review of published studies and data from clinical trials found that hospital admissions for intracerebral hemorrhage have increased by 18% in the past 10 years, probably because of increases in the number of elderly people, many of whom lack adequate BP control, as well as the increasing use of anticoagulants, thrombolytics, and antiplatelet agents. Mexican Americans, Latin Americans, blacks, Native Americans, Japanese people, and Chinese people have higher incidences than do white Americans.23
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In the GCNKSS, the annual incidence of anticoagulant-associated intracerebral hemorrhage per 100 000 people increased from 0.8 (95% CI 0.3–1.3) in 1988 to 1.9 (95% CI 1.1–2.7) in 1993/1994 and 4.4 (95% CI 3.2–5.5) in 1999 (P<0.001 for trend). Among people ≥80 years of age, the rate of anticoagulant-associated intracerebral hemorrhage increased from 2.5 (95% CI 0–7.4) in 1988 to 45.9 (95% CI 25.6–66.2) in 1999 (P<0.001 for trend). Over this period of time, incidence rates of cardioembolic ischemic stroke were similar, whereas warfarin distribution in the United States quadrupled on a per capita basis. The increase in incidence is therefore attributable to prescribing behavior and patterns of care.24
TIA: Prevalence and Incidence
•
In a nationwide survey of US adults, the estimated prevalence of self-reported physician-diagnosed TIA was 2.3%, which translates into ≈5 million people. The true prevalence of TIA is greater, because many patients who experience neurological symptoms consistent with a TIA fail to report it to their healthcare provider.25
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•
•
Approximately 15% of all strokes are heralded by a TIA.28
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TIAs confer a substantial short-term risk of stroke, hospitalization for CVD events, and death. Of 1707 TIA patients evaluated in the ED of Kaiser Permanente Northern California, a large, integrated healthcare delivery system, 180 (10%) experienced a stroke within 90 days. Ninety-one patients (5%) had a stroke within 2 days. Predictors of stroke included age >60 years, DM, focal symptoms of weakness or speech impairment, and TIA that lasted >10 minutes.29
•
•
Individuals who have a TIA and survive the initial high-risk period have a 10-year stroke risk of roughly 19% and a combined 10-year stroke, MI, or vascular death risk of 43% (4% per year).32
•
Within 1 year of TIA, ≈12% of patients will die.26
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It is estimated that one third of episodes characterized as TIA according to the classic definition (ie, focal neurological deficits that resolve within 24 hours) would be considered infarctions on the basis of diffusion-weighted magnetic resonance imaging findings.33
Stroke Mortality
•
On average, every 4 minutes, someone dies of a stroke (NCHS, NHLBI).33a
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Stroke accounted for ≈1 of every 18 deaths in the United States in 2008.33a
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When considered separately from other CVDs, stroke ranks No. 4 among all causes of death, behind diseases of the heart, cancer, and CLRD (NCHS mortality data). Stroke mortality in 2008 was 134 148; any-mention mortality in 2008 was 223 841 and the death rate was 40.7.33a See Chart 6-6 for sex and race comparisons.
•
•
Conclusions about changes in stroke death rates from 1980 to 2005 are as follows:
— There was a greater decline in stroke death rates in men than in women, with a male-to-female ratio decreasing from 1.11 to 1.03 (age adjusted).
— There were greater declines in stroke death rates in men than in women among people ≥65 years of age than among younger ages.34
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Approximately 54% of stroke deaths in 2008 occurred out of the hospital (unpublished NHLBI tabulation of NCHS 2008 Mortality Data Set).
•
Among people 45 to 64 years of age, 8% to 12% of ischemic strokes and 37% to 38% of hemorrhagic strokes result in death within 30 days, according to 1987 to 2001 data from the ARIC study of the NHLBI.35
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In a study of people ≥65 years of age recruited from a random sample of Health Care Financing Administration Medicare Part B eligibility lists in 4 US communities (CHS), over the time period 1989 to 2000, the 1-month case fatality rate was 12.6% for all strokes, 8.1% for ischemic strokes, and 44.6% for hemorrhagic strokes.36
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More women than men die of stroke each year because of the larger number of elderly women. Women accounted for 60.1% of US stroke deaths in 2008.
•
From 1995 to 1998, age-standardized mortality rates for ischemic stroke, subarachnoid hemorrhage, and intracerebral hemorrhage were higher among blacks than whites. Death rates attributable to intracerebral hemorrhage also were higher among Asians/Pacific Islanders than among whites. All minority populations had higher death rates attributable to subarachnoid hemorrhage than did whites. Among adults 25 to 44 years of age, blacks and American Indian/Alaska Natives had higher risk ratios than did whites for all 3 stroke subtypes.37
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Age-adjusted stroke mortality rates began to level off in the 1980s and stabilized in the 1990s for both men and women, according to the Minnesota Heart Study. Women had lower rates of stroke mortality than did men throughout the period. Some of the improvement in stroke mortality may be the result of improved acute stroke care, but most is thought to be the result of improved detection and treatment of hypertension.38
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In 2002, death certificate data showed that the mean age at stroke death was 79.6 years; however, males had a younger mean age at stroke death than females. Blacks, American Indian/Alaska Natives, and Asian/Pacific Islanders had younger mean ages than whites, and the mean age at stroke death was also younger among Hispanics than non-Hispanics.39
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A report released by the CDC in collaboration with the Centers for Medicare & Medicaid Services, the Atlas of Stroke Hospitalizations Among Medicare Beneficiaries, found that in Medicare beneficiaries over the time period 1995 to 2002, 30-day mortality rate varied by age: 9% in patients 65 to 74 years of age, 13.1% in those 74 to 84 years of age, and 23% in those ≥85 years of age.40
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The black/white disparity in stroke mortality varies by age in a similar fashion to stroke incidence as described above.
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There are substantial geographic disparities in stroke mortality, with higher rates in the southeastern United States, known as the “stroke belt” (Chart 6-7). This area is usually defined to include the 8 southern states of North Carolina, South Carolina, Georgia, Tennessee, Mississippi, Alabama, Louisiana, and Arkansas. These geographic differences have existed since at least 1940,41 and despite some minor shifts,42 they persist.43–45 Within the stroke belt, a “buckle” region along the coastal plain of North Carolina, South Carolina, and Georgia has been identified with even a higher stroke mortality rate than the remainder of the stroke belt.46 The overall average stroke mortality is ≈20% higher in the stroke belt than in the rest of the nation and ≈40% higher in the stroke buckle.
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Racial and regional patterns in stroke incidence have been shown to be similar to patterns for stroke mortality, which suggests that disparities in incidence play a substantial role in mortality disparities. However, incidence only partly explains mortality disparities, and differences in case fatality or other factors likely contribute to racial and geographic disparities in stroke mortality.47
Stroke Risk Factors
For prevalence and other information on any of these specific risk factors, refer to the specific risk factor chapters:
■ High blood pressure: Chapter 7
■ Disorders of heart rhythm (including atrial fibrillation): Chapter 10
■ Smoking/Tobacco Use: Chapter 13
■ High blood cholesterol and other lipids: Chapter 14
■ Physical inactivity: Chapter 15
■ Diabetes mellitus: Chapter 17
■ End-stage renal disease and chronic kidney disease: Chapter 18
(See Table 6-2 for data on modifiable stroke risk factors.)
•
BP is a powerful determinant of risk for both ischemic stroke and intracranial hemorrhage. Subjects with BP <120/80 mm Hg have approximately half the lifetime risk of stroke of subjects with hypertension. The treatment and lowering of BP among hypertensive individuals was associated with a significant reduction in stroke risk.48
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In REGARDS (NINDS), black participants were more aware than whites of their hypertension and more likely to be undergoing treatment if aware of their diagnosis, but among those treated for hypertension, they were less likely than whites to have their BP controlled.49
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REGARDS (NINDS) also showed no evidence of a difference between the stroke belt and other regions in awareness of hypertension, but there was a trend for better treatment and BP control in the stroke belt region. The lack of substantial geographic differences in hypertension awareness and the trend toward better treatment and control in the stroke belt suggest that differences in hypertension management may not be a major contributor to the geographic disparity in stroke mortality.49
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Impaired glucose tolerance nearly doubled the stroke risk compared with patients with normal glucose levels and tripled the risks for patients with DM.50
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Age-specific incidence rates and rate ratios show that DM increases ischemic stroke incidence at all ages, but this risk is most prominent before 55 years of age in blacks and before 65 years of age in whites. Ischemic stroke patients with DM are younger, more likely to be black, and more likely to have hypertension, MI, and high cholesterol than nondiabetic patients.51
•
•
Because AF is often asymptomatic54,55 and likely frequently clinically undetected,56 the stroke risk attributed to AF may be substantially underestimated.57 Therefore, although AF is an important stroke risk factor, both patients and treating physicians may be unaware of its presence. A related point is that no strategy to pursue normal sinus rhythm, including cardioversion, antiarrhythmic drug therapy, and/or ablation, has definitively been shown to reduce the risk of stroke.
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Data from the Honolulu Heart Program/NHLBI found that in Japanese men 71 to 93 years of age, low concentrations of HDL cholesterol were more likely to be associated with a future risk of thromboembolic stroke than were high concentrations.58
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In the FHS, a documented parental ischemic stroke by the age of 65 years was associated with a 300% increase in documented ischemic stroke risk in offspring, even after adjustment for other known stroke risk factors. The absolute magnitude of the increased risk was greatest in those in the highest quintile of the FRS. By age 65 years, people in the highest FRS quintile with an early parental ischemic stroke had a 25% risk of stroke compared with a 7.5% risk of ischemic stroke for those without such a history.59
Risk Factor Issues Specific to Women
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Analysis of data from the FHS found that women with natural menopause before 42 years of age had twice the ischemic stroke risk of women with natural menopause after age 42.62 Investigators from the Nurse's Health Study, however, did not find an association between age at natural menopause and risk of ischemic or hemorrhagic stroke.63
•
•
Among postmenopausal women who were generally healthy, the Women's Health Initiative (WHI), a randomized trial of 16 608 women (95% of whom had no preexisting CVD), found that estrogen plus progestin increased ischemic stroke risk by 44%, with no effect on hemorrhagic stroke.64
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In the WHI trial, among 10 739 women with hysterectomy, it was found that conjugate equine estrogen alone increased the risk of ischemic stroke by 55% and that there was no significant effect on hemorrhagic stroke.66
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In postmenopausal women with known CHD, the Heart and Estrogen/Progestin Replacement Study (HERS), a secondary CHD prevention trial, found that estrogen plus progestin hormone therapy did not reduce stroke risk.67
•
The Women's Estrogen for Stroke Trial (WEST) found that estrogen alone in postmenopausal women with a recent stroke or TIA had no significant overall effect on recurrent stroke or fatality.68
•
Analysis of data from the FHS found that women with menopause at 42 to 54 years of age and at ≥55 years of age had lower stroke risk than those with menopause at <42 years of age, even after adjustment for potential confounders. Women with menopause before 42 years of age had twice the stroke risk of all other women in different age groups.62
•
The risk of ischemic stroke or intracerebral hemorrhage during pregnancy and the first 6 weeks after giving birth was 2.4 times greater than for nonpregnant women of similar age and race, according to the Baltimore-Washington Cooperative Young Stroke Study. The risk of ischemic stroke during pregnancy was not increased during pregnancy per se but was increased 8.7-fold during the first 6 postpartum weeks. Intracerebral hemorrhage showed a small RR of 2.5 during pregnancy but increased dramatically to an RR of 28.3 in the first 6 postpartum weeks. The excess risk of stroke (all types except subarachnoid hemorrhage) attributable to the combined pregnancy/postpregnancy period was 8.1 per 100 000 pregnancies.69
•
In the US Nationwide Inpatient Sample from 2000 to 2001, the rate of events per 100 000 pregnancies was 9.2 for ischemic stroke, 8.5 for intracerebral hemorrhage, 0.6 for cerebral venous thrombosis, and 15.9 for the ill-defined category of pregnancy-related cerebrovascular events, for a total rate of 34.2 per 100 000, not including subarachnoid hemorrhage. The risk was increased in blacks and among older women. Death occurred during hospitalization in 4.1% of women with these events and in 22% of survivors after discharge to a facility other than home.70
•
Analyses of the US Nationwide Inpatient Sample from 1994 to 1995 and from 2006 to 2007 show a temporal increase in the proportion of pregnancy hospitalizations that were associated with a stroke, with a 47% increase for antenatal hospitalizations and 83% increase for postpartum hospitalizations, but no increase for delivery hospitalizations. Increases in the prevalence of heart disease and hypertensive disorders accounted for almost all the increase in postpartum stroke hospitalizations but not the antenatal stroke hospitalizations.71
Physical Inactivity as a Risk Factor for Stroke
•
In NOMAS, a prospective cohort that included white, black, and Hispanic men and women in an urban setting followed up for a median of 9 years, baseline PA was associated with an overall 35% reduction in risk of ischemic stroke.74
•
The NOMAS study found that only moderate- to vigorous-intensity exercise was associated with reduced stroke incidence, whereas light exercise (such as walking) showed no benefit.75
•
Timing of PA in relation to stroke onset has also been examined in several studies. In a hospital-based case-control study from Heidelberg, Germany, recent activity (within the prior months) was associated with reduced odds of having a stroke or TIA, whereas sports activity during young adulthood that was not continued showed no benefit.76 In a Danish case-control study, ischemic stroke patients were less physically active in the week preceding the stroke than age- and sex-matched control subjects, with the highest activity scores associated with the greatest reduction in odds of stroke.77
Smoking
(See Chapter 13 for more information.)
Sleep Apnea
•
•
•
Awareness of Stroke Warning Signs and Risk Factors
•
Correct knowledge of at least 1 stroke warning sign increased from 48% in 1995% to 68% in 2000, with no significant improvement to 2005 (68%) on the basis of a telephone survey conducted in a biracial population in the greater Cincinnati/Northern Kentucky region. Knowledge of 3 correct warning signs was low but increased over time: 5.4% in 1995, 12.0% in 2000, and 15.7% in 2005. Knowledge of at least 1 stroke risk factor increased from 59% in 1995% to 71% in 2000, but there was no improvement to 2005 (71%). Only 3.6% of those surveyed were able to independently identify tissue-type plasminogen activator as an available drug therapy, and only 9% of these were able to identify a window of <3 hours for treatment.99
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In the 2005 BRFSS, among respondents in 14 states, 38.1% were aware of 5 stroke warning symptoms and would first call 9-1-1 if they thought that someone was having a heart attack or stroke. Awareness of all 5 stroke warning symptoms and calling 9-1-1 was higher among whites than blacks and Hispanics (41.3%, 29.5%, and 26.8%, respectively), women than men (41.5% versus 34.5%), and people with higher versus lower educational attainment (47.6% for people with a college degree or more versus 22.5% for those who had not received a high school diploma).100
•
A study was conducted of patients admitted to an ED with possible stroke to determine their knowledge of the signs, symptoms, and risk factors of stroke. Of the 163 patients able to respond, 39% did not know a single sign or symptom. Patients ≥65 years of age were less likely than those <65 years old to know a sign or symptom of stroke (28% versus 47%), and 43% did not know a single risk factor. Overall, almost 40% of patients did not know the signs, symptoms, and risk factors of stroke.101
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In 2004, 800 adults ≥45 years of age were surveyed to assess their perceived risk for stroke and their history of stroke risk factors. Overall, 39% perceived themselves to be at risk. Younger age, current smoking, a history of DM, high BP, high cholesterol, HD, and stroke/TIA were independently associated with perceived risk for stroke. Respondents with AF were no more likely to report being at risk than were respondents without AF. Perceived risk for stroke increased as the number of risk factors increased; however, 46% of those with ≥3 risk factors did not perceive themselves to be at risk.102
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A study of patients who have had a stroke found that only 60.5% were able to accurately identify 1 stroke risk factor and that 55.3% were able to identify 1 stroke symptom. Patients' median delay time from onset of symptoms to admission in the ED was 16 hours, and only 31.6% accessed the ED in <2 hours. Analysis showed that the appearance of nonmotor symptoms as the primary symptom and nonuse of the 9-1-1 system were significant predictors of delay >2 hours. Someone other than the patient made the decision to seek treatment in 66% of the cases.103
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Spanish-speaking Hispanics are less likely to know all stroke symptoms than English-speaking Hispanics, non-Hispanic blacks, and non-Hispanic whites. Lack of English proficiency is strongly associated with lack of stroke knowledge among Hispanics.104
Aftermath
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Stroke is a leading cause of serious long-term disability in the United States (Survey of Income and Program Participation, a survey of the US Bureau of the Census).105
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In the NHLBI's FHS, among ischemic stroke survivors who were ≥65 years of age, these disabilities were observed at 6 months after stroke106:
— 50% had some hemiparesis
— 30% were unable to walk without some assistance
— 26% were dependent in activities of daily living
— 19% had aphasia
— 35% had depressive symptoms
— 26% were institutionalized in a nursing home
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Data from the BRFSS (CDC) 2005 survey on stroke survivors in 21 states and the District of Columbia found that 30.7% of stroke survivors received outpatient rehabilitation. The findings indicated that the prevalence of stroke survivors receiving outpatient stroke rehabilitation was lower than would be expected if clinical practice guideline recommendations for all stroke patients had been followed.107
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Black stroke survivors had greater limitations in ambulation than did white stroke survivors, after adjustment for age, sex, and educational attainment but not stroke subtype, according to data from the NHIS (2000–2001, NCHS) as analyzed by the CDC.108 A national study of inpatient rehabilitation after first stroke found that blacks were younger, had a higher proportion of hemorrhagic stroke, and were more disabled on admission. Compared with non-Hispanic whites, blacks and Hispanics also had a poorer functional status at discharge but were more likely to be discharged to home rather than to another institution even after adjustment for age and stroke subtype. After adjustment for the same covariates, compared with non-Hispanic whites, blacks also had less improvement in functional status per inpatient day.109
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After stroke, women have greater disability than men. A cross-sectional analysis of 5888 community-living elderly people (>65 years of age) in the CHS who were ambulatory at baseline found that women were half as likely to be independent in activities of daily living after stroke, even after controlling for age, race, education, and marital status.110 A prospective study from a Michigan-based stroke registry found that women had a 63% lower probability of achieving independence in activities of daily living 3 months after discharge, even after controlling for age, race, subtype, prestroke ambulatory status, and other patient characteristics.111
Hospital Discharges/Ambulatory Care Visits
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From 1999 to 2009, the number of inpatient discharges from short-stay hospitals with stroke as the first-listed diagnosis remained about the same, with discharges of 961 000 and 971 000, respectively (NHLBI tabulation, NHDS, NCHS).
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Data from 2009 from the Hospital Discharge Survey of the NCHS showed that the average length of stay for discharges with stroke as the first-listed diagnosis was 5.3 days.
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In 2003, men and women accounted for roughly the same number of hospital stays for stroke in the 18- to 44-year-old age group. After 65 years of age, women were the majority. Among people 65 to 84 years of age, 54.5% of stroke patients were women, whereas among the oldest age group, women constituted 69.7% of all stroke patients.112
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A first-ever county-level Atlas of Stroke Hospitalizations Among Medicare Beneficiaries was released in 2008 by the CDC in collaboration with the Centers for Medicare & Medicaid Services. It found that the stroke hospitalization rate for blacks was 27% higher than for the US population in general, 30% higher than for whites, and 36% higher than for Hispanics. In contrast to whites and Hispanics, the highest percentage of strokes in blacks (42.3%) occurred in the youngest Medicare age group (65–74 years of age).40
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In 2009, there were 768 000 ED visits and 127 000 outpatient department visits with stroke as the first-listed diagnosis. In 2009, physician office visits for a first-listed diagnosis of stroke totaled 3 327 000 (unpublished data, NCHS, NHAMCS, NHLBI tabulation).113
Stroke in Children
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On the basis of pathogenic differences, pediatric strokes are typically classified as either perinatal, occurring at ≤28 days of life and including in utero strokes, or (later) childhood.
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Recent estimates of the overall annual incidence of stroke in US children are 6.4 per 100 000 children (0–15 years) in 1999 in GCNKSS114 and 4.6 per 100 000 children (0–19 years) from 1997 to 2003 according to Kaiser Permanente of Northern California, a large, integrated healthcare delivery system.115 Approximately half of all incident childhood strokes are hemorrhagic.114–116
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The prevalence of perinatal strokes is 29 per 100 000 live births, or 1 per 3500 live births in the 1997 to 2003 Kaiser Permanente of Northern California population.115
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A history of infertility, preeclampsia, prolonged rupture of membranes, and chorioamnionitis were found to be independent risk factors for perinatal arterial ischemic stroke in the Kaiser Permanente of Northern California population. The RR of perinatal stroke increased ≈25-fold, with an absolute risk of 1 per 200 deliveries, when ≥3 antenatally determined risk factors were present.117
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Although children with sickle cell disease and congenital HD are at high risk for ischemic stroke, the most common cause in a previously healthy child is a cerebral arteriopathy, found in approximately two thirds of cases.118
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Congenital HD accounted for 25% of pediatric arterial ischemic strokes in a population based study in Utah, Wyoming, Idaho, and Nevada; it increased the odds of stroke 16-fold compared with the general population.119
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Thrombophilias (genetic and acquired) are risk factors for childhood stroke, with summary ORs ranging from 1.6 to 8.8 in a recent meta-analysis.120
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From 1979 to 1998 in the United States, childhood mortality resulting from stroke declined by 58% overall, with reductions in all major subtypes.121
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The incidence of stroke in children has been stable over the past 10 years, whereas the 30-day case fatality rates declined from 18% in 1988–1989 to 9% in 1993–1994 and 9% in 1999 in the GCNKSS population.114
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Compared with girls, boys have a 1.28-fold higher risk of stroke.122 Compared with white children, black children have a 2-fold risk of both incident stroke and death attributable to stroke.121,122 The increased risk among blacks is not fully explained by the presence of sickle cell disease, nor is the excess risk among boys fully explained by trauma.122
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Strokes in children can be mistaken for a postictal Todd's paresis: 22% of children with acute arterial ischemic stroke have a seizure on presentation; younger age predicts presentation with seizures.123
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At a median follow-up time of 6.3 years, half of 53 childhood ischemic stroke survivors and two thirds of 80 neonatal ischemic stroke survivors had at least 1 neurological deficit; only 10% to 20% had mild deficits, whereas the remainder had moderate or severe deficits.124 Involvement of deep structures (basal ganglia, posterior limb of the internal capsule) as opposed to pure cortical lesions predicts motor deficits.125
Barriers to Stroke Care
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On the basis of NHIS data, the inability to afford medications among stroke survivors increased significantly from 8.1% to 12.7% between 1997 and 2004, totaling 76 000 US stroke survivors in 2004. Compared with stroke survivors able to afford medications, those unable to afford them more frequently reported lack of transportation, no health insurance, no usual place of care, income <$20 000, and out-of-pocket medical expenses ≥$2000.129
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In 2002, ≈21% of US counties did not have a hospital, 31% lacked a hospital with an ED, and 77% did not have a hospital with neurological services.130
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Of patients with ischemic stroke in the California Acute Stroke Pilot Registry, 23.5% arrived at the ED within 3 hours of symptom onset, and 4.3% received thrombolysis. If all patients had called 9-1-1 immediately, the expected overall rate of thrombolytic treatment within 3 hours would have increased to 28.6%. If all patients with known onset had arrived within 1 hour and had been treated optimally, 57% could have received thrombolytic treatment.131
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Data from the Paul Coverdell National Acute Stroke Registry were analyzed from the 142 hospitals that participated in the 4 registry states. More patients were transported by ambulance than by other means (43.6%). Time of stroke symptom onset was recorded for 44.8% of the patients. Among these patients, 48% arrived at the ED within 2 hours of symptom onset. Significantly fewer blacks (42.4%) arrived within 2 hours of symptom onset than did whites (49.5%), and significantly fewer nonambulance patients (36.2%) arrived within 2 hours of symptom onset than did patients transported by ambulance (58.6%).132
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NHIS data from 1998 to 2002 found that younger stroke survivors (45–64 years) self-reported worse access to physician care and medication affordability than older stroke survivors. Compared with older patients, younger stroke survivors were more likely to be male (52% versus 47%), to be black (19% versus 10%), and to lack health insurance (11% versus 0.4%). Lack of health insurance was associated with reduced access to care.133
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Data from 142 hospitals participating in the Paul Coverdell National Acute Stroke Registry found that fewer than 48% of stroke patients arrived at the ED within 2 hours of symptom onset in 2005 to 2006. Blacks were less likely to arrive within the 2-hour window than whites (42.4% versus 49.5%). Among those arriving within 2 hours, 65.2% received imaging within 1 hour of ED arrival; significantly fewer women received imaging within 1 hour than men (62.9% versus 67.6%), but no differences were observed by racial group.132
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Results from the BASIC project found that women were less likely to arrive at the ED within 3 hours of stroke symptom onset than men (OR 0.7, 95% CI 0.5–0.9). Mexican Americans were 40% less likely to arrive by EMS than non-Hispanic whites, even after adjustment for age, National Institutes of Health Stroke Scale score, education, history of stroke, and insurance status. Language fluency was not associated with time to hospital arrival or use of EMS. The receipt of tissue-type plasminogen activator was low (1.5%) but did not differ by sex or race.134
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A national study of academic medical centers found no change in the proportion of patients with stroke arriving at hospitals within 2 hours of symptom onset between 2001 and 2004 (37% versus 38%); however, the rate of intravenous tissue-type plasminogen activator use increased over this time period (14% to 38%), which suggests system-level improvements in the organization of in-hospital care. In risk-adjusted analyses, black patients were 45% less likely to arrive within 2 hours than white patients.135
Operations and Procedures
Among stroke or TIA patients with high-grade carotid stenosis, carotid endarterectomy has been the recommended treatment for the prevention of stroke, whereas carotid stenting has been proposed as a therapeutic option for patients at high risk for surgical revascularization.
•
In 2009, an estimated 93 000 inpatient endarterectomy procedures were performed in the United States. Carotid endarterectomy is the most frequently performed surgical procedure to prevent stroke (NHDS, NCHS, NHLBI tabulation).
•
Although rates of carotid endarterectomy in the Medicare population decreased slightly between 1998 and 2004, the use of carotid artery stenting increased dramatically136 (Chart 6-12).
•
The randomized Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) compared carotid endarterectomy and stenting for symptomatic and asymptomatic carotid stenosis. There was no overall difference in the primary end point of stroke, MI, or death; however, carotid endarterectomy showed superiority with increasing age, with the crossover point at approximately age 70, and was associated with fewer strokes, which had a greater impact on quality of life than MI.137
Cost
The direct and indirect cost of stroke in 2008 was $34.3 billion (MEPS, NHLBI tabulation).
•
The estimated direct medical cost of stroke for 2008 is $18.8 billion. This includes hospital outpatient or office-based provider visits, hospital inpatient stays, ED visits, prescribed medicines, and home health care.138
•
The mean expense per person for stroke care in the United States in 2007 was estimated at $7657.138
•
The mean lifetime cost of ischemic stroke in the United States is estimated at $140 048. This includes inpatient care, rehabilitation, and follow-up care necessary for lasting deficits. (All numbers were converted to 1999 dollars by use of the medical component of the Consumer Price Index.)139
•
The estimated cost of acute pediatric stroke in the United States was $42 million in 2003. The mean cost of short-term hospital care was $20 927 per discharge.140
•
After adjustment for routine healthcare costs, the average 5-year cost of a neonatal stroke was $51 719 and that of a childhood stroke was $135 161. Costs among children with stroke continued to exceed those in age-matched control children even in the fifth year by an average of $2016.141
•
In a study of stroke costs within 30 days of an acute event between 1987 and 1989 in the Rochester Stroke Study, the average cost was $13 019 for mild ischemic strokes and $20 346 for severe ischemic strokes (4 or 5 on the Rankin Disability Scale).142
•
Inpatient hospital costs for an acute stroke event account for 70% of first-year poststroke costs.115
•
The largest components of short-term care costs were room charges (50%), medical management (21%), and diagnostic costs (19%).143
•
Death within 7 days, subarachnoid hemorrhage, and stroke while hospitalized for another condition are associated with higher costs in the first year. Lower costs are associated with mild cerebral infarctions or residence in a nursing home before the stroke.142
•
Demographic variables (age, sex, and insurance status) are not associated with stroke cost. Severe strokes (National Institutes of Health Stroke Scale score >20) cost twice as much as mild strokes, despite similar diagnostic testing. Comorbidities such as ischemic HD and AF predict higher costs.143,144
•
The total cost of stroke from 2005 to 2050, in 2005 dollars, is projected to be $1.52 trillion for non-Hispanic whites, $313 billion for Hispanics, and $379 billion for blacks. The per capita cost of stroke estimates is highest in blacks ($25 782), followed by Hispanics ($17 201) and non-Hispanic whites ($15 597). Loss of earnings is expected to be the highest cost contributor in each race/ethnic group.145
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Agrawal N, Johnston SC, Wu YW, Sidney S, Fullerton HJ. Imaging data reveal a higher pediatric stroke incidence than prior US estimates. Stroke. 2009;40:3415–3421.
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Broderick J, Brott T, Kothari R, Miller R, Khoury J, Pancioli A, Gebel J, Mills D, Minneci L, Shukla R. The Greater Cincinnati/Northern Kentucky Stroke Study: preliminary first-ever and total incidence rates of stroke among blacks. Stroke. 1998;29:415–421.
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Lee J, Croen LA, Backstrand KH, Yoshida CK, Henning LH, Lindan C, Ferriero DM, Fullerton HJ, Barkovich A, Wu YW. Maternal and infant characteristics associated with perinatal arterial stroke in the infant. JAMA. 2005;293:723–729.
118.
Ganesan V, Prengler M, McShane MA, Wade AM, Kirkham FJ. Investigation of risk factors in children with arterial ischemic stroke. Ann Neurol. 2003;53:167–173.
119.
Hoffman JL, Mack GK, Minich LL, Benedict SL, Heywood M, Stoddard GJ, Saarel EV. Failure to impact prevalence of arterial ischemic stroke in pediatric cardiac patients over three decades. Congenit Heart Dis. 2011;6:211–218.
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Kenet G, Lütkhoff LK, Albisetti M, Bernard T, Bonduel M, Brandao L, Chabrier S, Chan A, deVeber G, Fiedler B, Fullerton HJ, Goldenberg NA, Grabowski E, Günther G, Heller C, Holzhauer S, Iorio A, Journeycake J, Junker R, Kirkham FJ, Kurnik K, Lynch JK, Male C, Manco-Johnson M, Mesters R, Monagle P, van Ommen CH, Raffini L, Rostásy K, Simioni P, Sträter RD, Young G, Nowak-Göttl U. Impact of thrombophilia on risk of arterial ischemic stroke or cerebral sinovenous thrombosis in neonates and children: a systematic review and meta-analysis of observational studies. Circulation. 2010;121:1838–1847.
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Fullerton H, Chetkovich D, Wu Y, Smith W, Johnston SC. Deaths from stroke in US children, 1979 to 1998. Neurology. 2002;59:34–39.
122.
Fullerton HJ, Wu YW, Zhao S, Johnston SC. Risk of stroke in children: ethnic and gender disparities. Neurology. 2003;61:189–194.
123.
Abend NS, Beslow LA, Smith SE, Kessler SK, Vossough A, Mason S, Agner S, Licht DJ, Ichord RN. Seizures as a presenting symptom of acute arterial ischemic stroke in childhood. J Pediatr.2011;159:479–483.
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Neuner B, von Mackensen S, Krümpel A, Manner D, Friefeld S, Nixdorf S, Frühwald M, Deveber G, Nowak-Göttl U. Health-related quality of life in children and adolescents with stroke, self-reports, and parent/proxies reports: cross-sectional investigation. Ann Neurol.2011;70:70–78.
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Husson B, Hertz-Pannier L, Renaud C, Allard D, Presles E, Landrieu P, Chabrier S; AVCnn Group. Motor outcomes after neonatal arterial ischemic stroke related to early MRI data in a prospective study. Pediatrics. 2010;126:912–918.
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Sträter R, Becker S, von Eckardstein A, Heinecke A, Gutsche S, Junker R, Kurnik K, Schobess R, Nowak-Göttl U. Prospective assessment of risk factors for recurrent stroke during childhood: a 5-year follow-up study. Lancet. 2002;360:1540–1545.
127.
Fullerton HJ, Wu YW, Sidney S, Johnston SC. Recurrent hemorrhagic stroke in children: a population-based cohort study. Stroke. 2007;38:2658–2662.
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Fullerton HJ, Wu YW, Sidney S, Johnston SC. Risk of recurrent childhood arterial ischemic stroke in a population-based cohort: the importance of cerebrovascular imaging. Pediatrics. 2007;119:495–501.
129.
Levine DA, Kiefe CI, Howard G, Howard VJ, Williams OD, Allison JJ. Reduced medication access: a marker for vulnerability in US stroke survivors. Stroke. 2007;38:1557–1564.
130.
First-ever county level report on stroke hospitalizations [press release]. Atlanta, GA: Centers for Disease Control and Prevention; March 28, 2008. http://www.cdc.gov/media/pressrel/2008/r080328.htm. Accessed July 19, 2011.
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Prioritizing interventions to improve rates of thrombolysis for ischemic stroke. Neurology. 2005;64:654–659.
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Centers for Disease Control and Prevention (CDC). Prehospital and hospital delays after stroke onset–United States, 2005–2006. MMWR Morb Mortal Wkly Rep. 2007;56:474–478.
133.
Levine DA, Kiefe CI, Houston TK, Allison JJ, McCarthy EP, Ayanian JZ. Younger stroke survivors have reduced access to physician care and medications: National Health Interview Survey from years 1998 to 2002. Arch Neurol. 2007;64:37–42.
134.
Smith MA, Lisabeth LD, Bonikowski F, Morgenstern LB. The role of ethnicity, sex, and language on delay to hospital arrival for acute ischemic stroke. Stroke. 2010;41:905–909.
135.
Lichtman JH, Watanabe E, Allen NB, Jones SB, Dostal J, Goldstein LB. Hospital arrival time and intravenous t-PA use in US academic medical centers, 2001–2004. Stroke. 2009;40:3845–3850.
136.
Goodney PP, Lucas FL, Travis LL, Likosky DS, Malenka DJ, Fisher ES. Changes in the use of carotid revascularization among the Medicare population [published correction appears in Arch Surg. 2009;144:769]. Arch Surg. 2008;143:170–173.
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Brott TG, Hobson RW, Howard G, Roubin GS, Clark WM, Brooks W, Mackey A, Hill MD, Leimgruber PP, Sheffet AJ, Howard VJ, Moore WS, Voeks JH, Hopkins LN, Cutlip DE, Cohen DJ, Popma JJ, Ferguson RD, Cohen SN, Blackshear JL, Silver FL, Mohr JP, Lal BK, Meschia JF; CREST Investigators. Stenting versus endarterectomy for treatment of carotid-artery stenosis [published corrections appear in N Engl J Med. 2010;363:498 and N Engl J Med. 2010;363:198]. N Engl J Med. 2010;363: 11– 23.
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Medical Expenditure Panel Survey (MEPS) of the Agency for Healthcare Research and Quality (AHRQ). Household component summary data table. Table 4: Total Expenses and Percent Distribution for Selected Conditions by Source of Payment: United States, 2008. http://www.meps.ahrq.gov/mepsweb/data_stats/tables_compendia_hh_interactive.jsp?_SERVICE=MEPSSocket0&_PROGRAM=MEPSPGM.TC.SAS&File=HCFY2008&Table=HCFY2008_CNDXP_D&_Debug=. Accessed November 7, 2011.
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Taylor TN, Davis PH, Torner JC, Holmes J, Meyer JW, Jacobson MF. Lifetime cost of stroke in the United States. Stroke. 1996;27:1459–1466.
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Perkins E, Stephens J, Xiang H, Lo W. The cost of pediatric stroke acute care in the United States [published correction appears in Stroke. 2010;41:e600]. Stroke.2009;40:2820–2827.
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Gardner MA, Hills NK, Sidney S, Johnston SC, Fullerton HJ. The 5-year direct medical cost of neonatal and childhood stroke in a population-based cohort. Neurology. 2010;74:372–378.
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Leibson CL, Hu T, Brown RD, Hass SL, O'Fallon WM, Whisnant JP. Utilization of acute care services in the year before and after first stroke: a population-based study. Neurology. 1996;46:861–869.
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Diringer MN, Edwards DF, Mattson DT, Akins PT, Sheedy CW, Hsu CY, Dromerick AW. Predictors of acute hospital costs for treatment of ischemic stroke in an academic center. Stroke. 1999;30:724–728.
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Matz R. Cost-effective, risk-free, evidence-based medicine. Arch Intern Med. 2003;163:2795.
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Brown DL, Boden-Albala B, Langa KM, Lisabeth LD, Fair M, Smith MA, Sacco RL, Morgenstern LB. Projected costs of ischemic stroke in the United States. Neurology. 2006;67:1390–1395.
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Schiller J, Lucas J, Ward B, Peregoy J. Summary health statistics for U.S. adults: National Health Interview Survey, 2010. Vital Health Stat 10. In press.
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Wolf PA, D'Agostino RB, Belanger AJ, Kannel WB. Probability of stroke: a risk profile from the Framingham Study. Stroke. 1991; 22: 312– 318.
7. High Blood Pressure
| Population Group | Prevalence, 2008: Age ≥20 y | Mortality,* 2008: All Ages | Hospital Discharges, 2009: All Ages | Estimated Cost, 2008 |
|---|---|---|---|---|
| Both sexes | 76 400 000 (33.5%) | 61 005 | 579 000 | $50.6 billion |
| Males | 36 500 000 (34.1%) | 26 776 (43.9%)† | 260 000 | … |
| Females | 39 900 000 (32.7%) | 34 229 (56.1%)† | 319 000 | … |
| NH white males | 33.9% | 19 576 | … | … |
| NH white females | 31.3% | 26 342 | … | … |
| NH black males | 43.0% | 6370 | … | … |
| NH black females | 45.7% | 7002 | … | … |
| Mexican American males | 27.8% | … | … | … |
| Mexican American females | 28.9% | … | … | … |
| Hispanic or Latino‡ | 24.7% | … | … | … |
| Asian‡ | 20.5% | … | … | |
| American Indian/Alaska Native‡ | 30.0% | … | … |
Ellipses (…) indicate data not available; NH, non-Hispanic.
*
Mortality data for the white, black, Asian or Pacific Islander, and American Indian/Alaska Native populations include deaths among persons of Hispanic and non-Hispanic origin. Numbers of deaths for the American Indian/Alaska Native and Asian or Pacific Islander populations are known to be underestimated.
†
These percentages represent the portion of total high blood pressure mortality that is for males vs females.
‡
National Health Interview Survey (2010), National Center for Health Statistics; data are weighted percentages for Americans ≥18 years of age. Source: Schiller et al.19
Sources: Prevalence: National Health and Nutrition Examination Survey (2005–2008, National Center for Health Statistics) and National Heart, Lung, and Blood Institute. Percentages for racial/ethnic groups are age adjusted for Americans ≥20 years of age. Age-specific percentages are extrapolated to the 2008 US population estimates. Mortality: National Center for Health Statistics. These data represent underlying cause of death only. Hospital discharges: National Hospital Discharge Survey, National Center for Health Statistics; data include those discharged alive, dead, or status unknown. Cost: Medical Expenditure Panel Survey data include estimated direct costs for 2007; indirect costs calculated by National Heart, Lung, and Blood Institute for 2007.
Hypertension is defined in terms of National Health and Nutrition Examination Survey blood pressure measurements and health interviews. A subject was considered hypertensive if systolic blood pressure was ≥140 mm Hg or diastolic blood pressure was ≥90 mm Hg, if the subject said “yes” to taking antihypertensive medication, or if the subject was told on 2 occasions that he or she had hypertension.
| Awareness, % | Treatment, % | Control, % | ||||
|---|---|---|---|---|---|---|
| 1988–1994 | 1999–2008 | 1988–1994 | 1999–2008 | 1988–1994 | 1999–2008 | |
| NH white male | 63.0 | 73.5 | 46.2 | 63.8 | 22.0 | 44.1 |
| NH white female | 74.7 | 78.2 | 61.6 | 70.0 | 32.2 | 42.7 |
| NH black male | 62.5 | 70.8 | 42.3 | 60.3 | 16.6 | 35.2 |
| NH black female | 77.8 | 85.8 | 64.6 | 77.0 | 30.0 | 45.3 |
| Mexican American male | 47.8 | 59.5 | 30.9 | 46.1 | 13.5 | 30.3 |
| Mexican American female | 69.3 | 70.1 | 47.8 | 59.9 | 19.4 | 34.2 |
NHANES indicates National Health and Nutrition Examination Survey; NH, non-Hispanic.
Sources: NHANES (1988–1994, 1999–2008) and National Heart, Lung, and Blood Institute.
| ARIC | Atherosclerosis Risk in Communities Study |
| BP | blood pressure |
| BRFSS | Behavioral Risk Factor Surveillance System |
| CDC | Centers for Disease Control and Prevention |
| CHD | coronary heart disease |
| CHF | congestive heart failure |
| CHS | Cardiovascular Health Study |
| CVD | cardiovascular disease |
| DBP | diastolic blood pressure |
| DM | diabetes mellitus |
| FHS | Framingham Heart Study |
| HBP | high blood pressure |
| HD | heart disease |
| HHANES | Hispanic Health and Nutrition Examination Survey |
| ICD-9 | International Classification of Diseases, 9th Revision |
| ICD-9-CM | International Classification of Diseases, Clinical Modification, 9th Revision |
| ICD-10 | International Classification of Diseases, 10th Revision |
| LDL | low-density lipoprotein |
| MEPS | Medical Expenditure Panel Survey |
| MESA | Multi-Ethnic Study of Atherosclerosis |
| NAMCS | National Ambulatory Medical Care Survey |
| NCHS | National Center for Health Statistics |
| NHAMCS | National Hospital Ambulatory Medical Care Survey |
| NHANES | National Health and Nutrition Examination Survey |
| NHDS | National Hospital Discharge Survey |
| NHES | National Health Examination Survey |
| NHIS | National Health Interview Survey |
| NHLBI | National Heart, Lung, and Blood Institute |
| NINDS | National Institute of Neurological Disorders and Stroke |
| PA | physical activity |
| REGARDS | REasons for Geographic And Racial Differences in Stroke study |
| SBP | systolic blood pressure |
| SEARCH | Search for Diabetes in Youth Study |
Prevalence
•
HBP is defined as:
— SBP ≥140 mm Hg or DBP ≥90 mm Hg or taking antihypertensive medicine, or
— Having been told at least twice by a physician or other health professional that one has HBP.
•
One in 3 US adults has HBP.1
•
Data from NHANES 1999–2006 found that ≈8% of US adults have undiagnosed hypertension.2
•
An estimated 76 400 000 adults ≥20 years of age have HBP, extrapolated to 2008 with NHANES 2005–2008 data (Table 7-1).
•
NHANES data show that a higher percentage of men than women have hypertension until 45 years of age. From 45 to 54 and from 55 to 64 years of age, the percentages of men and women with hypertension are similar. After that, a higher percentage of women have hypertension than men.3
•
HBP is 2 to 3 times more common in women taking oral contraceptives, especially among obese and older women, than in women not taking them.4
•
Data from NHANES 2005–2006 found that 29% of US adults ≥18 years of age were hypertensive. The prevalence of hypertension was nearly equal between men and women; 7% of adults had HBP but had never been told that they had hypertension. Among hypertensive adults, 78% were aware of their condition, 68% were using antihypertensive medication, and 64% of those treated had their hypertension controlled.5
•
Data from the 2009 BRFSS/CDC indicate that the percentage of adults ≥18 years of age who had been told that they had HBP ranged from 21.6% in Minnesota to 37.6% in West Virginia. The median percentage was 28.7%.6
— According to NHANES data 2003–2008, among US adults with hypertension, 8.9% met the criteria for resistant hypertension (BP was ≥140/90 mm Hg, and they reported using antihypertensive medications from 3 different drug classes or drugs from ≥4 antihypertensive drug classes regardless of BP). This represents 12.8% of the population taking antihypertensive medication.7
•
According to data from NHANES from 1988–1994 and 2007–2008, HBP control rates improved from 27.3% to 50.1%, treatment improved from 54.0% to 73.5%, and the control/treated rates improved from 50.6% to 72.3%.8
•
Projections show that by 2030, an additional 27 million people could have hypertension, a 9.9% increase in prevalence from 2010.9
Older Adults
•
In 2007 to 2008, diagnosed chronic conditions that were more prevalent among older (≥65 years of age) women than men included hypertension (58% for women, 53% for men). Ever-diagnosed conditions that were more prevalent among older men than older women included HD (38% for men, 27% for women) and DM (20% for men, 18% for women) on the basis of data from NHIS/NCHS.10
•
The age-adjusted prevalence of hypertension (both diagnosed and undiagnosed) in 2003 to 2006 was 75% for older women and 65% for older men on the basis of data from NHANES/NCHS.11
Children and Adolescents
•
Analysis of the NHES, the Hispanic Health and Nutrition Examination Survey, and the NHANES/NCHS surveys of the NCHS (1963–2002) found that the BP, pre-HBP, and HBP trends in children and adolescents 8 to 17 years of age moved downward from 1963 to 1988 and upward thereafter. Pre-HBP and HBP increased 2.3% and 1%, respectively, between 1988 and 1999. Increased obesity (more so abdominal obesity than general obesity) partially explained the HBP and pre-HBP rise from 1988 to 1999. BP and HBP reversed their downward trends 10 years after the increase in the prevalence of obesity. In addition, an ethnic and sex gap appeared in 1988 for pre-HBP and in 1999 for HBP: Non-Hispanic blacks and Mexican Americans had a greater prevalence of HBP and pre-HBP than non-Hispanic whites, and the prevalence was greater in boys than in girls. In that study, HBP in children and adolescents was defined as SBP or DBP that was, on repeated measurement, ≥95th percentile.12
•
A study in Ohio of >14 000 children and adolescents 3 to 18 years of age who were observed at least 3 times between 1999 and 2006 found that 3.6% had hypertension. Of these, 26% had been diagnosed and 74% were undiagnosed. In addition, 3% of those with hypertension had stage 2 hypertension, and 41% of those with stage 2 hypertension were undiagnosed. Criteria for prehypertension were met by 485 children. Of these, 11% were diagnosed. In this study, HBP in children and adolescents was defined as SBP or DBP that was, on repeated measurement, ≥95th percentile.13
•
A study from 1988–1994 through 1999–2000 of children and adolescents 8 to 17 years of age showed that among non-Hispanic blacks, mean SBP levels increased by 1.6 mm Hg among girls and by 2.9 mm Hg among boys compared with non-Hispanic whites. Among Mexican Americans, girls' SBP increased 1.0 mm Hg and boys' SBP increased 2.7 mm Hg compared with non-Hispanic whites.14
•
Analysis of data from the Search for Diabetes in Youth Study (SEARCH), which included children 3 to 17 years of age with type 1 and type 2 DM, found the prevalence of elevated BP among those with type 1 DM to be 5.9% and the prevalence of elevated BP among those with type 2 DM to be 23.7%.15
Race/Ethnicity and HBP
•
The prevalence of hypertension in blacks in the United States is among the highest in the world, and it is increasing. From 1988 to 1994 through 1999 to 2002, the prevalence of HBP in adults increased from 35.8% to 41.4% among blacks, and it was particularly high among black women at 44.0%. Prevalence among whites also increased, from 24.3% to 28.1%.16
•
Compared with whites, blacks develop HBP earlier in life, and their average BPs are much higher. As a result, compared with whites, blacks have a 1.3-times greater rate of nonfatal stroke, a 1.8-times greater rate of fatal stroke, a 1.5-times greater rate of death attributable to HD, and a 4.2-times greater rate of end-stage kidney disease (fifth and sixth reports of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure).
•
Within the black community, rates of hypertension vary substantially16,17:
— Those with the highest rates are more likely to be middle-aged or older, less educated, overweight or obese, and physically inactive and are more likely to have DM.
— Those with the lowest rates are more likely to be younger but also overweight or obese.
— Those with uncontrolled HBP who are not taking antihypertensive medication tend to be male, to be younger, and to have infrequent contact with a physician.
•
Analysis from the REGARDS study of the NINDS suggests that efforts to raise awareness of prevalent hypertension among blacks apparently have been successful (31% greater odds in blacks relative to whites), and efforts to communicate the importance of receiving treatment for hypertension have been successful (69% greater odds among blacks relative to whites); however, substantial racial disparities remain with regard to the control of BP (SBP <140 mm Hg, DBP <90 mm Hg), with the odds of control being 27% lower in blacks than in whites. In contrast, geographic disparities in hypertension awareness, treatment, and control were minimal.18
•
Data from the 2010 NHIS showed that black adults ≥18 years of age were more likely (33.8%) to have been told on ≥2 occasions that they had hypertension than white adults (23.6%) or Asian adults (20.5%); there was no significant difference between the estimates for American Indian/Alaska Native adults (30.0%) and black adults.19
•
The CDC analyzed death certificate data from 1995 to 2002 (any-mention mortality; ICD-9 codes 401–404 and ICD-10 codes I10–I13). The results indicated that Puerto Rican Americans had a consistently higher hypertension-related death rate than all other Hispanic subpopulations and non-Hispanic whites. The age-standardized hypertension-related mortality rate was 127.2 per 100 000 population for all Hispanics, similar to that of non-Hispanic whites (135.9). The age-standardized rate for Hispanic females (118.3) was substantially lower than that observed for Hispanic males (135.9). Hypertension-related mortality rates for males were higher than rates for females for all Hispanic subpopulations. Puerto Rican Americans had the highest hypertension-related death rate among all Hispanic subpopulations (154.0); Cuban Americans had the lowest (82.5).20
•
Some studies suggest that Hispanic Americans have rates of HBP similar to or lower than those of non-Hispanic white Americans. Findings from a new analysis of combined data from the NHIS of 2000 to 2002 point to a health disparity between black and white adults of Hispanic descent. Black Hispanics were at slightly greater risk than white Hispanics, although non-Hispanic black adults had by far the highest rate of HBP. The racial disparity among Hispanics also was evident in the fact that higher-income, better-educated black Hispanics still had a higher rate of HBP than lower-income, less-educated white Hispanics.21 Data from the NHLBI's ARIC study found that hypertension was a particularly powerful risk factor for CHD in black people, especially black women.22
•
Data from MESA found that being born outside the United States, speaking a language other than English at home, and living fewer years in the United States were each associated with a decreased prevalence of hypertension.23
•
Filipino (27%) and Japanese (25%) adults were more likely than Chinese (17%) or Korean (17%) adults to have ever been told that they had hypertension.24
Mortality
HBP mortality in 2008 was 61 005. Any-mention mortality in 2008 was 347 689 (NHLBI tabulation of NCHS mortality data). The 2008 death rate was 18.3.25
•
•
The 2008 overall death rate resulting from HBP was 18.3. Death rates were 16.5 for white males, 50.3 for black males, 14.5 for white females, and 38.6 for black females. When any-mention mortality for 2008 was used, the overall death rate was 108.5. Death rates were 108.6 for white males, 228.8 for black males, 90.7 for white females, and 174.8 for black females (NHLBI tabulation of NCHS mortality data).
•
Analysis of NHANES I and II comparing hypertensive and nonhypertensive individuals found a reduction in age-adjusted mortality rate of 4.6/1000 person-years among people with hypertension compared with a reduction of 4.2/1000 person-years among those without hypertension.26
•
Assessment of 30-year follow-up of the Hypertension Detection and Follow-Up Program identified the long-term benefit of stepped care, and the increased survival for hypertensive African Americans.27
•
Assessment of the Charleston Heart Study and Evans County Heart Study identified the excess burden of elevated BP for African Americans and its effect on long-term health outcomes.28
Risk Factors
•
Numerous risk factors and markers for development of hypertension, including age, ethnicity, family history of hypertension and genetic factors, lower education and socioeconomic status, greater weight, lower PA, tobacco use, psychosocial stressors, sleep apnea, and dietary factors (including dietary fats, higher sodium intake, lower potassium intake, and excessive alcohol intake), have been identified.
•
A study of related individuals in the NHLBI's FHS suggested that different sets of genes regulate BP at different ages.29
•
Recent data from the Nurses' Health Study suggest that a large proportion of incident hypertension in women can be prevented by controlling dietary and lifestyle risk factors.30
•
A meta-analysis identified the benefit of a goal BP of 130/80 mm Hg for individuals with hypertension and type 2 DM but less evidence for treatment below this value.31
Aftermath
•
Approximately 69% of people who have a first heart attack, 77% of those who have a first stroke, and 74% of those who have CHF have BP >140/90 mm Hg (NHLBI unpublished estimates from ARIC, CHS, and FHS Cohort and Offspring studies).
•
Data from FHS/NHLBI indicate that recent (within the past 10 years) and remote antecedent BP levels may be an important determinant of risk over and above the current BP level.32
•
Data from the FHS/NHLBI indicate that hypertension is associated with shorter overall life expectancy, shorter life expectancy free of CVD, and more years lived with CVD.33
— Total life expectancy was 5.1 years longer for normotensive men and 4.9 years longer for normotensive women than for hypertensive people of the same sex at 50 years of age.
— Compared with hypertensive men at 50 years of age, men with untreated BP <140/90 mm Hg survived on average 7.2 years longer without CVD and spent 2.1 fewer years of life with CVD. Similar results were observed for women.
Hospital Discharges/Ambulatory Care Visits
•
From 1999 to 2009, the number of inpatient discharges from short-stay hospitals with HBP as the first-listed diagnosis increased from 439 000 to 579 000 (no significant difference; NCHS, NHDS). The number of all-listed discharges increased from 7 629 000 to 11 591 000 (NHLBI, unpublished data from the NHDS, 2009).
•
Data from ambulatory medical care utilization estimates for 2009 showed that the number of visits for essential hypertension was 55 148 000. Of these, 49 966 000 were physician office visits, 1 000 000 were ED visits, and 4 182 000 were outpatient department visits (NCHS, NAMCS and NHAMCS, NHLBI tabulation).
•
In 2009, there were 372 000 hospitalizations with a first-listed diagnosis of essential hypertension (ICD-9-CM code 401), but essential hypertension was listed as either a primary or a secondary diagnosis 9 317 000 times for hospitalized inpatients (NHLBI, unpublished data from the NHDS, 2009).
Awareness, Treatment, and Control
•
Data from NHANES/NCHS 2005–2008 showed that of those with hypertension who were ≥20 years of age, 79.6% were aware of their condition, 70.9% were under current treatment, 47.8% had their hypertension under control, and 52.2% did not have it controlled (NHLBI tabulation, NCHS, NHANES data).
•
Data from NHANES 1999–2006 showed that 11.2% of adults ≥20 years of age had treated and controlled BP levels.34
•
Analysis of NHANES/NCHS data from 1999–2004 through 2005–2006 found that there were substantial increases in awareness and treatment rates of hypertension. The control rates increased in both sexes, in non-Hispanic blacks, and in Mexican Americans. Among the group ≥60 years of age, awareness, treatment, and control rates of hypertension increased significantly.5,35
•
In NHANES/NCHS 2005–2006, rates of control were lower in Mexican Americans (35.2%) than in non-Hispanic whites (46.1%) and non-Hispanic blacks (46.5%).5
•
The awareness, treatment, and control of HBP among those ≥65 years of age in the CHS/NHLBI improved during the 1990s. The percentages of those aware of and treated for HBP were higher among blacks than among whites. Prevalence rates with HBP under control were similar. For both groups combined, the control of BP to <140/90 mm Hg increased from 37% in 1990 to 49% in 1999. Improved control was achieved by an increase in antihypertensive medications per person and by an increase in the proportion of the CHS population treated for hypertension from 34.5% to 51.1%.36
•
Data from the FHS of the NHLBI show that:
— Among those ≥80 years of age, only 38% of men and 23% of women had BPs that met targets set forth in the National High Blood Pressure Education Program's clinical guidelines. Control rates in men <60, 60 to 79, and ≥80 years of age were 38%, 36%, and 38%, respectively; for women in the same age groups, they were 38%, 28%, and 23%, respectively.37
•
Data from the WHI observational study of nearly 100 000 postmenopausal women across the country enrolled between 1994 and 1998 indicate that although prevalence rates ranged from 27% of women 50 to 59 years of age to 41% of women 60 to 69 years of age to 53% of women 70 to 79 years of age, treatment rates were similar across age groups: 64%, 65%, and 63%, respectively. Despite similar treatment rates, hypertension control is especially poor in older women, with only 29% of hypertensive women 70 to 79 years of age having clinic BPs <140/90 mm Hg compared with 41% and 37% of those 50 to 59 and 60 to 69 years of age, respectively.38
•
Among a cohort of postmenopausal women taking hormone replacement, hypertension was the most common comorbidity, with a prevalence of 34%.39
•
A study of >300 women in Wisconsin showed a need for significant improvement in BP and LDL levels. Of the screened participants, 35% were not at BP goal, 32.4% were not at LDL goal, and 53.5% were not at both goals.40
•
In 2005, a survey of people in 20 states conducted by the BRFSS of the CDC found that 19.4% of respondents had been told on ≥2 visits to a health professional that they had HBP. Of these, 70.9% reported changing their eating habits; 79.5% reduced the use of or were not using salt; 79.2% reduced the use of or eliminated alcohol; 68.8% were exercising; and 73.4% were taking antihypertensive medication.41
•
On the basis of NHANES 2003–2004 data, it was found that nearly three fourths of adults with CVD comorbidities have hypertension. Poor control rates of systolic hypertension remain a principal problem that further compromises their already high CVD risk.42
•
According to data from NHANES 2001–2006, non-Hispanic blacks had 90% higher odds of poorly controlled BP than non-Hispanic whites. Among those who were hypertensive, non-Hispanic blacks and Mexican Americans had 40% higher odds of uncontrolled BP than non-Hispanic whites.43
Cost
•
The estimated direct and indirect cost of HBP for 2008 is $50.6 billion (MEPS, NHLBI tabulation).
Prehypertension
•
Prehypertension is untreated SBP of 120 to 139 mm Hg or untreated DBP of 80 to 89 mm Hg and not having been told on 2 occasions by a physician or other health professional that one has hypertension.
•
Data from NHANES 1999–2006 estimate that 29.7% of adults ≥20 years of age have prehypertension.34
•
Follow-up of 9845 men and women in the FHS/NHLBI who attended examinations from 1978 to 1994 revealed that at 35 to 64 years of age, the 4-year incidence of hypertension was 5.3% for those with baseline BP <120/80 mm Hg, 17.6% for those with SBP of 120 to 129 mm Hg or DBP of 80 to 84 mm Hg, and 37.3% for those with SBP of 130 to 139 mm Hg or DBP of 85 to 89 mm Hg. At 65 to 94 years of age, the 4-year incidences of hypertension were 16.0%, 25.5%, and 49.5% for these BP categories, respectively.44
•
Data from FHS/NHLBI also reveal that prehypertension is associated with elevated relative and absolute risks for CVD outcomes across the age spectrum. Compared with normal BP (<120/80 mm Hg), prehypertension was associated with a 1.5- to 2-fold increased risk for major CVD events in those <60, 60 to 79, and ≥80 years of age. Absolute risks for major CVD associated with prehypertension increased markedly with age: 6-year event rates for major CVD were 1.5% in prehypertensive people <60 years of age, 4.9% in those 60 to 79 years of age, and 19.8% in those ≥80 years of age.37
•
In a study of NHANES 1999–2000 (NCHS), people with prehypertension were more likely than those with normal BP levels to have above-normal cholesterol levels, overweight/obesity, and DM, whereas the probability of currently smoking was lower. People with prehypertension were 1.65 times more likely to have 1 or more of these adverse risk factors than were those with normal BP.45
•
Assessment of the REGARDS data identified high risk of prehypertension to be associated with increased age and black race.46
References
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Fields LE, Burt VL, Cutler JA, Hughes J, Roccella EJ, Sorlie P. The burden of adult hypertension in the United States 1999 to 2000: a rising tide. Hypertension. 2004;44:398–404.
2.
Fryar CD, Hirsch R, Eberhardt MS, Yoon SS, Wright JD. Hypertension, high serum total cholesterol, and diabetes: racial and ethnic prevalence differences in U.S. adults, 1999–2006. NCHS Data Brief. 2010: (36):1– 8.
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National Center for Health Statistics. Health, United States, 2010: With Special Feature on Death and Dying. Hyattsville, MD: National Center for Health Statistics; 2011. http://www.cdc.gov/nchs/data/hus/hus10.pdf. Accessed July 5, 2011.
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Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL, Jones DW, Materson BJ, Oparil S, Wright JT, Roccella EJ; Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42:1206–1252.
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Ostchega Y, Yoon SS, Hughes J, Louis T. Hypertension awareness, treatment, and control—continued disparities in adults: United States, 2005–2006. NCHS Data Brief No. 3. Hyattsville, MD: National Center for Health Statistics; 2008.
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Centers for Disease Control and Prevention Web site. Behavioral Risk Factor Surveillance System: prevalence and trends data. http://apps.nccd.cdc.gov/brfss/index.asp. Accessed July 5, 2011.
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Persell SD. Prevalence of resistant hypertension in the United States, 2003–2008. Hypertension. 2011;57:1076–1080.
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Egan BM, Zhao Y, Axon RN. US trends in prevalence, awareness, treatment, and control of hypertension, 1988–2008. JAMA. 2010;303:2043–2050.
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Heidenreich PA, Trogdon JG, Khavjou OA, Butler J, Dracup K, Ezekowitz MD, Finkelstein EA, Hong Y, Johnston SC, Khera A, Lloyd-Jones DM, Nelson SA, Nichol G, Orenstein D, Wilson PW, Woo YJ. Forecasting the future of cardiovascular disease in the United States: a policy statement from the American Heart Association. Circulation. 2011;123:933–944.
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Federal Interagency Forum on Aging-Related Statistics. Older Americans 2010: Key Indicators of Well-Being. Washington, DC: US Government Printing Office; 2010. http://www.agingstats.gov. Accessed July 25, 2011.
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Crescioni M, Gorina Y, Bilheimer L, Gillum RF. Trends in health status and health care use among older men. Hyattsville, MD: National Center for Health Statistics; 2010. National Health Statistics Report No. 24. http://www.cdc.gov/nchs/data/nhsr/nhsr024.pdf. Accessed July 20, 2011.
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Din-Dzietham R, Liu Y, Bielo MV, Shamsa F. High blood pressure trends in children and adolescents in national surveys, 1963 to 2002. Circulation. 2007;116:1488–1496.
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Hansen ML, Gunn PW, Kaelber DC. Underdiagnosis of hypertension in children and adolescents. JAMA. 2007;298:874–879.
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Muntner P, He J, Cutler JA, Wildman RP, Whelton PK. Trends in blood pressure among children and adolescents. JAMA. 2004;291:2107–2113.
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Rodriguez BL, Dabelea D, Liese AD, Fujimoto W, Waitzfelder B, Liu L, Bell R, Talton J, Snively BM, Kershnar A, Urbina E, Daniels S, Imperatore G; SEARCH Study Group. Prevalence and correlates of elevated blood pressure in youth with diabetes mellitus: the SEARCH for Diabetes in Youth Study. J Pediatr. 2010;157:245–251.
16.
Hertz RP, Unger AN, Cornell JA, Saunders E. Racial disparities in hypertension prevalence, awareness, and management. Arch Intern Med. 2005;165:2098–2104.
17.
Collins R, Winkleby MA. African American women and men at high and low risk for hypertension: a signal detection analysis of NHANES III, 1988–1994. Prev Med. 2002;35:303–312.
18.
Howard G, Prineas R, Moy C, Cushman M, Kellum M, Temple E, Graham A, Howard V. Racial and geographic differences in awareness, treatment, and control of hypertension: the REasons for Geographic And Racial Differences in Stroke study. Stroke. 2006;37:1171–1178.
19.
Schiller J, Lucas J, Ward B, Peregoy J. Summary health statistics for U.S. adults: National Health Interview Survey, 2010. Vital Health Stat 10. In press.
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Centers for Disease Control and Prevention (CDC). Hypertension-related mortality among Hispanic subpopulations–United States, 1995–2002. MMWR Morb Mortal Wkly Rep.2006;55:177–180.
21.
Borrell LN. Self-reported hypertension and race among Hispanics in the National Health Interview Survey. Ethn Dis. 2006;16:71–77.
22.
Jones DW, Chambless LE, Folsom AR, Heiss G, Hutchinson RG, Sharrett AR, Szklo M, Taylor HA Risk factors for coronary heart disease in African Americans: the Atherosclerosis Risk in Communities study, 1987–1997. Arch Intern Med. 2002;162:2565–2571.
23.
Moran A, Roux AV, Jackson SA, Kramer H, Manolio TA, Shrager S, Shea S. Acculturation is associated with hypertension in a multiethnic sample. Am J Hypertens. 2007;20:354–363.
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Barnes PM, Adams PF, Powell-Griner E. Health characteristics of the Asian adult population: United States, 2004–2006. Advance Data From Vital and Health Statistics; No. 394. Hyattsville, MD: National Center for Health Statistics; 2008.
25.
Centers for Disease Control and Prevention. Vital Statistics Public Use Data Files - 2008 Mortality Multiple Cause Files. Available at: http://www.cdc.gov/nchs/data_access/Vitalstatsonline.htm#Mortality_Multiple. Accessed September 23, 2011.
25a.
Centers for Disease Control and Prevention. National Center for Health Statistics. Health Data Interactive. http://www.cdc.gov/nchs/hdi.htm. Accessed July 19, 2011.
26.
Ford ES. Trends in mortality from all causes and cardiovascular disease among hypertensive and nonhypertensive adults in the United States. Circulation. 2011;123:1737–1744.
27.
Lackland DT, Egan BM, Mountford WK, Boan AD, Evans DA, Gilbert G, McGee DL. Thirty-year survival for black and white hypertensive individuals in the Evans County Heart Study and the Hypertension Detection and Follow-up Program. J Am Soc Hypertens. 2008;2:448–454.
28.
Gazes PC, Lackland DT, Mountford WK, Gilbert GE, Harley RA. Comparison of cardiovascular risk factors for high brachial pulse pressure in blacks versus whites (Charleston Heart Study, Evans County Study, NHANES I and II Studies). Am J Cardiol. 2008;102:1514–1517.
29.
Kraft P, Bauman L, Yuan JY, Horvath S. Multivariate variance-components analysis of longitudinal blood pressure measurements from the Framingham Heart Study. BMC Genet. 2003; 4 (suppl 1): S55.
30.
Forman JP, Stampfer MJ, Curhan GC. Diet and lifestyle risk factors associated with incident hypertension in women. JAMA. 2009;302:401–411.
31.
Bangalore S, Kumar S, Lobach I, Messerli FH. Blood pressure targets in subjects with type 2 diabetes mellitus/impaired fasting glucose: observations from traditional and bayesian random-effects meta-analyses of randomized trials. Circulation. 2011;123:2799–2810.
32.
Vasan RS, Massaro JM, Wilson PW, Seshadri S, Wolf PA, Levy D, D'Agostino RB; Framingham Heart Study. Antecedent blood pressure and risk of cardiovascular disease: the Framingham Heart Study. Circulation. 2002;105:48–53.
33.
Franco OH, Peeters A, Bonneux L, de Laet C. Blood pressure in adulthood and life expectancy with cardiovascular disease in men and women: life course analysis. Hypertension. 2005;46:280–286.
34.
Ogunniyi MO, Croft JB, Greenlund KJ, Giles WH, Mensah GA. Racial/ethnic differences in microalbuminuria among adults with prehypertension and hypertension: National Health and Nutrition Examination Survey (NHANES), 1999–2006. Am J Hypertens. 2010;23:859–864.
35.
Ong KL, Cheung BM, Man YB, Lau CP, Lam KS. Prevalence, awareness, treatment, and control of hypertension among United States adults 1999–2004. Hypertension. 2007;49:69–75.
36.
Psaty BM, Manolio TA, Smith NL, Heckbert SR, Gottdiener JS, Burke GL, Weissfeld J, Enright P, Lumley T, Powe N, Furberg CD. Time trends in high blood pressure control and the use of antihypertensive medications in older adults: the Cardiovascular Health Study. Arch Intern Med. 2002;162:2325–2332.
37.
Lloyd-Jones DM, Evans JC, Levy D. Hypertension in adults across the age spectrum: current outcomes and control in the community. JAMA. 2005;294:466–472.
38.
Wassertheil-Smoller S, Anderson G, Psaty BM, Black HR, Manson J, Wong N, Francis J, Grimm R, Kotchen T, Langer R, Lasser N. Hypertension and its treatment in postmenopausal women: baseline data from the Women's Health Initiative. Hypertension. 2000;36:780–789.
39.
Hawkins K, Mittapally R, Chang J, Nahum GG, Gricar J. Burden of illness of hypertension among women using menopausal hormone therapy: a US perspective. Curr Med Res Opin. 2010;26:2823–2832.
40.
Sanchez RJ, Khalil L. Badger Heart Program: health screenings targeted to increase cardiovascular awareness in women at four northern sites in Wisconsin. WMJ. 2005;104:24–29.
41.
Centers for Disease Control and Prevention (CDC). Prevalence of actions to control high blood pressure–20 states, 2005. MMWR Morb Mortal Wkly Rep.2007;56:420–423.
42.
Wong ND, Lopez VA, L'Italien G, Chen R, Kline SE, Franklin SS. Inadequate control of hypertension in US adults with cardiovascular disease comorbidities in 2003–2004. Arch Intern Med. 2007;167:2431–2436.
43.
Redmond N, Baer HJ, Hicks LS. Health behaviors and racial disparity in blood pressure control in the National Health and Nutrition Examination Survey. Hypertension. 2011;57:383–389.
44.
Vasan RS, Larson MG, Leip EP, Kannel WB, Levy D. Assessment of frequency of progression to hypertension in non-hypertensive participants in the Framingham Heart Study: a cohort study. Lancet. 2001;358:1682–1686.
45.
Greenlund KJ, Croft JB, Mensah GA. Prevalence of heart disease and stroke risk factors in persons with prehypertension in the United States, 1999–2000. Arch Intern Med. 2004;164:2113–2118.
46.
Glasser SP, Judd S, Basile J, Lackland D, Halanych J, Cushman M, Prineas R, Howard V, Howard G. Prehypertension, racial prevalence and its association with risk factors: analysis of the REasons for Geographic And Racial Differences in Stroke (REGARDS) study. Am J Hypertens. 2011;24:194–199.
8. Congenital Cardiovascular Defects
ICD-9 745 to 747, ICD-10 Q20 to Q28. See Tables 8-1 through 8-4.
| Population Group | Estimated Prevalence, 2002: All Ages | Mortality, 2008: All Ages | Hospital Discharges,2009: All Ages |
|---|---|---|---|
| Both sexes | 650 000 to 1.3 million11 | 3415 | 52 000 |
| Males | … | 1839 (53.9%)* | 25 000 |
| Females | … | 1576 (46.1%)* | 27 000 |
| NH white males | … | 1427 | … |
| NH white females | … | 1236 | … |
| NH black males | … | 335 | … |
| NH black females | … | 270 | … |
Ellipses (…) indicate data not available; NH, non-Hispanic.
*
These percentages represent the portion of total congenital cardiovascular mortality that is for males vs females.
Sources: Mortality: National Center for Health Statistics (NCHS). These data represent underlying cause of death only; data for white and black males and females include Hispanics. Hospital discharges: National Hospital Discharge Survey, NCHS; data include those inpatients discharged alive, dead, or status unknown.
| Type of Presentation | Rate per 1000 Live Births | Estimated N (Variable With Yearly Birth Rate) |
|---|---|---|
| Fetal loss | Unknown | Unknown |
| Invasive procedure during the first year | 2.4 | 9200 |
| Detected during first year* | 8 | 36 000 |
| Bicuspid aortic valve | 13.7 | 54 800 |
*
Includes stillbirths and pregnancy termination at <20 weeks' gestation; includes some defects that resolve spontaneously or do not require treatment.
| Prevalence, n | Percent of Total | |||||
|---|---|---|---|---|---|---|
| Type | Total | Children | Adults | Total | Children | Adults |
| Total | 994 | 463 | 526 | 100 | 100 | 100 |
| VSD† | 199 | 93 | 106 | 20.1 | 20.1 | 20.1 |
| ASD | 187 | 78 | 109 | 18.8 | 16.8 | 20.6 |
| Patent ductus arteriosus | 144 | 58 | 86 | 14.2 | 12.4 | 16.3 |
| Valvular pulmonic stenosis | 134 | 58 | 76 | 13.5 | 12.6 | 14.4 |
| Coarctation of aorta | 76 | 31 | 44 | 7.6 | 6.8 | 8.4 |
| Valvular aortic stenosis | 54 | 25 | 28 | 5.4 | 5.5 | 5.2 |
| TOF | 61 | 32 | 28 | 6.1 | 7 | 5.4 |
| Atrioventricular septal defect | 31 | 18 | 13 | 3.1 | 3.9 | 2.5 |
| TGA | 26 | 17 | 9 | 2.6 | 3.6 | 1.8 |
| Hypoplastic right heart syndrome | 22 | 12 | 10 | 2.2 | 2.5 | 1.9 |
| Double-outlet right ventricle | 9 | 9 | 0 | 0.9 | 1.9 | 0.1 |
| Single ventricle | 8 | 6 | 2 | 0.8 | 1.4 | 0.3 |
| Anomalous pulmonary venous connection | 9 | 5 | 3 | 0.9 | 1.2 | 0.6 |
| Truncus arteriosus | 9 | 6 | 2 | 0.7 | 1.3 | 0.5 |
| HPLHS | 3 | 3 | 0 | 0.3 | 0.7 | 0 |
| Other | 22 | 12 | 10 | 2.1 | 2.6 | 1.9 |
VSD indicates ventricular septal defect; ASD, atrial septal defect; TOF, tetralogy of Fallot; TGA, transposition of the great arteries; and HPLHS, hypoplastic left heart syndrome.
*
Excludes an estimated 3 million bicuspid aortic valve prevalence (2 million in adults and 1 million in children).
†
Small VSD, 117 000 (65 000 adults and 52 000 children); large VSD, 82 000 (41 000 adults and 41 000 children).
| Sample | Population, Weighted | |
|---|---|---|
| Surgery for congenital heart disease | 14 888 | 25 831 |
| Deaths | 736 | 1253 |
| Mortality rate, % | 4.9 | 4.8 |
| By sex (81 missing in sample) | ||
| Males | 8127 | 14 109 |
| Deaths | 420 | 714 |
| Mortality rate, % | 5.2 | 5.1 |
| Females | 6680 | 11 592 |
| Deaths | 315 | 539 |
| Mortality rate, % | 4.7 | 4.6 |
| By type of surgery | ||
| ASD secundum surgery | 834 | 1448 |
| Deaths | 3 | 6 |
| Mortality rate, % | 0.4 | 0.4 |
| Norwood procedure for HPLHS | 161 | 286 |
| Deaths | 42 | 72 |
| Mortality rate, % | 26.1 | 25.2 |
ASD indicates atrial septal defect; HPLHS, hypoplastic left heart syndrome.
In 2003, 25 000 cardiovascular operations for congenital cardiovascular defects were performed on children <20 years of age. Inpatient mortality rate after all types of cardiac surgery was 4.8%. Nevertheless, mortality risk varies substantially for different defect types, from 0.4% for ASD repair to 25.2% for first-stage palliation for HPLHS. Fifty-five percent of operations were performed in males. In unadjusted analysis, mortality after cardiac surgery was somewhat higher for males than for females (5.1% vs 4.6%).
Source: Analysis of 2003 Kids' Inpatient Database38 and personal communication with Kathy Jenkins, MD, Children's Hospital of Boston, MA, October 1, 2006.
| ASD | atrial septal defect |
| AV | atrioventricular |
| CDC | Centers for Disease Control and Prevention |
| CHD | coronary heart disease |
| CI | confidence interval |
| DM | diabetes mellitus |
| HD | heart disease |
| HPLHS | hypoplastic left heart syndrome |
| ICD-9 | International Classification of Diseases, 9th Revision |
| ICD-10 | International Classification of Diseases, 10th Revision |
| MACDP | Metropolitan Atlanta Congenital Defects Program |
| NCHS | National Center for Health Statistics |
| NH | non-Hispanic |
| NHLBI | National Heart, Lung, and Blood Institute |
| TGA | transposition of the great arteries |
| TOF | tetralogy of Fallot |
| VSD | ventricular septal defect |
Congenital cardiovascular defects, also known as congenital heart defects, are structural problems that arise from abnormal formation of the heart or major blood vessels. ICD-9 lists 25 congenital heart defects codes, of which 21 designate specified anatomic or hemodynamic lesions.
Defects range in severity from tiny pinholes between chambers that may resolve spontaneously to major malformations that can require multiple surgical procedures before school age and may result in death in utero, in infancy, or in childhood. The common complex defects include the following:
•
Tetralogy of Fallot (TOF)
•
Transposition of the great arteries (TGA)
•
Atrioventricular (AV) septal defects
•
Coarctation of the aorta
•
Hypoplastic left heart syndrome
Congenital heart defects are serious and common conditions that have significant impact on morbidity, mortality, and healthcare costs in children and adults.1–4
Incidence
The most commonly reported incidence of congenital heart defects in the United States is between 4 and 10 per 1000, clustering around 8 per 1000 live births.5,6 Variations in reported number of incident cases are largely accounted for by the age at detection and the method of diagnosis. Major defects may be apparent in the prenatal or neonatal period, but minor defects may not be detected until adulthood. Detection rates have increased since the advent of cardiac ultrasound.4 Thus, true measures of the incidence of congenital HD would need to record new cases of defects that present from fetal life onward. Because most estimates are available for new cases detected between birth and the first year of life, birth prevalence is the best proxy for incident congenital heart defects. These are typically reported as cases per 1000 live births per year and do not distinguish between tiny defects that resolve without treatment and major malformations. To distinguish more serious defects, some studies also report new cases of sufficient severity to require an invasive procedure or that result in death within the first year of life. Despite the absence of true incidence figures, some data are available and are provided inTable 8-2.
•
Using population-based data from the Metropolitan Atlanta Congenital Defects Program (MACDP) in metropolitan Atlanta, GA, congenital heart defects occurred in 1 of every 111 to 125 births (live, still, or >20 weeks' gestation) from 1995 to 1997 and from 1998 to 2005, with variations in sex and racial distribution of some lesions.4,5
•
Analysis of contemporary birth cohorts with MACDP data revealed that the most common defects at birth were ventricular septal defect (VSD; 4.2/1000), atrial septal defect (ASD; 1.3/1000), valvar pulmonic stenosis (0.6/1000); TOF (0.5/1000), aortic coarctation (0.4/1000), AV septal defect (0.4/1000), and TGA (0.2/1000).5,7
•
An estimated minimum of 32 000 infants are expected to be affected each year in the United States. Of these, an approximate 25%, or 2.4 per 1000 live births, require invasive treatment in the first year of life.1
•
Estimates also are available for bicuspid aortic valves, which occur in 13.7 per 1000 people; these defects may not require treatment in infancy but can cause problems later in adulthood.8
•
Data collected by the National Birth Defects Prevention Network from 11 states from 1999 to 2001 showed the average prevalence of 18 selected major birth defects. These data indicated that there are >6500 estimated annual cases of 5 cardiovascular defects: truncus arteriosus, TGA, TOF, AV septal defect, and hypoplastic left heart syndrome.9
Prevalence
The 32nd Bethesda Conference estimated that the total number of adults living with congenital HD in the United States in 2000 was 800 000.2,3 In the United States, 1 in 150 adults are expected to have some form of congenital HD.3 Nearly 2 decades ago, the estimated number of children with congenital heart defects in the United States was 600 000.1 In population data from Canada, the measured prevalence of congenital cardiac defects in the general population was 11.89 per 1000 children and 4.09 per 1000 adults in the year 2000.10 Extrapolated to the US population in the same year, this yields published estimates of 859 000 children and 850 000 adults over a decade ago,7 with expected growth rates of the congenital heart defects population varying from 1% to 5% per year depending on the age and distribution of lesions.2,10
Estimates of the distribution of lesions in the congenital heart defects population using available data vary with assumptions made. If all those born were treated, there would be 750 000 survivors with simple lesions, 400 000 with moderate lesions, and 180 000 with complex lesions; in addition, there would be 3 000 000 subjects alive with bicuspid aortic valves.11 Without treatment, the number of survivors in each group would be 400 000, 220 000, and 30 000, respectively. The actual numbers surviving are projected to be between these 2 sets of estimates as of 1 decade ago.11 Using measurements from population data in Canada, the prevalence of severe forms of congenital heart defects increased 85% in adults and 22% in children from 1985 to 2000.10 The most common types of defects in children are (at a minimum) VSD, 620 000 people; ASD, 235 000 people; valvular pulmonary stenosis, 185 000 people; and patent ductus arteriosus, 173 000 people.11 The most common lesions seen in adults are ASD and TOF.2
Risk Factors
•
Numerous intrinsic and extrinsic nongenetic risk factors contribute to CHD.12
•
Attributable risks or fractions have been shown to include paternal anesthesia in TOF (3.6%), sympathomimetic medication for coarctation of the aorta (5.8%), pesticides for VSD (5.5%), and solvents for hypoplastic left heart syndrome (4.6%).13
•
A study of infants born with heart defects unrelated to genetic syndromes who were included in the National Birth Defects Prevention Study found that women who reported smoking in the month before becoming pregnant or in the first trimester were more likely to give birth to a child with a septal defect. Compared with the infants of mothers who did not smoke during pregnancy, infants of mothers who were heavy smokers (≥25 cigarettes daily) were twice as likely to have a septal defect.14
•
Data from the Baltimore-Washington Infant Study reported that maternal smoking during the first trimester of pregnancy was associated with at least a 30% increased risk of the following lesions in the fetus: ASD, pulmonary valvar stenosis, truncus arteriosus, and TGA.15
•
Associations between exposure to air pollutants during first-trimester pregnancy and risks of congenital heart defects were documented from 1986 to 2003 by the MACDP that related carbon monoxide, nitrogen dioxide, and sulfur dioxide measurements to the risk of ASD, VSD, TGA, and TOF.16
•
The results of a population-based study examining pregnancy obesity found a weak to moderate positive association of maternal obesity with 7 of 16 categories of birth defects, including heart defects.17
•
Although folic acid supplementation is recommended during pregnancy to potentially reduce the risk of congenital heart defects,12 there has been only 1 US population-based case-control study, performed with the Baltimore-Washington Infant Study between 1981 and 1989, that showed an inverse relationship between folic acid use and the risk of TGA.18 A study from Quebec, Canada, that analyzed 1.3 million births from 1990 to 2005 found a significant 6% per year reduction in severe congenital heart defects using a time-trend analysis before and after public health measures were instituted that mandated folic acid fortification of grain and flour products in Canada.19
•
Pregestational DM was significantly associated with cardiac defects, both isolated and multiple. Gestational DM was associated with a limited group of birth defects.20
Mortality
Mortality related to congenital cardiovascular defects in 2008 was 3415. Any-mention mortality related to congenital cardiovascular defects in 2008 was 5359.21
•
Congenital cardiovascular defects are the most common cause of infant death resulting from birth defects; >24% of infants who die of a birth defect have a heart defect.21
•
The mortality rate attributable to congenital heart defects in the United States has continued to decline from 1979 to 1997 and from 1999 to 2006. Age-adjusted death rates attributable to all congenital heart defects declined 21% to 39%, and deaths tended to occur at progressively older ages. Nevertheless, mortality in infants <1 year of age continues to account for nearly half of the deaths, with persistence of ethnicity differences revealing higher mortality rates in non-Hispanic blacks.15,22
•
When CDC death registry data were used to examine mortality in cyanotic and acyanotic lesions between 1979 and 2005, all-age mortality rates had declined by 60% for VSD and 40% for TOF.23
•
In population-based data from Canada, 8123 deaths occurred among 71 686 congenital HD patients followed up for nearly 1 million patient-years. Overall mortality decreased by 31%, and the median age of death increased from 2 to 23 years between 1987 and 2005.24
•
The 2008 death rate attributable to congenital cardiovascular defects was 1.1. Death rates were 1.2 for white males, 1.5 for black males, 1.0 for white females, and 1.2 for black females. Infant mortality rates (<1 year of age) were 34.9 for white infants and 46.5 for black infants.21
•
According to CDC multiple-cause death data, from 1999 to 2006, sex differences in mortality over time varied with age. Between the ages of 18 and 34 years, mortality over time decreased significantly in females but not in males.25
•
On the basis of data from the Healthcare Cost and Utilization Project's Kids' Inpatient Database from 2000, 2003, and 2006, male children had more congenital heart defect surgeries in infancy, more high-risk surgeries, and more procedures to correct multiple congenital heart defects. Female infants with high risk congenital heart defects had a 39% higher adjusted mortality.26
•
In 2007, 189 000 life-years were lost before 55 years of age because of deaths attributable to congenital cardiovascular defects. This is almost as many as life-years as were lost from leukemia and asthma combined (NHLBI tabulation of NCHS mortality data).
•
Data from the Pediatric Heart Network conducted in 15 North American centers revealed that even in lesions associated with the highest mortality among congenital lesions, such as hypoplastic left heart syndrome, aggressive palliation can lead to an increase in the 12-month survival rate from 64% to 74%.27
•
Data analysis from the Society of Thoracic Surgeons, a voluntary registry with self-reported data for a 4-year cycle (2006–2009) from 68 centers performing congenital heart surgery (67 from the United States and 1 from Canada), showed that for 88 989 total operations, the overall aggregate hospital discharge mortality rate was 3.6%28; specifically, for neonates (0–30 days of age), the mortality rate was 10.2%29; for infants (31 days to 1 year of age), it was 2.8%30; for children (>1 year to 18 years of age), it was 1.1%31; and for adults (>18 years of age), it was 1.8%.32
•
Using the Nationwide Inpatient Sample 1988–2003, mortality was examined for 12 congenital heart defects procedures. A total of 30 250 operations were identified, which yielded a national estimate of 152 277±7875 operations. Of these, 27% were performed in patients ≥18 years of age. The overall in-hospital mortality rate for adult congenital heart defect patients was 4.71% (95% CI 4.19% to 5.23%), with a significant reduction in mortality observed when surgery was performed on adult congenital heart defect patients by pediatric versus nonpediatric heart surgeons (1.87% versus 4.84%; P<0.0001).33
Hospitalizations
In 2004, birth defects accounted for >139 000 hospitalizations, representing 47.4 stays per 100 000 people. Cardiac and circulatory congenital anomalies accounted for 34% of all hospital stays for birth defects. Although the most common congenital lesions were shunts, including patent ductus arteriosus, VSDs, and ASDs, TOF accounted for a higher proportion of in-hospital death than any other birth defect. Between 1997 and 2004, hospitalization rates increased by 28.5% for cardiac and circulatory congenital anomalies.34
Cost
•
From 2003 data from the Healthcare Cost and Utilization Project 2003 Kids' Inpatient Database and information on birth defects in the Congenital Malformations Surveillance Report, it was found that the most expensive average neonatal hospital charges were for 2 congenital heart defects: hypoplastic left heart syndrome ($199 597) and common truncus arteriosus ($192 781). Two other cardiac defects, coarctation of the aorta and TGA, were associated with average hospital charges in excess of $150 000. For the 11 selected cardiovascular congenital defects (of 35 birth defects considered), there were 11 578 hospitalizations in 2003 and 1550 in-hospital deaths (13.4%). Estimated total hospital charges for these 11 conditions were $1.4 billion.35
•
In 2004, hospital costs for congenital cardiovascular defect conditions totaled $2.6 billion. The highest aggregate costs were for stays related to cardiac and circulatory congenital anomalies, which accounted for ≈$1.4 billion, more than half of all hospital costs for birth defects.34
References
1.
Moller J. Prevalence and incidence of cardiac malformation. In:, Moller JH ed. Perspectives in Pediatric Cardiology: Surgery of Congenital Heart Disease: Pediatric Cardiac Care Consortium, 1984–1995. Armonk, NY: Futura Publishing; 1998:19–26.
2.
Warnes CA, Liberthson R, Danielson GK, Dore A, Harris L, Hoffman JI, Somerville J, Williams RG, Webb GD. Task force 1: the changing profile of congenital heart disease in adult life. J Am Coll Cardiol. 2001;37:1170–1175.
3.
Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA, del Nido P, Fasules JW, Graham TP, Hijazi ZM, Hunt SA, King ME, Landzberg MJ, Miner PD, Radford MJ, Walsh EP, Webb GD. ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to develop guidelines on the management of adults with congenital heart disease). Circulation. 2008;118:e714–e833.
4.
Botto LD, Correa A, Erickson JD. Racial and temporal variations in the prevalence of heart defects. Pediatrics. 2001;107:E32.
5.
Reller MD, Strickland MJ, Riehle-Colarusso T, Mahle WT, Correa A. Prevalence of congenital heart defects in metropolitan Atlanta, 1998–2005. J Pediatr. 2008;153:807–813.
6.
Roguin N, Du ZD, Barak M, Nasser N, Hershkowitz S, Milgram E. High prevalence of muscular ventricular septal defect in neonates. J Am Coll Cardiol. 1995;26:1545–1548.
7.
Marelli AJ, Therrien J, Mackie AS, Ionescu-Ittu R, Pilote L. Planning the specialized care of adult congenital heart disease patients: from numbers to guidelines: an epidemiologic approach. Am Heart J. 2009;157:1–8.
8.
Hoffman JI, Kaplan S. The incidence of congenital heart disease. J Am Coll Cardiol. 2002;39:1890–1900.
9.
Centers for Disease Control and Prevention (CDC). Improved national prevalence estimates for 18 selected major birth defects–United States, 1999–2001. MMWR Morb Mortal Wkly Rep.2006;54:1301–1305.
10.
Marelli AJ, Mackie AS, Ionescu-Ittu R, Rahme E, Pilote L. Congenital heart disease in the general population: changing prevalence and age distribution. Circulation. 2007;115:163–172.
11.
Hoffman JI, Kaplan S, Liberthson RR. Prevalence of congenital heart disease. Am Heart J. 2004;147:425–439.
12.
Jenkins KJ, Correa A, Feinstein JA, Botto L, Britt AE, Daniels SR, Elixson M, Warnes CA, Webb CL. Noninherited risk factors and congenital cardiovascular defects: current knowledge: a scientific statement from the American Heart Association Council on Cardiovascular Disease in the Young. Circulation. 2007;115:2995–3014.
13.
Wilson PD, Loffredo CA, Correa-Villaseñor A, Ferencz C. Attributable fraction for cardiac malformations. Am J Epidemiol. 1998;148:414–423.
14.
Malik S, Cleves MA, Honein MA, Romitti PA, Botto LD, Yang S, Hobbs CA. Maternal smoking and congenital heart defects. Pediatrics. 2008;121:e810–e816.
15.
Alverson CJ, Strickland MJ, Gilboa SM, Correa A. Maternal smoking and congenital heart defects in the Baltimore-Washington Infant Study. Pediatrics. 2011;127:e647–e653.
16.
Strickland MJ, Klein M, Correa A, Reller MD, Mahle WT, Riehle-Colarusso TJ, Botto LD, Flanders WD, Mulholland JA, Siffel C, Marcus M, Tolbert PE. Ambient air pollution and cardiovascular malformations in Atlanta, Georgia, 1986–2003. Am J Epidemiol. 2009;169:1004–1014.
17.
Waller DK, Shaw GM, Rasmussen SA, Hobbs CA, Canfield MA, Siega-Riz AM, Gallaway MS, Correa A; for the National Birth Defects Prevention Study. Prepregnancy obesity as a risk factor for structural birth defects. Arch Pediatr Adolesc Med. 2007;161:745–750.
18.
Scanlon KS, Ferencz C, Loffredo CA, Wilson PD, Correa-Villaseñor A, Khoury MJ, Willett WC; Baltimore-Washington Infant Study Group. Preconceptional folate intake and malformations of the cardiac outflow tract. Epidemiology. 1998;9:95–98.
19.
Ionescu-Ittu R, Marelli AJ, Mackie AS, Pilote L. Prevalence of severe congenital heart disease after folic acid fortification of grain products: time trend analysis in Quebec, Canada. BMJ. 2009;338:b1673.
20.
Correa A, Gilboa SM, Besser LM, Botto LD, Moore CA, Hobbs CA, Cleves MA, Riehle-Colarusso TJ, Waller DK, Reece EA. Diabetes mellitus and birth defects. Am J Obstet Gynecol.2008;199:237.e231–e239.
21.
Centers for Disease Control and Prevention. Vital Statistics Public Use Data Files - 2008 Mortality Multiple Cause Files. Available at: http://www.cdc.gov/nchs/data_access/Vitalstatsonline.htm#Mortality_Multiple. Accessed September 23, 2011.
22.
Boneva RS, Botto LD, Moore CA, Yang Q, Correa A, Erickson JD. Mortality associated with congenital heart defects in the United States: trends and racial disparities, 1979–1997. Circulation. 2001;103:2376–2381.
23.
Pillutla P, Shetty KD, Foster E. Mortality associated with adult congenital heart disease: trends in the US population from 1979 to 2005. Am Heart J. 2009;158:874–879.
24.
Khairy P, Ionescu-Ittu R, Mackie AS, Abrahamowicz M, Pilote L, Marelli AJ. Changing mortality in congenital heart disease. J Am Coll Cardiol. 2010;56:1149–1157.
25.
Gilboa SM, Salemi JL, Nembhard WN, Fixler DE, Correa A. Mortality resulting from congenital heart disease among children and adults in the United States, 1999 to 2006. Circulation. 2010;122:2254–2263.
26.
Marelli A, Gauvreau K, Landzberg M, Jenkins K. Sex differences in mortality in children undergoing congenital heart disease surgery: a United States population-based study. Circulation. 2010; 122(suppl): S234– S240.
27.
Ohye RG, Sleeper LA, Mahony L, Newburger JW, Pearson GD, Lu M, Goldberg CS, Tabbutt S, Frommelt PC, Ghanayem NS, Laussen PC, Rhodes JF, Lewis AB, Mital S, Ravishankar C, Williams IA, Dunbar-Masterson C, Atz AM, Colan S, Minich LL, Pizarro C, Kanter KR, Jaggers J, Jacobs JP, Krawczeski CD, Pike N, McCrindle BW, Virzi L, Gaynor JW; Pediatric Heart Network Investigators. Comparison of shunt types in the Norwood procedure for single-ventricle lesions. N Engl J Med. 2010;362:1980–1992.
28.
Society of Thoracic Surgeons. STS congenital heart surgery data summary: July 2006–June 2010 procedures: all patients. Society of Thoracic Surgeons Web site. http://www.sts.org/sites/default/files/documents/STSCONG-AllPatientsSummary_Fall2010.pdf. Accessed July 18, 2011.
29.
Society of Thoracic Surgeons. STS congenital heart surgery data summary: July 2006–June 2010 procedures: neonates (0–30 days). Society of Thoracic Surgeons Web site. http://www.sts.org/sites/default/files/documents/STSCONG-NeonatesSummary_Fall2010.pdf. Accessed July 18, 2011.
30.
Society of Thoracic Surgeons. STS congenital heart surgery data summary: July 2006–June 2010 procedures: infants (31 days–1 year). Society of Thoracic Surgeons Web site. http://www.sts.org/sites/default/files/documents/STSCONG-InfantsSummary_Fall2010.pdf. Accessed July 18, 2011.
31.
Society of Thoracic Surgeons. STS congenital heart surgery data summary: July 2006–June 2010 procedures: children (>1 year to <18 years). Society of Thoracic Surgeons Web site. http://www.sts.org/sites/default/files/documents/STSCONG-ChildrenSummary_Fall2010.pdf. Accessed July 18, 2011.
32.
Society of Thoracic Surgeons. STS congenital heart surgery data summary: July 2006–June 2010 procedures: adult (18 years+). Society of Thoracic Surgeons Web site. http://www.sts.org/sites/default/files/documents/STSCONG-AdultsSummary_Fall2010.pdf. Accessed July 18, 2011.
33.
Karamlou T, Diggs BS, Person T, Ungerleider RM, Welke KF. National practice patterns for management of adult congenital heart disease: operation by pediatric heart surgeons decreases in-hospital death. Circulation. 2008;118:2345–2352.
34.
Russo CA, Elixhauser A. Hospitalizations for Birth Defects, 2004. HCUP Statistical Brief No. 24. Rockville, MD: US Agency for Healthcare Research and Quality; January 2007. http://www.hcup-us.ahrq.gov/reports/statbriefs/sb24.pdf. Accessed July 18, 2011.
35.
Centers for Disease Control and Prevention (CDC). Hospital stays, hospital charges, and in-hospital deaths among infants with selected birth defects–United States, 2003. MMWR Morb Mortal Wkly Rep.2007;56:25–29.
36.
Sands AJ, Casey FA, Craig BG, Dornan JC, Rogers J, Mulholland HC. Incidence and risk factors for ventricular septal defect in “low risk” neonates. Arch Dis Child Fetal Neonatal Ed. 1999;81:F61–F63.
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Larson EW, Edwards WD. Risk factors for aortic dissection: a necropsy study of 161 cases. Am J Cardiol. 1984;53:849–855.
38.
Kids' Inpatient Database, HCUPnet, Healthcare Cost and Utilization Project, Agency for Healthcare Research and Quality. http://www.hcup-us.ahrq.gov/kidoverview.jsp. Accessed November 7, 2011.
9. Cardiomyopathy and Heart Failure
| Population Group | Prevalence, 2008: Age ≥20 y | Incidence (New Cases): Age ≥45 y | Mortality 2008: All Ages * | Hospital Discharges, 2009: All Ages |
|---|---|---|---|---|
| Both sexes | 5 700 000 (2.4%) | 670 000 | 56 830 | 1 094 000 |
| Males | 3 100 000 (3.0%) | 350 000 | 23 017 (40.5%)† | 531 000 |
| Females | 2 600 000 (2.0%) | 320 000 | 33 813 (59.5%)† | 563 000 |
| NH white males | 2.7% | … | 20 278 | … |
| NH white females | 1.8% | … | 30 244 | … |
| NH black males | 4.5% | … | 2391 | … |
| NH black females | 3.8% | … | 3068 | … |
| Mexican American males | 2.3% | … | … | … |
| Mexican American females | 1.3% | … | … | … |
NH indicates non-Hispanic; ellipses (…), data not available.
Heart failure includes persons who answered “yes” to the question of ever having congestive heart failure.
*
Mortality data are for whites and blacks and include Hispanics.
†
These percentages represent the portion of total mortality attributable to heart failure that is for males vs females.
Sources: Prevalence: National Health and Nutrition Examination Survey 2005–2008 (National Center for Health Statistics) and National Heart, Lung, and Blood Institute. Percentages are age adjusted for Americans ≥20 years of age. Age-specific percentages are extrapolated to the 2008 US population estimates. These data are based on self-reports. Incidence: Framingham Heart Study, 1980–2003 from National Heart, Lung, and Blood Institute Incidence and Prevalence Chart Book, 2006. Mortality: National Center for Health Statistics.
Cardiomyopathy
ICD-9 425; ICD-10 I42.
Mortality—24 703. Any-mention mortality—48 579. Hospital discharges—52 000.
•
Since 1996, the NHLBI-sponsored Pediatric Cardiomyopathy Registry has collected data on all children with newly diagnosed cardiomyopathy in New England and the Central Southwest (Texas, Oklahoma, and Arkansas).1
— The overall incidence of cardiomyopathy is 1.13 cases per 100 000 among children <18 years of age.
— Among children <1 year of age, the incidence is 8.34, and among children 1 to 18 years of age, it is 0.70 per 100 000.
— The annual incidence is lower in white than in black children, higher in boys than in girls, and higher in New England (1.44 per 100 000) than in the Central Southwest (0.98 per 100 000).
•
Hypertrophic cardiomyopathy (HCM) is the most common inherited heart defect, occurring in 1 of 500 individuals. In the United States, ≈500 000 people have HCM, yet most are unaware of it.2 See Chapter 10, Disorders of Heart Rhythm, for statistics regarding sudden death in HCM.
•
In a recent report of the Pediatric Cardiomyopathy Registry, the overall annual incidence of HCM in children was 4.7 per 1 million children. There was a higher incidence in the New England than in the Central Southwest region, in boys than in girls, and in children diagnosed at <1 year of age than in older children.3
•
Dilated cardiomyopathy is the most common form of cardiomyopathy. The Pediatric Cardiomyopathy Registry recently reported an annual incidence of dilated cardiomyopathy in children <18 years of age of 0.57 per 100 000 overall. The annual incidence was higher in boys than in girls (0.66 versus 0.47 cases per 100 000), in blacks than in whites (0.98 versus 0.46 cases per 100 000), and in infants (<1 year of age) than in children (4.40 versus 0.34 cases per 100 000). The majority of children (66%) had idiopathic disease. The most common known causes were myocarditis (46%) and neuromuscular disease (26%).4
•
Tachycardia-induced cardiomyopathy develops slowly and appears reversible, but recurrent tachycardia causes rapid decline in left ventricular function and development of HF. Sudden death is possible.5
| ABC | Aging, Body and Composition |
| ARIC | Atherosclerosis Risk in Communities Study |
| BP | blood pressure |
| CARDIA | Coronary Artery Risk Development in Young Adults Study |
| CHS | Cardiovascular Health Study |
| CVD | cardiovascular disease |
| DM | diabetes mellitus |
| EF | ejection fraction |
| FHS | Framingham Heart Study |
| HbA1c | hemoglobin A1c |
| HCM | Hypertrophic cardiomyopathy |
| HF | heart failure |
| ICD-9 | International Classification of Diseases, 9th Revision |
| ICD-10 | International Classification of Diseases, 10th Revision |
| MESA | Multi-Ethnic Study of Atherosclerosis |
| MI | Myocardial infarction |
| NCHS | National Center for Health Statistics |
| NH | Non-Hispanic |
| NHAMCS | National Hospital Ambulatory Medical Care Survey |
| NHANES | National Health and Nutrition Examination Survey |
| NHDS | National Hospital Discharge Survey |
| NHLBI | National Heart, Lung, and Blood Institute |
| PAR | Population-attributable risk |
Heart Failure
ICD-9 428; ICD-10 I50.
Prevalence
Incidence
•
Data from the NHLBI-sponsored FHS7 indicate the following:
— HF incidence approaches 10 per 1000 population after 65 years of age.
— Seventy-five percent of HF cases have antecedent hypertension.
— At 40 years of age, the lifetime risk of developing HF for both men and women is 1 in 5. At 80 years of age, remaining lifetime risk for development of new HF remains at 20% for men and women, even in the face of a much shorter life expectancy.
— At 40 years of age, the lifetime risk of HF occurring without antecedent MI is 1 in 9 for men and 1 in 6 for women.
— The lifetime risk for people with BP >160/90 mm Hg is double that of those with BP <140/90 mm Hg.
•
The annual rates per 1000 population of new HF events for white men are 15.2 for those 65 to 74 years of age, 31.7 for those 75 to 84 years of age, and 65.2 for those ≥85 years of age. For white women in the same age groups, the rates are 8.2, 19.8, and 45.6, respectively. For black men, the rates are 16.9, 25.5, and 50.6,* and for black women, the estimated rates are 14.2, 25.5, and 44.0,* respectively (CHS, NHLBI).8
•
In MESA, African Americans had the highest risk of developing HF, followed by Hispanic, white, and Chinese Americans (4.6, 3.5, 2.4, and 1.0 per 1000 person-years, respectively). This higher risk reflected differences in the prevalence of hypertension, DM, and socioeconomic status. African Americans had the highest proportion of incident HF not preceded by clinical MI (75%).9
•
In Olmsted County, Minnesota, the incidence of HF did not decline between 1979 and 2000.10
•
In the ARIC study of the NHLBI, the age-adjusted incidence rate per 1000 person-years was 3.4 for white women, less than for all other groups; that is, white men (6.0), black women (8.1), and black men (9.1). The 30-day, 1-year, and 5-year case fatality rates after hospitalization for HF were 10.4%, 22%, and 42.3%, respectively. Blacks had a greater 5-year case fatality rate than whites (P<0.05). HF incidence rates in black women were more similar to those of men than of white women. The greater HF incidence in blacks than in whites is explained largely by blacks' greater levels of atherosclerotic risk factors.11
•
Data from Kaiser Permanente indicated an increase in the incidence of HF among the elderly, with the effect being greater in men.12
•
Data from hospitals in Worcester, MA, indicate that during 2000, the incidence and attack rates for HF were 219 per 100 000 and 897 per 100 000, respectively. HF was more frequent in women and the elderly. The hospital fatality rate was 5.1%.13
•
In the CARDIA study, HF before 50 years of age was more common among blacks than whites. Hypertension, obesity, and systolic dysfunction are important risk factors that may be targets for prevention.14
Mortality
•
In 2008, HF any-mention mortality was 281 437 (124 598 males and 156 839 females). HF was the underlying cause in 56 830 of those deaths in 2008 (NCHS, NHLBI). Table 9-1 shows the numbers of these deaths that are coded for HF as the underlying cause.
•
The 2008 overall any-mention death rate for HF was 84.6. Any-mention death rates were 98.9 for white males, 102.7 for black males, 75.9 for white females, and 78.8 for black females (NCHS, NHLBI).
•
One in 9 deaths has HF mentioned on the death certificate (NCHS, NHLBI).
•
The number of any-mention deaths from HF was approximately as high in 1995 (287 000) as it was in 2008 (283 000; NCHS, NHLBI).
•
•
In the elderly, data from Kaiser Permanente indicate that survival after the onset of HF has also improved.12
•
In the CHS, depression and amino-terminal pro-B-type natriuretic peptide were independent risk factors for CVD-related and all-cause mortality.17
Risk Factors
•
•
In the Framingham Offspring Study, among 2739 participants, increased circulating concentrations of resistin were associated with incident HF independent of prevalent coronary disease, obesity, insulin resistance, and inflammation.20
•
Among 20 900 male physicians in the Physicians Health Study, the lifetime risk of HF was higher in men with hypertension; healthy lifestyle factors (normal weight, not smoking, regular exercise, moderate alcohol intake, consumption of breakfast cereals, and consumption of fruits and vegetables) were related to lower risk of HF.21
•
Among 2934 participants in the Health Aging, Body and Composition (ABC) study, the incidence of HF was 13.6 per 1000 person-years. Men and black participants were more likely to develop HF. Coronary disease (population attributable risk 23.9% for white participants, 29.5% for black participants) and uncontrolled BP (population attributable risk 21.3% for white participants, 30.1% for black participants) had the highest population attributable risks in both races. There was a higher overall proportion of HF attributable to modifiable risk factors in black participants than white participants (67.8% versus 48.9%). Hospitalizations were higher among black participants.22 Inflammatory markers (interleukin-6 and tumor necrosis factor-α) and serum albumin levels were also associated with HF risk.23,24
•
In the CHS, baseline cardiac troponin and changes in cardiac troponin levels measured by a sensitive assay were significantly associated with incident HF.25
Left Ventricular Function
•
Data from Olmsted County, Minnesota, indicate that:
— Among asymptomatic individuals, the prevalence of left ventricular diastolic dysfunction was 21% for mild diastolic dysfunction and 7% for moderate or severe diastolic dysfunction. The prevalence of systolic dysfunction was 6%. The presence of any left ventricular dysfunction (systolic or diastolic) was associated with an increased risk of developing overt HF, and diastolic dysfunction was predictive of all-cause death.29
— Among individuals with symptomatic HF, the prevalence of left ventricular diastolic dysfunction was 6% for mild diastolic dysfunction and 75% for moderate or severe diastolic dysfunction.30 The proportion of people with HF and preserved ejection fraction (EF) increased over time. Survival improved over time among individuals with reduced EF but not among those with preserved EF.31
Hospital Discharges/Ambulatory Care Visits
•
Hospital discharges for HF were essentially unchanged from 1999 to 2009, with first-listed discharges of 975 000 and 1 094 000, respectively (unpublished data from the NHDS 2009, NCHS, NHLBI).
•
In 2009, there were 3 041 000 physician office visits with a primary diagnosis of HF. In 2009, there were 668 000 ED visits and 293 000 outpatient department visits for HF (NCHS, NHAMCS, NHLBI tabulation).
•
Among 1077 patients with HF in Olmsted County, Minnesota, hospitalizations were common after HF diagnosis, with 83% patients hospitalized at least once and 43% hospitalized at least 4 times. More than one half of all hospitalizations were related to noncardiovascular causes.32
References
1.
Lipshultz SE, Sleeper LA, Towbin JA, Lowe AM, Orav EJ, Cox GF, Lurie PR, McCoy KL, McDonald MA, Messere JE, Colan SD. The incidence of pediatric cardiomyopathy in two regions of the United States. N Engl J Med. 2003;348:1647–1655.
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Maron BJ, McKenna WJ, Danielson GK, Kappenberger LJ, Kuhn HJ, Seidman CE, Shah PM, Spencer WH, Spirito P, Ten Cate FJ, Wigle ED. American College of Cardiology/European Society of Cardiology clinical expert consensus document on hypertrophic cardiomyopathy: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines. J Am Coll Cardiol. 2003;42:1687–1713.
3.
Colan SD, Lipshultz SE, Lowe AM, Sleeper LA, Messere J, Cox GF, Lurie PR, Orav EJ, Towbin JA. Epidemiology and cause-specific outcome of hypertrophic cardiomyopathy in children: findings from the Pediatric Cardiomyopathy Registry. Circulation. 2007;115:773–781.
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Towbin JA, Lowe AM, Colan SD, Sleeper LA, Orav EJ, Clunie S, Messere J, Cox GF, Lurie PR, Hsu D, Canter C, Wilkinson JD, Lipshultz SE. Incidence, causes, and outcomes of dilated cardiomyopathy in children. JAMA. 2006;296:1867–1876.
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Nerheim P, Birger-Botkin S, Piracha L, Olshansky B. Heart failure and sudden death in patients with tachycardia-induced cardiomyopathy and recurrent tachycardia. Circulation. 2004;110:247–252.
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Heidenreich PA, Trogdon JG, Khavjou OA, Butler J, Dracup K, Ezekowitz MD, Finkelstein EA, Hong Y, Johnston SC, Khera A, Lloyd-Jones DM, Nelson SA, Nichol G, Orenstein D, Wilson PW, Woo YJ; on behalf of the American Heart Association Advocacy Coordinating Committee, Stroke Council, Council on Cardiovascular Radiology and Intervention, Council on Clinical Cardiology, Council on Epidemiology and Prevention, Council on Arteriosclerosis, Thrombosis and Vascular Biology, Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation, Council on Cardiovascular Nursing, Council on the Kidney in Cardiovascular Disease, Council on Cardiovascular Surgery and Anesthesia, and Interdisciplinary Council on Quality of Care and Outcomes Research. Forecasting the future of cardiovascular disease in the United States: a policy statement from the American Heart Association. Circulation. 2011;123:933–944.
7.
Lloyd-Jones DM, Larson MG, Leip EP, Beiser A, D'Agostino RB, Kannel WB, Murabito JM, Vasan RS, Benjamin EJ, Levy D; Framingham Heart Study. Lifetime risk for developing congestive heart failure: the Framingham Heart Study. Circulation. 2002;106:3068–3072.
8.
Incidence and Prevalence: 2006 Chart Book on Cardiovascular and Lung Diseases. Bethesda, MD: National Heart, Lung, and Blood Institute; 2006.
9.
Bahrami H, Kronmal R, Bluemke DA, Olson J, Shea S, Liu K, Burke GL, Lima JAC. Differences in the incidence of congestive heart failure by ethnicity: the Multi-Ethnic Study of Atherosclerosis. Arch Intern Med. 2008;168:2138–2145.
10.
Roger VL, Weston SA, Redfield MM, Hellermann-Homan JP, Killian J, Yawn BP, Jacobsen SJ. Trends in heart failure incidence and survival in a community-based population. JAMA. 2004;292:344–350.
11.
Loehr LR, Rosamond WD, Chang PP, Folsom AR, Chambless LE. Heart failure incidence and survival (from the Atherosclerosis Risk in Communities study). Am J Cardiol. 2008;101:1016–1022.
12.
Barker WH, Mullooly JP, Getchell W. Changing incidence and survival for heart failure in a well-defined older population, 1970–1974 and 1990–1994. Circulation. 2006;113:799–805.
13.
Goldberg RJ, Spencer FA, Farmer C, Meyer TE, Pezzella S. Incidence and hospital death rates associated with heart failure: a community-wide perspective. Am J Med. 2005;118:728–734.
14.
Bibbins-Domingo K, Pletcher MJ, Lin F, Vittinghoff E, Gardin JM, Arynchyn A, Lewis CE, Williams OD, Hulley SB. Racial differences in incident heart failure among young adults. N Engl J Med. 2009;360:1179–1190.
15.
Matsushita K, Blecker S, Pazin-Filho A, Bertoni A, Chang PP, Coresh J, Selvin E. The association of hemoglobin A1c with incident heart failure among people without diabetes: the Atherosclerosis Risk in Communities Study. Diabetes. 2010;59:2020–2026.
16.
Levy D, Kenchaiah S, Larson MG, Benjamin EJ, Kupka MJ, Ho KK, Murabito JM, Vasan RS. Long-term trends in the incidence of and survival with heart failure. N Engl J Med. 2002;347:1397–1402.
17.
van den Broek KC, Defilippi CR, Christenson RH, Seliger SL, Gottdiener JS, Kop WJ. Predictive value of depressive symptoms and B-type natriuretic peptide for new-onset heart failure and mortality. Am J Cardiol. 2011;107:723–729.
18.
Velagaleti RS, Gona P, Larson MG, Wang TJ, Levy D, Benjamin EJ, Selhub J, Jacques PF, Meigs JB, Tofler GH, Vasan RS. Multimarker approach for the prediction of heart failure incidence in the community. Circulation. 2010;122:1700–1706.
19.
Dhingra R, Gona P, Wang TJ, Fox CS, D'Agostino RB, Vasan RS. Serum gamma-glutamyl transferase and risk of heart failure in the community. Arterioscler Thromb Vasc Biol. 2010;30:1855–1860.
20.
Frankel DS, Vasan RS, D'Agostino RB, Benjamin EJ, Levy D, Wang TJ, Meigs JB. Resistin, adiponectin, and risk of heart failure: the Framingham offspring study. J Am Coll Cardiol. 2009;53:754–762.
21.
Djoussé L, Driver JA, Gaziano JM. Relation between modifiable lifestyle factors and lifetime risk of heart failure. JAMA. 2009;302:394–400.
22.
Kalogeropoulos A, Georgiopoulou V, Kritchevsky SB, Psaty BM, Smith NL, Newman AB, Rodondi N, Satterfield S, Bauer DC, Bibbins-Domingo K, Smith AL, Wilson PW, Vasan RS, Harris TB, Butler J. Epidemiology of incident heart failure in a contemporary elderly cohort: the Health, Aging, and Body Composition Study. Arch Intern Med. 2009;169:708–715.
23.
Kalogeropoulos A, Georgiopoulou V, Psaty BM, Rodondi N, Smith AL, Harrison DG, Liu Y, Hoffmann U, Bauer DC, Newman AB, Kritchevsky SB, Harris TB, Butler J; Health ABC Study Investigators. Inflammatory markers and incident heart failure risk in older adults: the Health ABC (Health, Aging, and Body Composition) study. J Am Coll Cardiol. 2010;55:2129–2137.
24.
Gopal DM, Kalogeropoulos AP, Georgiopoulou VV, Tang WW, Methvin A, Smith AL, Bauer DC, Newman AB, Kim L, Harris TB, Kritchevsky SB, Butler J; Health ABC Study. Serum albumin concentration and heart failure risk The Health, Aging, and Body Composition Study. Am Heart J. 2010;160:279–285.
25.
deFilippi CR, de Lemos JA, Christenson RH, Gottdiener JS, Kop WJ, Zhan M, Seliger SL. Association of serial measures of cardiac troponin T using a sensitive assay with incident heart failure and cardiovascular mortality in older adults. JAMA. 2010;304:2494–2502.
26.
Blecker S, Matsushita K, Kottgen A, Loehr LR, Bertoni AG, Boulware LE, Coresh J. High-normal albuminuria and risk of heart failure in the community. Am J Kidney Dis. 2011;58:47–55.
27.
Saunders JT, Nambi V, de Lemos JA, Chambless LE, Virani SS, Boerwinkle E, Hoogeveen RC, Liu X, Astor BC, Mosley TH, Folsom AR, Heiss G, Coresh J, Ballantyne CM. Cardiac troponin T measured by a highly sensitive assay predicts coronary heart disease, heart failure, and mortality in the Atherosclerosis Risk in Communities Study. Circulation. 2011;123:1367–1376.
28.
Roberts CB, Couper DJ, Chang PP, James SA, Rosamond WD, Heiss G. Influence of life-course socioeconomic position on incident heart failure in blacks and whites: the Atherosclerosis Risk in Communities Study. Am J Epidemiol. 2010;172:717–727.
29.
Redfield MM, Jacobsen SJ, Burnett JC, Mahoney DW, Bailey KR, Rodeheffer RJ. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA. 2003;289:194–202.
30.
Bursi F, Weston SA, Redfield MM, Jacobsen SJ, Pakhomov S, Nkomo VT, Meverden RA, Roger VL. Systolic and diastolic heart failure in the community. JAMA. 2006;296:2209–2216.
31.
Owan TE, Hodge DO, Herges RM, Jacobsen SJ, Roger VL, Redfield MM. Trends in prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med. 2006;355:251–259.
32.
Dunlay SM, Redfield MM, Weston SA, Therneau TM, Hall Long K, Shah ND, Roger VL. Hospitalizations after heart failure diagnosis: a community perspective. J Am Coll Cardiol. 2009;54:1695–1702.
10. Disorders of Heart Rhythm
See Table 10-1.
| Incidence per 100 000 Resident Population, Mean (95% CI) | |||
|---|---|---|---|
| Overall | Adults | Children | |
| EMS-assessed | 124.0 (121.6, 126.4) | 140.9 (138.0, 143.8) | 13.8 (12.2, 15.4) |
| EMS treated, non-traumatic cardiac arrest | 67.2 (65.5, 68.9) | 85.2 (82.9, 87.5) | 10.5 (9.1, 11.9) |
| Bystander-witnessed VF | 8.0 (7.4, 8.6) | 10.5 (9.7, 11.3) | 0.4 (0.1, 0.6) |
CI indicates confidence interval; EMS, emergency medical services; VF, ventricular fibrillation.
Source: Resuscitation Outcomes Consortium Investigators, unpublished data, June 20, 2011.
Bradyarrhythmias
ICD-9 426.0, 426.1, 427.81; ICD-10 I44.0 to I44.3, I49.5.
Mortality—835. Any-mention mortality—4818. Hospital discharges—120 000.
AV Block
Prevalence and Incidence
•
The prevalence of first-degree AV block in NHANES III is 3.7% (313 of 8434 participants with ECG data readable for PR interval).1
•
In a healthy sample of subjects from the ARIC study (mean age 53 years), the prevalence of first-degree AV block was 7.8% in black men, 3.0% in black women, 2.1% in white men, and 1.3% in white women.2 Smaller prevalence estimates were noticed in the relatively younger population (mean age 45 years) of the CARDIA study at its year-20 follow-up examination: 2.6% in black men, 1.9% in black women, 1.2% in white men, and 0.1% in white women.3
•
Mobitz II second-degree AV block is rare in healthy individuals (≈0.003%), whereas Mobitz I (Wenckebach) is observed in 1% to 2% of healthy young people, especially during sleep.4
•
Third-degree AV block is very rare in apparently healthy individuals. Johnson et al7 found only 1 case among >67 000 symptom-free individuals; Rose et al,8 in their study of >18 000 civil servants, did not find any cases. On the other hand, among 293 124 patients with DM and 552 624 with hypertension enrolled with Veterans Health Administration hospitals, third-degree AV block was present in 1.1% and 0.6% of those patients, respectively.9
•
Congenital complete AV block is estimated to occur in 1 of 15 000 to 25 000 live births.4
| AHA | American Heart Association |
| AF | Atrial fibrillation |
| AMI | Acute myocardial infarction |
| ARIC | Atherosclerosis Risk in Communities study |
| AV | Atrioventricular |
| BMI | Body mass index |
| BP | Blood pressure |
| CAD | Coronary artery disease |
| CARDIA | C |