Heart Disease and Stroke Statistics—2006 Update
Table of Contents
About These Statistics
Coronary Heart Disease, Acute Coronary Syndrome and Angina Pectoris
Stroke and Stroke in Children
High Blood Pressure (and End-Stage Renal Disease)
Congenital Cardiovascular Defects
Other Cardiovascular Diseases
–Arrhythmias (Disorders of Heart Rhythm)
–Arteries, Diseases of (including Peripheral Arterial Disease)
–Rheumatic Fever/Rheumatic Heart Disease
–Valvular Heart Disease
–High Blood Cholesterol and Other Lipids
–Overweight and Obesity
Quality of Care
Economic Cost of Cardiovascular Diseases
At-a-Glance Summary Tables
–Men and Cardiovascular Diseases
–Women and Cardiovascular Diseases
–Ethnic Groups and Cardiovascular Diseases
–Children, Youth and Cardiovascular Diseases
Glossary and Abbreviation Guide
Appendix I: List of Statistical Fact Sheets. URL: http://www.americanheart.org/presenter.jhtml?identifier=2007
1. About These Statistics
The American Heart Association works with the Centers for Disease Control and Prevention’s National Center for Health Statistics (CDC/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 update. This section describes the most important sources we use. For more details and an alphabetical list of abbreviations, see the Glossary and Abbreviation Guide.
All statistics are for the most recent year available. Prevalence, mortality and hospitalizations are computed for 2003 unless otherwise noted. Mortality as an underlying or contributing cause of death is for 2002. Economic cost estimates are for 2006. Due to late release of data, some disease mortality are not updated to 2003. Mortality for 2003 are underlying preliminary data, obtained from the NCHS publication National Vital Statistics Report: Deaths: Preliminary Data for 2003 (NVSR, 2005;53:15) and from unpublished tabulations furnished by Robert Anderson of NCHS. US and state death rates and prevalence rates are age-adjusted per 100 000 population (unless otherwise specified) using the 2000 US standard for age standardization.
Morbidity (illness) and mortality (death) data in the United States use a standard classification system—the International Classification of Diseases (ICD). About every 10–20 years, the ICD codes are revised to reflect changes over time in medical technology, diagnosis or terminology. Effective with mortality data for 1999, we’re using the tenth revision (ICD/10). It will be a few more years before the tenth revision is used for hospital discharge data.
Prevalence is an estimate of how many people have a disease at a given point in time. Government agencies periodically conduct health examination surveys. Rates for specific diseases are calculated from those surveys. These rates are applied as the population changes for several years, until a new health examination survey is done and new rates are established. It’s important to realize that the prevalence rates do not change from year to year until there is a new survey.
The annual changes in prevalence as reported in this update only reflect changes in the population. It’s impossible to develop a prevalence “trend” by comparing numbers from yearly versions of this update or its precursors. Many of our prevalence estimates come from the NHANES studies of the CDC/NCHS, and the ARIC, CHS and FHS studies of the NHLBI. Coronary heart disease (CHD), myocardial infarction (MI), angina pectoris (AP) and stroke prevalence are based on self-reports in national health interviews.
Incidence is an estimate of the number of new cases of a disease that develop in a population in a 1-year period. For some statistics, new and recurrent attacks or cases are combined.
The incidence of a specific cardiovascular disease (CVD) in the United States is estimated by multiplying the incidence rates reported in community- or hospital-based studies by the US population. The rates change only when new data are available; they are not computed annually. The estimates were revised to reflect the 2000 US Census. Do not compare the incidence or the rates with those in past issues of the Heart and Stroke Statistical Update (renamed Heart Disease and Stroke Statistics Update). Doing so can lead to serious misinterpretation of time trends.
Our incidence estimates for the various cardiovascular diseases are extrapolations from the Framingham Heart Study (FHS), Atherosclerosis Risk in Communities (ARIC) study and Cardiovascular Health Study (CHS) conducted by the NHLBI and Greater Cincinnati/Northern Kentucky Stroke Study and others conducted by the NIH.
Note: data published by governmental agencies for some racial groups, are considered unreliable due to the small sample size in the studies. Since we try to provide data for as many racial groups as possible, we show these data for informational and comparative purposes, etc.
If you have questions about statistics or any points made in this booklet, please contact the Biostatistics Program Coordinator at the American Heart Association National Center, [email protected], 214-706-1423. 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’ll provide corrections at our Web site, http://www.americanheart.org/statistics.
2. Cardiovascular Diseases
(ICD/9 390–459, 745–747) (ICD/10 I00–I99, Q20–Q28; see Glossary for details and definitions). See Table 2A.
|Population Group||Prevalence 2003||Mortality 2003#||Hospital Discharges 2003||Cost 2006|
|Note: (…) = data not available. NH = non-Hispanic.|
|*These percentages represent the portion of total CVD mortality that is for males vs. females.|
|Sources: Prevalence: NHANES (1999–02), CDC/NCHS and NHLBI. Percentages for racial/ethnic groups are age-adjusted for Americans age 20 and older. These data are based on self reports. Estimates from NHANES 1999–2002 applied to 2003 population estimates. Mortality: CDC/NCHS; these data represent underlying cause of death only; data for white and black males and females include Hispanics; data include congenital cardiovascular disease. Hospital discharges: National Hospital Discharge Survey, CDC/NCHS; data include people discharged alive and dead. Cost: NHLBI; data include estimated direct and indirect costs for 2006.|
|Total||71 300 000 (34.2%)||910 614||6 434 000||$403.1 billion|
|Total males||33 100 000 (34.4%)||426 772 (46.9%)*||3 239 000||…|
|Total females||38 200 000 (33.9%)||483 842 (53.1%)*||3 196 000||…|
|NH white males||34.3%||368 182||…||…|
|NH white females||32.4%||419 248||…||…|
|NH black males||41.1%||49 032||…||…|
|NH black females||44.7%||55 803||…||…|
Of the 71 300 000 American adults with 1 or more types of cardiovascular disease (CVD), 27 400 000 are estimated to be age 65 or older (National Health and Nutrition Examination Survey [NHANES 1999–2002], CDC/NCHS). Bullet points below are from NHANES 1999–2002 unless otherwise noted.
The following are the latest estimates of prevalence for these conditions. Due to overlap, it is not possible to add these conditions to arrive at a total.
High blood pressure (HBP)—65 000 000. (Defined as systolic pressure 140 mm Hg or greater and/or diastolic pressure 90 mm Hg or greater, taking antihypertensive medication or being told at least twice by a physician or other health professional that you have high blood pressure.)
Coronary heart disease (CHD)—13 200 000.
–Myocardial infarction (MI, or heart attack)—7 200 000.
–Angina pectoris (AP, or chest pain)—6 500 000.
Heart failure (HF)—5 000 000.
Stroke—5 500 000.
Congenital cardiovascular defects—1 000 000 (Unpublished NHIS survey data, 1993–95, CDC/NCHS).
1 in 3 adult men and women has some form of CVD (NHANES 1999–02, CDC/NCHS).
The following prevalence estimates are for people age 18 and older1:
–Among whites only, 11.4% have heart disease, 5.9% have CHD, 20.5% have hypertension and 2.3% have had a stroke.
–Among blacks or African Americans only, 9.9% have heart disease, 5.3% have CHD, 31.6% have hypertension and 3.5% have had a stroke.
–Among Hispanics or Latinos, 7.7% have heart disease, 4.5% have CHD, 19.0% have hypertension and 2.2% have had a stroke.
–Among Asians, 5.6% have heart disease, 3.8% have CHD, 16.1% have hypertension and 1.8% have had a stroke.
–Among Native Hawaiians or other Pacific Islanders, 16.6% have heart disease, 4.9% have CHD, and 18.2% have hypertension.
–Among American Indians or Alaska Natives, 13.8% have heart disease, 8.2% have CHD, 23.9% have hypertension and 3.1% have had a stroke.
Based on the NHLBI’s Framingham Heart Study (FHS) in its 44-year follow-up of participants and the 20-year follow-up of their offspring2…
–The average annual rates of first major cardiovascular events rise from 7 per 1000 men at ages 35–44 to 68 per 1000 at ages 85–94. For women, comparable rates occur 10 years later in life. The gap narrows with advancing age.
–Under age 75, a higher proportion of CVD events due to CHD occur in men than in women, and a higher proportion of events due to congestive heart failure (CHF) occur in women than in men.
Among American Indian men ages 45–74, the incidence of CVD ranges from 15 to 28 per 1000. Among women it ranges from 9 to 15 per 1000.3
Data from the FHS indicate that the lifetime risk for CVD is 2 in 3 for men and more than 1 in 2 for women at age 40 (personal communication, Donald Lloyd-Jones, MD).
Preliminary mortality data show that CVD as the underlying cause of death accounted for 37.3% of all 2 440 000 deaths in 2003 or 1 of every 2.7 deaths in the United States. CVD as an underlying or contributing cause of death (1 408 000 deaths in 2002) was about 58% of all deaths that year.
Since 1900, CVD has been the No. 1 killer in the United States every year but 1918. Nearly 2500 Americans die of CVD each day, an average of 1 death every 35 seconds. CVD claims more lives each year than the next 4 leading causes of death combined, which are cancer, chronic lower respiratory diseases, accidents, and diabetes mellitus.
The 2003 overall preliminary death rate from CVD was 308.8. The rates were 359.1 for white males and 479.6 for black males; 256.2 for white females and 354.8 for black females. From 1993–2003, death rates from CVD (ICD/10 I00–I99) declined 22.1%. In the same 10-year period actual CVD deaths declined 4.6%.
Other causes of death in 2003—cancer 554 643; accidents 105 695; Alzheimer’s disease 63 343; HIV (AIDS) 13 544. (preliminary data)
The 2003 preliminary CVD death rates were 364.2 for males and 262.5 for females. Cancer death rates were 232.3 for males and 160.2 for females. Breast cancer claimed the lives of 41 566 females in 2003; lung cancer claimed 67 894. Death rates for females were 25.2 for breast cancer and 41.1 for lung cancer. One in 30 female deaths are from breast cancer, while 1 in 2.6 are from CVD. Based on preliminary 2003 mortality, CVD caused about a death a minute among females—over 480 000 female lives every year. That’s more female lives than were claimed by the next five leading causes of death combined (cancer, COPD, Alzheimer’s, diabetes and accidents).
Over 152 000 Americans killed by CVD each year are under age 65. In 2002, 32% of deaths from CVD occurred prematurely (ie, before age 75, which is close to the average life expectancy).
In 2002, the age-adjusted death rate for diseases of the heart in American Indians or Alaska Natives was 201.2 for males and 123.6 for females; for Asians or Pacific Islanders it was 169.8 for males and 108.1 for females; for Hispanics or Latinos it was 219.8 for males and 149.7 for females (Health, United States, 2004; CDC/NCHS).
According to the CDC/NCHS, if all forms of major CVD were eliminated, life expectancy would rise by almost 7 years. If all forms of cancer were eliminated, the gain would be 3 years. According to the same study, the probability at birth of eventually dying from major CVD (I00–I78) is 47%, and the chance of dying from cancer is 22%. Additional probabilities are 3% for accidents, 2% for diabetes and 0.7% for HIV.4
Based on revised 2000 population data, the average life expectancy of people born in the United States in 2003 is 77.6 years (preliminary data for 2003. NSVR, Vol. 53, No. 15, Hyattsville, Md: National Center for Health Statistics, 2005).
In 2001, the proportion of premature deaths (<65 years) from diseases of the heart (I00–I09, I11, I13, I20–I51) was greatest among American Indians or Alaska Natives (36%) and blacks (31.5%) and lowest among whites (14.7%). Premature death was higher for Hispanics (23.5%) than non-Hispanics (16.5%), and for males (24%) than females (10%). Hispanic whites (23.3%) had lower proportions than Hispanic blacks (27.5%), and non-Hispanic (NH) whites (14.4%) had lower proportions than NH blacks (31.5%).5
Age-adjusted death rates for diseases of the heart from 1990–98 declined 17% for Hispanics, 15% for NH whites, 14% for Asians/Pacific Islanders, 11% for NH blacks, and 8% for American Indians or Alaska Natives. In 1998 the rate for NH blacks was 2.8 times the rate for Asian or Pacific Islanders.6
Out-of-Hospital Cardiac Arrest
There is a wide variation in the reported incidence and outcome for out-of-hospital cardiac arrest. These differences are due to in part to differences in definition and ascertainment of cardiac arrest, as well as differences in treatment after its onset.
Cardiac arrest is the cessation of cardiac mechanical activity as confirmed by the absence of signs of circulation.6a Available epidemiological databases do not record deaths due to cardiac arrest or the subset of cases that occur with sudden onset (sudden cardiac arrest). Therefore, surrogate data are often used for epidemiological purposes to estimate the incidence of cardiac arrest, especially in the out-of-hospital setting. Those surrogate data include deaths due to “coronary heart disease” (ICD codes I20-I25) and “cardiac arrest,” defined as coronary death that occurred within 1 hour of symptom onset in the out-of-hospital setting, and without other probable cause of death.6b Datasets based on either definition are not optimal. Out-of-hospital data that are based on the latter definition of cardiac arrest can be especially unreliable because of the difficulty in determining the duration of symptoms prior to the onset of the episode. The following information summarizes representative data from several sources in an attempt to characterize the incidence and outcome of sudden cardiac arrest and demonstrate the need for a comprehensive system of capturing more meaningful data.
330 000 coronary heart disease deaths occur out-of-hospital or in hospital emergency departments annually (2002) (ICD-10 codes I20-I25) (personal communication, Thomas Thom, NHLBI/NIH).
In 1998, 456 076 deaths from cardiac disease (ICD-9 code 390 to 398, 402, or 404 to 429) were reported in the United States (among people aged 35 years and above) in an emergency room, before reaching a hospital, or as “dead on arrival.”7
The annual incidence of sudden cardiac arrest in North America is about 0.55 per 1000 population.8,9 With an estimated US population of 296 766 821,10 this implies that about 163 221 out-of-hospital sudden cardiac arrests occur annually in the United States.
About two thirds of unexpected cardiac deaths occur without prior recognition of cardiac disease.11
About 60% of unexpected cardiac deaths are treated by EMS.12
Incidence of EMS-treated out-of-hospital cardiac arrest is 36/100 000–81/100 000.12,13 This implies EMS treats 107 000 to 240 000 cardiac arrests in the United States annually.
Of these, 20%–38% have ventricular fibrillation or ventricular tachycardia as the first recorded rhythm. This implies 21 000–91 000 ventricular fibrillation arrests annually.8,13
The incidence of ventricular fibrillation among cardiac arrest victims with any first initial rhythm is decreasing over time.13
The median reported survival to discharge after any first recorded rhythm is 6.4%.14 Survival during a recent one year experience in Seattle of all treated cardiac arrests, considered to be of cardiac origin, was reported to be 20%. (personal communication, L. Cobb, Seattle Medic One, December 7, 2005).
The average proportion of cases of out-of-hospital cardiac arrest that receive bystander CPR is 27.4%.14
The incidence of lay responder defibrillation is low, 2.05% in 2002, but increasing over time.15
Unexpected death in the pediatric patient is usually due to trauma, sudden infant death syndrome, respiratory causes or submersion.16 Ventricular fibrillation is an uncommon cause of cardiac arrest in children but it is observed in approximately 5% to 15% of children with out-of-hospital cardiac arrest.17
The reported incidences of out-of-hospital pediatric cardiac arrest vary widely in number (from 2.6–19.7 annual cases per 100 000) and inclusion criteria (age, cause of arrest, etc).18
Since there are 73 559 232 individuals aged <18 years in the United States,10 this implies that there are 1 900–14 000 pediatric out-of-hospital cardiac arrests, annually, from all causes (including trauma, sudden infant death syndrome, respiratory causes, cardiovascular causes and submersion).
The incidence of sudden cardiac arrest in children in the out-of-hospital setting is unknown. Studies that document voluntary reports of deaths among high school athletes suggest that the incidence of sudden cardiac arrest ranges from 0.28–1.0 deaths per 100 000 high school athletes annually nationwide.19,20 Although incomplete, these numbers provide a basis for estimating the number of deaths in this age range.
The reported average survival to discharge after pediatric out-of-hospital cardiac arrest is 6.7%.18
Black and Mexican-American women have higher prevalence of CVD risk factors than white women of comparable socioeconomic status (SES).21
Data from the 2003 BRFSS study of adults age 18 and older showed the prevalence of respondents reporting 2 or more risk factors for heart disease and stroke increased among successive age groups. The prevalence of having 2 or more risk factors was highest among blacks (48.7%) and American Indians/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 equivalent). Persons reporting household income of $50 000 or more had the lowest prevalence (28.8%) and those reporting $10 000 or less had the highest prevalence (52.5%). Adults who reported being unable to work had the highest prevalence (69.3%) of 2 or more risk factors, followed by retired persons (45.1%), unemployed adults (43.4%), homemakers (34.3%) and employed persons (34.0%). Prevalence of 2 or more 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% or more: Alabama, Arkansas, Georgia, Indiana, Kentucky, Louisiana, Mississippi, North Carolina, Ohio, Oklahoma, Tennessee, West Virginia, Guam and Puerto Rico.22
Data from the BRFSS study of the CDC showed that young women and men, ages 18–24, had poor health profiles and experienced adverse changes from 1990–2000. After adjustment for education and income, these young people had the highest prevalence of smoking (34–36% current smokers among whites); the largest increases in smoking (10–12% among whites and 9% among Hispanic women); large increases in obesity (4–9% increase in all groups). All groups had high levels of sedentary behavior (approximately 20–30%) and low vegetable or fruit intake (approximately 35–50%). In contrast, older Hispanics and older black men, ages 65–74, showed some of the most positive changes. They had the largest decreases in smoking (Hispanic women), largest decreases in sedentary behavior (Hispanic women and black men), and largest increases in vegetable or fruit intake (Hispanic women and black men).23
Data from the Chicago Heart Association Detection Project (1967–73, with an average follow-up of 31 years) showed that in younger women (ages 18–39) with favorable levels for all 5 major risk factors (blood pressure, serum cholesterol, BMI, diabetes and smoking), future incidence of CHD and CVD is rare, and long-term and all-cause mortality are much lower compared with those who have unfavorable or elevated risk factor levels at young ages. Similar findings applied to men in this study.24,25
Data from the BRFSS study of the CDC showed that in adults age 18 and over, disparities in CVD health 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 in both groups of educational status. CHD and stroke were inversely related to education, income and poverty status. Hospitalization was greater in men for total heart disease and acute MI but greater in women for CHF and stroke. Among Medicare enrollees, CHF hospitalization was higher in blacks, Hispanics, and American Indians/Alaska Natives than among whites, and stroke hospitalization was highest in blacks. Hospitalizations for CHF and stroke were highest in the southeastern United States. Life expectancy remains higher in women than in men and higher in whites than blacks by about 5 years. CVD mortality at all ages tended to be highest in blacks.26
In respondents ages 18–74, data from the 2000 BRFSS study showed the prevalence of Healthy Lifestyle Characteristics (HLC) was as follows: nonsmoking, 76.0%; healthy weight, 40.1%; 5 fruits and vegetables per day, 23.3%; and regular physical activity, 22.2%. The overall prevalence of the healthy lifestyle indicator (ie, having all 4 HLCs) was only 3%, with little variation among subgroups.27
Analysis of 5 cross-sectional, nationally representative surveys, from NHES 1960–62 to NHANES 1999–2000, showed that the prevalence of key risk factors, ie, high cholesterol, high blood pressure, current smoking, and total diabetes, decreased over time across all BMI groups, with the greatest reductions observed among overweight and obese groups. Total diabetes 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.28
The aging of the population will undoubtedly result in an increased incidence of chronic diseases, including coronary artery disease, heart failure and stroke.29
–The US Census estimates that there will be 40 million Americans age 65 and older in 2010.
–There’s been an explosive increase in the prevalence of obesity and type 2 diabetes. Their related complications—hypertension, hyperlipidemia and atherosclerotic vascular disease—also have increased.
–An alarming increase in unattended risk factors in the younger generations will continue to fuel the cardiovascular epidemic for years to come.
Hospital/Physician/Nursing Home Visits
From 1979–2003, the number of discharges from short-stay hospitals with CVD as the first listed diagnosis increased 31%. In 2003, CVD ranked highest among all disease categories in hospital discharges.30
In 2003, there were 70 681 000 physician office visits with a primary diagnosis of CVD.31
In 2003, there were 4 497 000 visits to emergency departments with a primary diagnosis of CVD.32
In 1999, 23% of nursing home residents age 65 or older had a primary diagnosis of CVD at admission. This was the highest disease category for these residents.33
In 2002, there were 6 024 000 outpatient department visits with a primary diagnosis of CVD.34
The estimated direct and indirect cost of CVD for 2006 is $403.1 billion.
In 2001, $29.3 billion in program payments were made to Medicare beneficiaries discharged from short-stay hospitals with a principal diagnosis of cardiovascular disease. That was an average of $8 354 per discharge.35
A study of the 1987 National Medicaid Expenditure Survey and the 2000 Medical Expenditure Panel Survey, Household Component, showed the 15 most costly medical conditions, and the estimated percent increase in total healthcare spending for each condition from 1987–2000. The following are some of the top 15 conditions, by order of rank, and their percentage impact on health care spending: heart disease (1) +8.06%; cancer (4) +5.36%; hypertension (5) +4.24%; cerebrovascular disease (7) +3.52%; diabetes (9) +2.37%; and kidney disease (15) +1.03%.36
Operations and Procedures
CHART 2S. 2002 Age-Adjusted Death Rates for Total Cardiovascular Disease, Coronary Heart Disease and Stroke by State (includes District of Columbia and Puerto Rico)
State Total Cardiovascular Disease* Coronary Heart Disease** Stroke# Rank## Death Rate % Change+ 1992 to 2002 Rank## Death Rate % Change+ 1992 to 2002 Rank## Death Rate % Change+ 1992 to 2002 Note: The AHRQ has released state level data for heart disease for all 50 states and the District of Columbia. The data is taken from the congressionally mandated 2004 National Healthcare Quality Report (NHQR) at: http://www.qualitytools.ahrq.gov/qualityreport/state. In addition, the Women’s Health and Mortality Chartbook of the CDC/NCHS has state-related data for women 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. BRFSS data is also collected within each state. www.cdc.gov/brfss. (…) = data not available. *Total cardiovascular disease is defined here as ICD/10 I00–I99. **Coronary heart disease is defined here as ICD/10 I20–I25. #Stroke is defined here as ICD/10 I60–I69. ##Rank is lowest to highest. +Percent change is based on log linear slope of rates for each year, 1992–2002. For stroke, the death rates in 1992–98 were comparability modified using the ICD/9 comparability ratio of 1.0588. Source: CDC/NCHS compressed mortality file 1979–2002. Data provided by personal communication with NHLBI. Alabama 49 378.5 −11.2 22 149.2 −22.1 49 69.7 −6.8 Alaska 3 242.1 −23.8 44 112.7 −36.5 22 55.1 -14.2 Arizona 9 271.9 −20.8 26 153.6 −26.3 8 48.0 −15.7 Arkansas 48 376.0 −12.4 44 192.1 −22.8 52 74.5 −14.3 California 26 305.7 −18.3 34 173.3 −26.2 30 58.1 −14.3 Colorado 7 266.0 −19.3 7 118.6 −34.8 21 54.8 −11.8 Connecticut 15 281.5 −22.9 21 149.1 −28.3 4 45.5 −16.5 Delaware 27 306.5 −20.0 35 173.5 −24.7 12 50.5 −13.6 District of Columbia 45 360.5 −11.9 49 211.6 +26.0 10 49.1 −35.2 Florida 20 289.2 −17.7 31 169.5 −23.9 5 46.1 −18.5 Georgia 42 356.1 −16.2 23 150.6 −31.2 44 65.6 −14.9 Hawaii 6 265.2 −17.2 22 104.8 −32.5 36 60.4 −5.1 Idaho 12 277.9 −18.8 12 136.6 −27.5 32 58.6 −17.2 Illinois 32 324.8 −21.8 36 173.6 −31.6 26 57.2 −16.8 Indiana 37 334.1 −19.9 29 167.8 −30.1 35 60.0 −17.7 Iowa 24 297.9 −18.7 33 171.2 −26.6 28 57.8 −9.5 Kansas 28 308.1 −17.1 13 139.9 −28.4 34 59.6 −9.7 Kentucky 46 372.9 −13.3 42 184.2 −23.5 42 63.9 −11.7 Louisiana 43 357.0 −18.7 32 170.4 −30.9 41 63.0 −14.1 Maine 18 283.0 −21.3 19 147.0 −31.2 16 53.9 −10.6 Maryland 31 316.7 −15.4 38 175.8 −20.1 23 56.5 -4.3 Massachusetts 8 270.6 −23.0 10 134.2 −33.7 9 48.3 −14.5 Michigan 41 348.0 −17.0 46 193.9 −27.1 29 58.0 −15.3 Minnesota 2 237.7 −28.3 3 107.1 −40.2 14 51.0 −27.5 Mississippi 52 420.7 −12.9 45 192.5 −24.9 48 69.6 −9.0 Missouri 44 357.1 −15.3 43 187.6 −24.0 39 62.5 −10.7 Montana 10 273.2 −19.2 6 116.6 −30.9 38 62.0 −14.9 Nebraska 22 290.7 −25.1 8 123.5 −37.4 20 54.6 −13.5 Nevada 35 327.5 −18.5 14 141.9 −32.9 24 56.9 −7.5 New Hampshire 21 290.5 −20.4 30 169.0 −25.0 11 50.1 −20.1 New Jersey 29 308.2 −19.9 40 179.3 −26.5 3 43.6 −21.9 New Mexico 4 255.9 −18.8 15 142.2 −20.9 2 41.7 −20.1 New York 36 333.8 −24.9 51 224.2 −29.0 1 37.4 −26.8 North Carolina 34 327.0 −19.5 28 163.6 −29.7 46 67.9 −16.8 North Dakota 11 276.2 −22.0 24 152.7 −21.5 18 54.3 −18.7 Ohio 40 341.5 −17.0 41 183.6 −25.3 33 59.4 −7.2 Oklahoma 51 398.8 −7.9 52 226.6 −8.8 45 66.4 −6.4 Oregon 19 287.9 −19.5 9 127.9 −34.9 47 69.3 −10.4 Pennsylvania 33 325.1 −20.8 37 173.9 −29.7 19 54.5 −13.7 Puerto Rico 1 233.7 … 5 116.5 … 7 46.2 … Rhode Island 25 302.4 −19.8 48 202.5 −18.7 6 46.1 −21.9 South Carolina 39 339.4 −22.9 27 155.3 −33.5 51 72.7 −19.8 South Dakota 17 282.1 −23.0 18 146.0 −33.6 17 54.2 −12.1 Tennessee 50 380.8 −13.0 50 214.3 −18.8 50 70.4 −17.9 Texas 38 337.0 −13.9 39 178.6 −22.4 40 62.5 −11.3 Utah 5 262.6 −18.2 1 100.0 −37.0 25 57.0 −10.2 Vermont 14 280.6 −27.8 25 153.3 −35.1 13 50.8 −20.4 Virginia 30 309.7 −23.4 17 144.9 −29.3 37 61.2 −16.6 Washington 13 280.2 −19.6 16 143.8 −23.4 43 65.2 −10.6 West Virginia 47 374.1 −15.1 47 202.2 −23.2 31 58.4 −6.5 Wisconsin 23 295.7 −19.8 20 147.2 −30.9 27 57.6 −16.3 Wyoming 16 281.8 −17.9 11 134.7 −26.2 15 51.9 −25.5 Total United States … 319.0 −19.7 … 170.8 −27.2 … 56.2 −14.7
3. Coronary Heart Disease, Acute Coronary Syndrome and Angina Pectoris
Coronary Heart Disease
(ICD/9 410–414, 429.2) (ICD/10 I20–I25; see Glossary for details and definitions). See Table 3A.
|Population Group||Prevalence CHD 2003||Prevalence MI 2003||New and Recurrent Heart Attacks and Fatal CHD||New and Recurrent MI||Mortality CHD 2003#||Mortality MI 2003#||Hospital Discharges CHD 2003||Cost CHD 2006|
|Note: CHD = coronary heart disease; includes acute myocardial infarction, other acute ischemic (coronary) heart disease, angina pectoris, atherosclerotic cardiovascular disease, and all other forms of heart disease. MI = myocardial infarction (heart attack). NH = non-Hispanic.|
|(…) = data not available.|
|*These percentages represent the portion of total CHD mortality that is for males vs. females.|
|**NHIS (2003) — data are estimates for Americans age 18 and older.|
|Sources: Prevalence: NHANES (1999–02), CDC/NCHS and NHLBI. Total data are for Americans age 20 and older; percentages for racial/ethnic groups are age-adjusted for age 20 and older. These data are based on self report. Estimates from NHANES 1999–2002 applied to 2003 population estimates. Incidence: ARIC (1987–2000), NHLBI. Mortality: CDC/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, CDC/NCHS; data include people discharged alive and dead. Cost: NHLBI; data include estimated direct and indirect costs for 2006.|
|Total||13 200 000 (6.9%)||7 200 000 (3.5%)||1 200 000||865 000||479 305||170 961||2 011 000||$142.5 billion|
|Total males||7 200 000 (8.4%)||4 200 000 (5.0%)||715 000||520 000||245 419 (51.2%)*||89 670 (52.3%)*||1 175 000||…|
|Total females||6 000 000 (5.6%)||3 000 000 (2.3%)||485 000||345 000||233 886 (48.8%)*||81 291 (47.7%)*||834 000||…|
|NH white males||8.9%||5.1%||650 000||…||216 220||79 387||…||…|
|NH white females||5.4%||2.4%||425 000||…||204 971||71 054||…||…|
|NH black males||7.4%||4.5%||65 000||…||23 957||8376||…||…|
|NH black females||7.5%||2.7%||60 000||…||24 897||8908||…||…|
|Hispanic or Latino**||4.5%||…||…||…||…||…||…||…|
|American Indian/Alaska Native**||8.2%||…||…||…||…||…||…||…|
Among Americans ages 40–74, NHANES data found the age-adjusted prevalence of self-reported MI and ECG-MI (verified by electrocardiogram) to be higher among men than women, but angina prevalence to be higher in women than men. Age-adjusted rates of self-reported MI increased among African-American men and women and Mexican-American men, but decreased among white men and women.38
This year an estimated 700 000 Americans will have a new coronary attack and about 500 000 will have a recurrent attack.39 It is estimated that an additional 175 000 silent first heart attacks occur each year.
The estimated incidence of MI (ICD/9 410) (ICD/10 I21, I22) is 565 000 new attacks and 300 000 recurrent attacks annually.39
The average age of a person having a first heart attack is 65.8 for men and 70.4 for women (ARIC and CHS, NHLBI).
Based on the NHLBI’s FHS in its 44-year follow-up of participants and the 20-year follow-up of their offspring2:
–CHD comprises more than half of all cardiovascular events in men and women under age 75.
–The lifetime risk of developing CHD after age 40 is 49% for men and 32% for women.40
–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.
In the NHLBI’s ARIC study, average age-adjusted CHD incidence rates per 1000 person-years were: white men, 12.5; black men, 10.6; white women, 4.0; and black women, 5.1. Incidence rates excluding revascularization procedures were: white men, 7.9; black men, 9.2; white women, 2.9; and black women, 4.9. Hypertension was a particularly powerful risk factor for CHD in black persons, especially in black women. Diabetes was a weaker predictor of CHD in black than in white persons.41
The annual rates per 1000 population of first heart attack (MI or CHD death) in non-black men are 19.2 for ages 65–74, 28.3 for ages 75–84, and 50.6 for age 85 and older. For non-black women in the same age groups the rates are 6.8, 14.2 and 33.2, respectively. For black men the rates are 21.6, 27.9 and 57.1, and for black women the rates are 8.6, 17.6 and 24.8, respectively (CHS [1989–2000], NHLBI).
Combining the rates for possible and definite CHD shows that 17 to 25 of every 100 American Indian men ages 45–74 had some evidence of heart disease.3
Among American Indians ages 65–74, the annual rates per 1000 population of new and recurrent heart attacks are 7.6 for men and 4.9 for women (SHS [1989-2002], NHLBI).
CHD rates in women after menopause are 2–3 times those of women the same age before menopause.42
CHD caused 1 of every 5 deaths in the United States in 2003. CHD mortality as an underlying or contributing cause of death—653 000. MI mortality as an underlying or contributing cause of death—221 000.
CHD is the single largest killer of American males and females. About every 26 seconds an American will suffer a coronary event, and about every minute someone will die from one. About 40% of the people who experience a coronary attack in a given year will die from it.
A study of 1275 HMO enrollees ages 50–79 who had cardiac arrest (CA), showed the incidence of out-of-hospital CA was 6.0/1000 subject-years in subjects with any clinically recognized heart disease compared to 0.8/1000 subject-years in subjects without heart disease. In subgroups with heart disease, incidence was 13.6/1000 subject-years in subjects with prior MI and 21.9/1000 subject-years in subjects with heart failure.43
An analysis of data from the FHS from 1950–99 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.44
From 1993–2003, the death rate from CHD declined 30.2%, but the actual number of deaths declined only 14.7%. In 2003, the overall CHD death rate was 162.6 per 100 000 population. The death rates were 209.2 for white males and 241.1 for black males; for white females the rate was 125.1 and for black females it was 160.3. The 2002 death rates for CHD were 138.3 for Hispanics or Latinos, 114.0 for American Indians or Alaska Natives, and 98.6 for Asians or Pacific Islanders (Health, United States, 2004).
Over 83% of people who die of CHD are age 65 or older (CDC/NCHS).
The estimated average number of years of life lost due to a heart attack is 14.2 (NHLBI).
Based on data from the FHS study of the NHLBI2:
–25% of men and 38% of women will die within 1 year after having an initial recognized MI. In part because women have heart attacks at older ages than men do, they’re more likely to die from them within a few weeks. Almost half of men and women under age 65 who have a heart attack (MI) die within 8 years.
–50% of men and 64% of women who died suddenly of CHD had no previous symptoms of this disease.
–Between 70% and 89% of sudden cardiac deaths occur in men, and the annual incidence is 3–4 times higher in men than in women. However, this disparity decreases with advancing age.
–People who’ve had a heart attack have a sudden death rate that’s 4–6 times that of the general population.
–Sudden cardiac death accounts for 19% of sudden deaths in children between 1 and 13 years of age and 30% between 14 and 21 years of age. The overall incidence is low, 600 cases per year.
According to data from the National Registry of Myocardial Infarction45:
–From 1990–1999, in-hospital AMI mortality declined from 11.2% to 9.4%.46
–Mortality increases for every 30 minutes that elapse before a patient with ST-segment elevation is recognized and treated.47
–The median door-to-drug time for thrombolytic therapy was reduced by nearly half, from 61.8 minutes to 37.8 minutes, during the NRMI data collection used in this study. However, many hospitals are still working to meet the goal of 30 minutes set in 1991 (www.nrmi.org).
–Women under 50 are twice as likely to die after an AMI than men in the same age group.48
A study of men and women in 3 prospective cohort studies found that antecedent major CHD risk factor exposures were very common among those who developed CHD. About 90% of the CHD patients 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 blood pressure-lowering drugs, current cigarette use, and clinical report of diabetes.49
According to a case-control study of 52 countries (INTERHEART), 9 easily measured and potentially modifiable risk factors account for over 90% of the risk of an initial acute MI. The effect of these risk factors is consistent in men and women, across different geographic regions, and by ethnic group, making the study applicable worldwide. These 9 risk factors include cigarette smoking, abnormal blood lipid levels, hypertension, diabetes, abdominal obesity, a lack of physical activity, low daily fruit and vegetable consumption, alcohol overconsumption, and psychosocial index.50
A study of over 3000 members of the FHS 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 MET (metabolic equivalent) increment in exercise capacity reduced risk by 13%.51
Low CHD risk is defined as blood pressure <120/80 mm Hg, cholesterol <200 mg/dL and not currently smoking. Age-adjusted prevalence was estimated in nondiabetic persons without a history of MI participating in 4 NHANES surveys conducted in 1971–75, 1976–80, 1988–94, and 1999–2000.52
–The prevalence of low risk rose from 6% in 1971–75 to 17% in 1988–94 and 1999–2000.
–Prevalence of low risk was about twice as high in women as in men throughout the period.
–Prevalence was initially higher in whites than in blacks (7% versus 3% in 1971–75); it increased more with time in blacks (17% versus 15% in 1999–2000).
–Prevalence of low risk in 1999–2000 was lowest in those ages 65–74 (3%) and was progressively greater at younger ages (29% at ages 25–34), with similar increases in prevalence over time across age groups.
–The greatest changes in the components of low risk from 1971–2000 were in prevalence of favorable diastolic blood pressure (from 38% to 71%), compared to favorable systolic blood pressure (from 32% to 47%), nonsmoking (from 60% to 79%), and favorable cholesterol (from 33% to 46%).
Taking into account CHD risk factors in combination provides a very potent predictor of 10-year risk of CHD compared with individual risk factors. Among participants ages 20–79 in the NHANES III study of the CDC/NCHS, without self-reported CHD, stroke, peripheral vascular disease and diabetes, 81.7% had a 10-year risk for CHD of <10%, 15.5% had a risk of 10–20%, and 2.9% had a risk of >20%. Among participants age 60 and over, 40.3% of men and 8.2% of women were at “intermediate risk (10% to 20%).” The proportion of participants with a 10-year risk of CHD of >20% increased with advancing age and was higher among men than women but varied little with race or ethnicity.53
A study of NH white persons, ages 35–74, in the Framingham Heart Study and the NHANES III studies, showed that 26% of men and 41% of women had at least 1 borderline risk factor in NHANES III. It is estimated that more than 90% of CHD events will occur in individuals with at least 1 elevated risk factor, and approximately 8% will occur in people with only borderline levels of multiple risk factors. Absolute 10-year CHD risk exceeded 10% in men older than age 45 who had 1 elevated risk factor and 4 more borderline risk factors and in those who had at least 2 elevated risk factors. In women, absolute CHD risk exceeded 10% only in those over age 55 who had at least 3 elevated risk factors.54
Depending on their gender and clinical outcome, people who survive the acute stage of a heart attack have a chance of illness and death that’s 1.5–15 times higher than that of the general population. The risk of another heart attack, sudden death, AP, HF and stroke—for both men and women—is substantial (FHS, NHLBI).2
A study conducted by the Mayo Clinic found that cardiac rehabilitation after a heart attack 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 than younger participants. Only 32% of men and women age 70 or older participated in cardiac rehabilitation, in comparison to 66% of 60– 69-year-olds and 81% of those under age 60.55
Within 6 years after a recognized heart attack (MI) (FHS, NHLBI)2…
–18% of men and 35% of women will have another heart attack.
–7% of men and 6% of women will experience sudden death.
–About 22% of men and 46% of women will be disabled with heart failure.
–8% of men and 11% of women will have a stroke.
From 1979–2003, the number of discharges from short-stay hospitals with CHD as the first listed diagnosis increased 16% (National Hospital Discharge Survey, CDC/NCHS).
From 1990–99, the median duration of hospital stay related to acute myocardial infarction dropped from 8.3 days to 4.3 days, according to an analysis of the NRMI. Findings were similar for both patients receiving primary PTCA and those receiving thrombolytic therapy.46
Data from Ambulatory Care Visits to Physician Offices, Hospital Outpatient Departments, and Emergency Departments: US, 1999–2000, showed the number of visits for CHD were 12.2 million.56
Awareness of Warning Signs and Risk Factors for Heart Disease
Surveys conducted by the AHA between 1997 and 2003 showed the awareness of heart disease as the leading cause of death in women rose from 30% in 1997 to 46% in 2003. Awareness in white women (55%) was nearly twice as high as among African-American (30%) and Hispanic (27%) women.57
In 2003, 46% of respondents to a nationally representative telephone survey of women age 25 and older, identified heart disease as the leading killer of women, up from 30% in 1997 and 34% in 2000.57
In 1997, a telephone survey of 1000 US households found that only 8% of women respondents identified heart disease as their greatest health concern; less than 33% identified heart disease as the leading cause of death.58
Data from the Women Veteran Cohort, age 35 and over, showed 42% of women were concerned about heart disease. Only 8–20% were aware that coronary artery disease (CAD) is the major cause of death for women.59
Data from the 2001 BRFSS study of the CDC showed that 95% of respondents recognized chest pain as a heart attack symptom. However, only 11% correctly classified all symptoms and knew to call 911 when someone was having a heart attack. This random digit-dialed telephone survey was conducted in 17 states and the US Virgin Islands.60
A study of public knowledge of CVD risk factors and risk-reduction techniques in 2 New England communities showed that prevention knowledge improved significantly over time in both locations and in every demographic subgroup. Scores were higher for native-born citizens, women, more educated individuals and English-speaking people. There was an increase in the identification of physical inactivity, and blood cholesterol/high-fat diet as CVD risk factors, while there was a decrease in the identification of overweight and blood pressure.61
Three population-based cross-sectional surveys in 2 northern California cities were conducted between 1980 and 1990. Significant differentials in baseline knowledge widened over the 10-year period. Individuals with less than 12 years of education had only slight improvement in their knowledge of CVD risk factors; those with more than 16 years of education had twice as much improvement. There were similar time-effect disparities in knowledge of risk-reduction strategies. In contrast, interest in risk modification was high for all educational groups and remained uniform across time.62
A national study of physician awareness and adherence to CVD prevention guidelines, conducted in late 2004, showed that fewer than 1 in 5 physicians knew that more women than men die each year from CVD.63
A recent community surveillance study in 4 US communities reported that in 2000, the overall proportion of persons with delays from onset of symptoms of acute MI to hospital arrival of 4 or more hours was 49.5%. The study also reported that there was no statistically significant change in the proportion of patients delaying 4 or more hours from 1987–2000, indicating that there has been little improvement in the speed at which patients with MI symptoms arrive at the hospital after onset. Although the proportion of MI patients who arrived at the hospital by emergency medical services increased over this period from 37% in 1987 to 55% in 2000, the total time between onset and hospital arrival did not change appreciably.64
In 2006, the estimated direct and indirect cost of CHD is $142.5 billion.
In 2001, $11.6 billion was paid to Medicare beneficiaries for CHD ($11 201 per discharge for acute MI; $11 308 per discharge for coronary atherosclerosis; and $3513 per discharge for other ischemic heart disease).35
Operations and Procedures
In 2003, an estimated 1 244 000 inpatient angioplasty procedures, 467 000 inpatient bypass procedures, 1 414 000 inpatient diagnostic cardiac catheterizations, 64 000 inpatient implantable defibrillators and 197 000 inpatient pacemaker procedures were performed in the United States.
Acute Coronary Syndrome (ACS)
(ICD/9 codes 410, 411)
The term “acute coronary syndrome” (ACS) is increasingly used to describe patients who present with either acute MI or UA. (UA is chest pain or discomfort that’s unexpected and usually occurs while at rest. The discomfort may be more severe and prolonged than typical angina or be the first time a person has angina.)
A conservative estimate for the number of discharges with ACS from hospitals in 2003 is 879 000. Of these, an estimated 497 000 are male and 382 000 are female. This estimate is derived by adding the first listed hospital discharges for myocardial infarction (767 000) to those for unstable angina (112 000) (CDC/NCHS).
When including secondary discharge diagnoses, the corresponding number of hospital discharges was 1 555 000 unique hospitalizations for ACS, 946 000 for MI, and 650 000 for UA (31 000 hospitalizations received both diagnoses) (CDC/NCHS).
Decisions regarding 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 electrocardiogram and abnormal (“positive”) elevations of myocardial biomarkers such as troponins, as follows:
ST elevation myocardial infarction (STEMI)
non-ST elevation myocardial infarction
Studies evaluating the percentage of ACS patients who have STEMI range from 30–45%.65 These are only preliminary estimates, in part because of dramatically changing practices in the unstable angina discharge diagnosis in the past decade. Factors affecting the UA diagnosis include changes in reimbursement policies, the advent of more sensitive assays for myocardial injury (leading to increased diagnosis of MI over UA), and greater care of patients in same-day “chest pain units” and same-day catheterization procedures.
A study of over 1300 elderly patients admitted to all intensive cardiovascular care units (CCUs) and cardiology departments in Israel, showed the mean age of women versus men was comparable. Comorbidities were more frequent in women, whereas previous coronary disease and typical anginal pain on admission were more frequent in men. Medical treatment and revascularization procedures during the index hospitalization were comparable. Crude and covariate-adjusted mortality rates were higher in women at 7 days, but not at 6 months. This difference was attributed to ST elevation (STE)-ACS in women versus men. Seven-day mortality rates were higher in patients with STE-ACS who were denied coronary angiography, especially women.66
(ICD/9 413) (ICD/10 I20). See Table 3B.
|Population Group||Prevalence 2003||Incidence of Stable Angina||Hospital Discharges 2003*|
|Note: Angina pectoris is chest pain or discomfort due to insufficient blood flow to the heart muscle. Stable angina is predictable chest pain on exertion or under mental or emotional stress. The incidence estimate is for angina without MI.|
|(…) = data not available. NH = non-Hispanic.|
|Sources: Prevalence: NHANES (1999–02), CDC/NCHS and NHLBI; percentages for racial/ethnic groups are age-adjusted for Americans age 20 and older. Estimates from NHANES 1999–2002 applied to 2003 population estimates. Incidence: FHS, NHLBI. Hospital discharges: National Hospital Discharge Survey, CDC/NCHS; data include people discharged alive and dead.|
|*There were 123 000 days of care for discharges with angina from short-stay hospitals in 2002.|
|Total||6 500 000 (3.8%)||400 000||63 000|
|Total males||3 200 000 (4.2%)||…||27 000|
|Total females||3 300 000 (3.6%)||…||36 000|
|NH white males||4.5%||…||…|
|NH white females||3.5%||…||…|
|NH black males||3.1%||…||…|
|NH black females||4.7%||…||…|
A study of 4 national cross-sectional health examination studies found that, among Americans ages 40–74, 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.38
Only 20% of coronary attacks are preceded by long-standing angina.2
The annual rates per 1000 population of new and recurrent episodes of angina for non-black men are 44.3 for ages 65–74, 56.4 for ages 75–84, and 42.6 for age 85 and older. For non-black women in the same age groups the rates are 18.8, 30.8 and 19.8, respectively. For black men the rates are 26.1, 52.2 and 43.5, and for black women the rates are 29.4, 37.7 and 15.2, respectively (CHS, NHLBI).
A small number of deaths due to CHD are coded as being from AP. These are included as a portion of total deaths from CHD.
|Population Group||Prevalence 2003||New and Recurrent Attacks||Mortality 2003#||Hospital Discharges 2003||Cost 2006|
|Note: (…) = data not available. NH = non-Hispanic.|
|*These percentages represent the portion of total stroke incidence or mortality that is for males vs. females.|
|**NHIS (2003) — data are estimates for Americans age 18 and older.|
|Sources: Prevalence: NHANES (1999–2002), CDC/NCHS and NHLBI. Total data include children; percentages for racial/ethnic groups are age-adjusted for Americans age 20 and older. These data are based on self report. Estimates from NHANES 1999–2002 applied to 2003 population estimates. Incidence: Broderick et al (GCNKSS).68 Mortality: CDC/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, CDC/NCHS; data include people discharged alive and dead. Cost: NHLBI; data include estimated direct and indirect costs for 2006.|
|Total||5 500 000 (2.6%)||700 000||157 804||965 000||$57.9 billion|
|Total males||2 400 000 (2.5%)||327 000 (47%)*||61 561 (39.0%)*||455 000||…|
|Total females||3 100 000 (2.6%)||373 000 (53%)*||96 243 (61.0%)*||510 000||…|
|NH white males||2.3%||277 000||51 849||…||…|
|NH white females||2.6%||312 000||83 187||…||…|
|NH black males||4.0%||50 000||7791||…||…|
|NH black females||3.9%||61 000||10 834||…||…|
|Hispanic or Latino**||2.2%||…||…||…||…|
|American Indian/Alaska Native**||3.1%||…||…||…||…|
From the early 1970s to the early 1990s, the estimated number of noninstitutionalized stroke survivors increased from 1.5 million to 2.4 million.69
The prevalence of stroke in American Indian men ages 45–74 ranges from 0.2–1.4% and in women from 0.2–0.7%.3
1999–2003 data from the NHIS study of the CDC/NCHS showed that 3.6% of American Indians/Alaska Natives, age 18 and over, have had a stroke. Among blacks or African Americans it was 3.3%, among whites it was 2.2%, and among Asians it was 2.0%.70
2003 data from the BRFSS survey of the CDC showed a higher prevalence of stroke in 10 southeastern states than in 13 non-southeastern states and the District of Columbia. Prevalence was higher in blacks than in whites. The highest age-adjusted prevalence of stroke was among southeastern blacks, followed by non-southeastern blacks, southeastern whites and non-southeastern whites.71
The prevalence of silent cerebral infarction between ages 55–64 is about 11%. This prevalence increases to 22% between ages 65 and 69, 28% between ages 70 and 74, 32% between ages 75 and 79, 40% between ages 80 and 85, and 43% above age 85. Applying these rates to 1998 US population estimates results in an estimated 13 million people with prevalent silent stroke.71a,71b
Transient Ischemic Attack (TIA)
The prevalence of transient ischemic attacks (TIA) in men is 2.7% for ages 65–69 and 3.6% for ages 75–79. (A TIA, or transient ischemic attack, is a mini-stroke that lasts less than 24 hours.) For women, TIA prevalence is 1.6% for ages 65–69 and 4.1% for ages 75–79.72
Approximately 15% of all strokes are heralded by a TIA.73
A third of spells characterized as TIAs using the classic definition (focal neurological deficits resolving within 24 hours) would be considered infarctions based on diffusion- weighted MRI findings.74
In population-based studies, the age and gender adjusted incidence rates for TIA range from 68.2–83/100 000. Males and blacks have higher rates of TIA.75,76 Approximately half of patients who experience a TIA fail to report it to their healthcare providers.77,78
After TIA, the 90-day risk of stroke is 3–17.3%, highest within the first 30 days.75–77,79,80
Within a year of TIA, up to a quarter of patients will die.76,81
Individuals who have a TIA have a 10-year stroke risk of 18.8%, and a combined 10-year stroke, MI or vascular death risk of 42.8% (4% a year).82
In the North American Symptomatic Carotid Endarterectomy Trial (NASCET) study, patients with a first-ever hemispheric TIA had a 90-day stroke risk of 20.1%. The risk of stroke after TIA exceeded the risk after hemispheric stroke.83
Each year about 700 000 people experience a new or recurrent stroke. About 500 000 of these are first attacks, and 200 000 are recurrent attacks (GCNKSS, FHS, ARIC).
On average, every 45 seconds someone in the United States has a stroke.
Each year, about 46 000 more women than men have a stroke (GCNKSS).
Men’s stroke incidence rates are 1.25 times greater than women’s. The difference in incidence rates between the sexes is somewhat higher at younger ages but nonexistent at older ages. The male/female incidence was 1.59 for ages 65–69; 1.46 for ages 70–74; 1.35 for ages 75–79 and 0.74 for age 80 and older (CHS, NHLBI).
Of all strokes, 88% are ischemic, 9% are intracerebral hemorrhage, and 3% are subarachnoid hemorrhage (GCNKSS, FHS, ARIC).
Blacks have almost twice the risk of first-ever stroke compared with whites. The age-adjusted stroke incidence rates (per 100 000) for first-ever strokes are 167 for white males, 138 for white females, 323 for black males and 260 for black females (GCNKSS, FHS, ARIC).
The Brain Attack Surveillance in Corpus Christi project (BASIC) clearly demonstrated an increased incidence of stroke among Mexican Americans compared with NH whites in this community. The crude cumulative incidence was 168/10 000 in Mexican Americans and 136/10 000 in NH whites. Specifically, Mexican Americans have an increased incidence of intracerebral hemorrhage and subarachnoid hemorrhage compared with NH whites adjusted for age, as well as an increased incidence of ischemic stroke and TIA at younger ages when compared with NH whites.86
The age-adjusted annual incidence rate (per 1000) for total stroke in Japanese-American men has declined markedly from 5.1 to 2.4; for thromboembolic stroke, from 3.5 to 1.9; and for hemorrhagic stroke, from 1.1 to 0.6. The estimated average annual declines are 5% for total stroke, 3.5% for thromboembolic stroke, and 4.3% for hemorrhagic stroke. The decline in stroke mortality in the Honolulu Heart Program (HHP) target population was similar to that reported for US white males ages 60–69 during the same period (during the 1969–88 follow-up period of the HHP, NHLBI).
Among American Indians ages 65–74, the annual rates per 1000 population of new and recurrent strokes are 6.1 for men and 6.6 for women (SHS [1989–2002], NHLBI).
Data from the Northern Manhattan Study showed the age-adjusted incidence of first ischemic stroke per 100 000 was 88 in whites, 149 in Hispanics and 191 in blacks. Among blacks compared with whites, the relative rate of intracranial atherosclerotic stroke was 5.85; extracranial atherosclerotic stroke, 3.18; lacunar stroke, 3.09; and cardioembolic stroke, 1.58. Among Hispanics compared with whites, the relative rate of intracranial atherosclerotic stroke was 5.00; extracranial atherosclerotic stroke, 1.71; lacunar stroke, 2.32; and cardioembolic stroke, 1.42.87
Stroke accounted for about 1 of every 15 deaths in the United States in 2003. About 50% of these deaths occurred out of hospital. Stroke as an underlying or contributing cause of death—about 273 000.
When considered separately from other cardiovascular diseases, stroke ranks No. 3 among all causes of death, behind diseases of the heart and cancer (CDC/NCHS).
On average, about every 3 minutes someone dies of a stroke.
Eight to 12% of ischemic strokes and 37–38% of hemorrhagic strokes result in death within 30 days.88
From 1993–2003, the stroke death rate fell 18.5%, and the actual number of stroke deaths declined 0.7% (CDC/NCHS).
The 2003 overall death rate for stroke was 54.3. Death rates were 51.9 for white males and 78.8 for black males; for white females it was 50.5 and for black females it was 69.1.
2002 age-adjusted death rates for stroke were 44.3 for Hispanic or Latino males and 38.6 for females; 50.8 for Asian or Pacific Islander males and 45.4 for females; and 37.1 for American Indians or Alaska Native males and 38.0 for females (Health, United States, 2004, CDC/NCHS).
Because women live longer than men, more women than men die of stroke each year. Women accounted for 61.0% of US stroke deaths in 2003.
From 1995–98, age-standardized mortality rates for ischemic stroke, subarachnoid hemorrhage and intracerebral hemorrhage were higher among blacks than whites. Death rates from intracerebral hemorrhage were also higher among Asian or Pacific Islanders than among whites. All minority populations had higher death rates from subarachnoid hemorrhage than did whites. Among adults ages 25–44, blacks and American Indians or Alaska Natives had higher risk ratios than did whites for all 3 stroke subtypes.90
In 2002, the mean age of stroke death was 79.6 years; however, males had a younger mean age at stroke death than females. Blacks, American Indians/Alaska Natives, and Asians/ Pacific Islanders had younger mean ages than whites, and the mean age at stroke death was also younger among Hispanics than non-Hispanics.85
TIAs carry a substantial short-term risk of stroke, hospitalization for cardiovascular events and death. Of 1707 TIA patients evaluated in the emergency department (ED) of a large health care plan, 180 patients, or 10%, developed stroke within 90 days. Ninety-one patients, or 5%, did so within 2 days. Predictors of stroke: more than 60 years of age, having diabetes mellitus, focal symptoms of weakness or speech impairment, and TIA lasting longer than 10 minutes.91
The relative risk (RR) of stroke in heavy smokers (more than 40 cigarettes a day) is twice that of light smokers (less than 10 cigarettes per day). Stroke risk decreases significantly after 2 years and is at the level of nonsmokers by 5 years after cessation of cigarette smoking.92
Atrial fibrillation (AF) is an independent risk factor for stroke, increasing risk about 5-fold. For details, see Section VII a: Arrhythmias.93
In adults over 55, the lifetime risk for stroke is greater than 1 in 6. Women have a higher risk than men, perhaps due to their survival advantage. Blood pressure (BP) is a powerful determinant of stroke risk. Subjects with BP less than 120/80 mm Hg have about half the lifetime risk of stroke, compared to subjects with hypertension.94
Data from the GCNKSS study shows that ischemic stroke patients with diabetes are younger, more likely to be African American, and more likely to have hypertension, MI, and high cholesterol than nondiabetic patients. Age-specific incidence rates and rate ratios show that diabetes increases ischemic stroke incidence at all ages, but this risk is most prominent before age 55 in African Americans and before age 65 in whites. One-year case fatality rates after ischemic stroke are not different between those patients with and without diabetes.95
Physical activity reduces stroke risk. Results from the Physicians’ Health Study showed a lower stroke risk associated with vigorous exercise among men (RR of total stroke = 0.86 for exercise 5 times a week or more).96 The Harvard Alumni Study showed a decrease in total stroke risk in men who were highly physically active (RR = 0.82).97
For women in the Nurses’ Health Study, RR for total stroke from the lowest to the highest physical activity levels were: 1.00, 0.98, 0.82, 0.74 and 0.66, respectively.98
The Northern Manhattan Study—which included whites, blacks and Hispanics, and men and women in an urban setting—showed a decrease in ischemic stroke risk associated with physical activity (PA) levels across all racial/ethnic and age groups, and for each gender (odds ratio = 0.37).99
A follow-up of the ARIC cohort found that PA —be it from sports, during leisure time, or at work—was related to reduced risk of ischemic stroke.100
Pregnancy and Stroke
The Baltimore–Washington Cooperative Young Stroke Study found the risk of ischemic stroke or intracerebral hemorrhage during pregnancy and the first 6 weeks postpartum was 2.4 times greater than for nonpregnant women of similar age and race. The risk of ischemic stroke during pregnancy was not increased during pregnancy per se, but was increased 8.7-fold during the 6 weeks postpartum. Intracerebral hemorrhage showed a small RR of 2.5 during pregnancy, but increased dramatically to an RR of 28.3 in the 6 weeks postpartum. The excess risk of stroke (all types except subarachnoid hemorrhage) attributable to the combined pregnant/post-pregnant period was 8.1 per 100 000 pregnancies.101
Using Swedish administrative data, it was found that ischemic stroke and intracerebral hemorrhage, including subarachnoid hemorrhage, are increased in association with pregnancy. Compared to the risk of stroke among women who were not pregnant or in early pregnancy (up to the first 27 gestational weeks), women in the peripartum (from 2 days before to 1 day after delivery), and the puerperium (from 2 days before to 6 complete weeks after delivery) periods were at increased risk for all 3 major stroke types. The 3 days surrounding delivery were the time of highest risk.102
Data from the HHP found that in elderly Japanese men ages 71–93, low concentrations of high-density lipoprotein (HDL) cholesterol were more likely to be associated with a future risk of thromboembolic stroke than were high concentrations.103
In the US Nationwide Inpatient Sample from 2000–01, 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, or a total rate of 34.2/100 000, not including subarachnoid hemorrhage. The risk was increased in African Americans and among older women. Among women with these events, death during hospitalization occurred in 4.1%, and in 22% of survivors after discharge to a facility other than home.104
Stroke is a major health issue for women, particularly for postmenopausal women, raising the question whether increased incidence is due to aging or to hormone status, and whether hormone therapy affects risk.105,106
Among postmenopausal women who are generally healthy, the Women’s Health Initiative primary prevention clinical trial among 16 608 women (95% of whom had no pre-existing CVD) found that estrogen plus progestin (PremPro) increased ischemic stroke risk by 44%, with no effect on hemorrhagic stroke. The excess risk was apparent in all age groups, in all categories of baseline stroke risk, and in women with and without hypertension, or prior history of CVD.107
In the Women’s Health Initiative trial of estrogen alone, among 10 739 women with hysterectomy, it was found that conjugate equine estrogen alone (Premarin) increased risk of stroke by 39%. The excess risk conferred by estrogen alone was 12 additional strokes per 10 000 person-years.108
In postmenopausal women with known CHD, the Heart and Estrogen/progestin Replacement Study (HERS), a secondary CHD prevention trial, found that a combination of estrogen plus progestin (conjugated equine estrogen [0.625 mg] and medroxyprogesterone acetate [2.5 mg] hormone therapy did not reduce stroke risk.109
The Women’s Estrogen for Stroke Trial (WEST) found that estrogen alone (1 mg of 17B-estradiol) in women of mean age 71 years, also had no significant overall effect on recurrent stroke or fatality, but there was an increased rate of fatal stroke and an early rise in overall stroke rate in the first 6 months.110
Clinical trials data indicate that estrogen plus progestin as well as estrogen alone increase stroke risk in postmenopausal, generally healthy women and provide no protection for women with established heart disease.107,108,111
Stroke is a leading cause of serious, long-term disability in the United States.112
The median time from stroke onset to arrival in an ER is between 3 and 6 hours, according to a study of at least 48 unique reports of prehospital delay time for patients with stroke, TIA or stroke-like symptoms. The study included data from 17 countries, including the United States. Improved clinical outcome at 3 months was seen for patients with acute ischemic stroke when intravenous thrombolytic treatment was started within 3 hours of the onset of symptoms.113
In 1999, more than 1 100 000 American adults reported difficulty with functional limitations, activities of daily living, etc, resulting from stroke (MMWR, Vol 50, No 7, Feb 23, 2001, CDC).
According to the NHLBI’s FHS2…
–14% of persons who survive a first stroke or TIA will have another one within 1 year.
–22% of men and 25% of women who have an initial stroke die within a year. This percentage is higher among people age 65 and older.
–51% of men and 53% of women under age 65 who have a stroke die within 8 years.
–The length of time to recover from a stroke depends on its severity. From 50–70% of stroke survivors regain functional independence, but 15–30% are permanently disabled, and 20% require institutional care at 3 months after onset.
In the NHLBI’s FHS, among ischemic stroke survivors who were at least 65 years old, these disabilities were observed at 6 months post-stroke114:
–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.
Data from the Paul Coverdell National Acute Stroke Registry showed the majority of stroke admissions were ischemic strokes (52–70%) with TIA and intracerebral hemorrhage comprising the bulk of the remainder. Between 19% and 26% of admissions were under 60 years of age, and between 52% and 58% were female. Blacks varied from 7–31% depending on state of residence. Between 20% and 25% of admissions arrived at the emergency department within 3 hours of onset. Treatment with recombinant tissue plasminogen activator (rtPA) was administered to between 3% and 8.5% of ischemic stroke admissions. Of those treated with rtPA, less than 20% received it within 60 minutes of arrival. Compliance with secondary prevention practices was poorest for smoking cessation counseling and best for antithrombotics.115
Of patients with ischemic stroke in the California Acute Stroke Pilot Registry, 23.5% arrived at the ER within 3 hours of symptom onset, and 4.3% received thrombolysis. If all patients had called 911 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 optimally treated, 57% could have been treated.116
Patients with a discharge diagnosis of ischemic stroke were identified in 7 California hospitals participating in the California Acute Stroke Pilot Registry. Six points of care were tracked: thrombolysis, receipt of antithrombotic medications within 48 hours, prophylaxis for deep vein thrombosis, smoking cessation counseling, and prescription of lipid-lowering and antithrombotic medications at discharge. Overall, rates of optimal treatment improved for patients treated in year 2 compared to year 1, with 63% of patients receiving a perfect score in year 2 compared to 44% in year 1. Rates significantly improved in 4 of the 6 hospitals and for 4 of the 6 interventions. A seventh hospital that participated in the registry but did not implement standardized orders showed no improvement in optimal treatment.117
From 1979–2003, the number of discharges from short-stay hospitals with stroke as the first listed diagnosis increased 29% (National Hospital Discharge Survey, CDC/NCHS).
During 1988–97, the age-adjusted stroke hospitalization rate increased 18.6% (from 560 to 664 per 100 000), while total hospitalizations increased 38.6% (from 592 811 to 821 760). Hospitalization rates did not change for ages 35–64 but increased for persons age 65 and older. This increase was greater for men than for women. The average length of hospital stay fell from 11.1 to 6.2 days. Total person-days in hospital decreased 22%.118 (Stroke in this study includes ICD/9 431–434 and 436–438. The American Heart Association uses 430–438.)
Between 1980 and 1999, hospital discharge rates for stroke increased for blacks and whites; the in-hospital mortality rates decreased for both black and white patients. Generally, the risk of a stroke hospitalization was more than 70% greater for blacks than for whites. Both groups were similar in terms of in-hospital mortality rates.119 Note: Estimates by race, especially time trends, are affected by the increasing underreporting of race in the National Hospital Discharge Survey.120
Data from Ambulatory Care Visits to Physician Offices, Hospital Outpatient Departments, and Emergency Departments: U.S., 1999–2000, showed the number of visits for stroke was 3.0 million.56
Awareness of Stroke Warning Signs and Risk Factors
2001 data from the BRFSS study of the CDC, in 17 states and the US Virgin Islands, showed that public awareness of the major stroke warning signs was high.
–Sudden numbness or weakness of the face, arm or leg—94.1%
–Sudden confusion, trouble speaking or understanding—87.9%
–Sudden trouble walking, dizziness or loss of balance or coordination—85%
–Sudden trouble seeing in 1 or both eyes—68.1%
–Sudden severe headache with no known cause—61.3%
–37.8% incorrectly reported sudden chest pain as a sign of stroke.121
A study was conducted of patients admitted to an emergency department with possible stroke, to determine 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 above age 65 were less likely than those under 65 to know a sign or symptom of stroke (47% versus 28%). Forty-three percent did not know a single risk factor for stroke. Overall, almost 40% of patients admitted with a possible stroke did not know the signs, symptoms and risk factors of stroke.122
A study of over 2100 respondents to a random-digit telephone survey in Cincinnati, Ohio, in 2000, showed that 70% of respondents correctly named at least 1 established stroke warning sign versus 57% in 1995, and 72% correctly named at least 1 established risk factor versus 68% in 1995.123
The Heart and Stroke Foundation of Ontario, Canada, conducted a public opinion polling in 4 communities to determine the level of awareness of the warning signs of stroke and to determine the impact of different media strategies. Television advertising significantly increased the ability to name the warning signs. There was no significant change in communities receiving print advertising.124
2001 BRFSS data from over 61 000 adults showed that only 17.2% overall correctly classified all stroke symptoms and indicated that they would call 911 if they thought someone was having a stroke.125
In 1995, a telephone survey was conducted in the Greater Cincinnati area. Fifty-seven percent of demographically eligible individuals correctly listed at least 1 of the established warning signs and 68% correctly listed 1 of the established risk factors. Respondents age 75 or older were less likely to correctly list 1 warning sign and were less likely to list 1 stroke risk factor.126
Patients were recruited from the Academic Medical Center Consortium, the Cardiovascular Health Study and United HealthCare. Only 41% were aware of their increased risk for stroke. About 74% of patients recalled being told of their increased stroke risk by a physician in comparison with 28% who did not recall. Younger patients, depressed patients, those in poor current health, and those with a history of TIA were most likely to be aware of their risk.127
An AHA-sponsored random-digit dialing telephone survey was conducted in mid 2003. Only 26% of women over age 65 reported being well informed about stroke. Correct identification of the warning signs of stroke was low among all racial/ethnic and age groups.128
Among participants in a study by the National Stroke Association, 2.3% reported having been told be a physician that they had a TIA. Of those with a TIA, only 64% saw a physician within 24 hours of the event. Only 8.2% correctly related the definition of TIA and 8.6% could identify a typical symptom. Men, nonwhites, and those with lower income and fewer years of education were less likely to be knowledgeable about TIA.75
Participants in the 1999 World Senior Games received 1 or more free screening tests and completed an awareness questionnaire. Results indicate that stroke education should be targeted at the very elderly, those who have less than a college education and those who do not have a history of chronic disease. It also may be effectively directed toward those with higher cholesterol.129
The estimated direct and indirect cost of stroke for 2006 is $57.9 billion.
In 2001, $3.7 billion ($6037 per discharge) was paid to Medicare beneficiaries discharged from short-stay hospitals for stroke.35
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 converted to 1999 dollars using the medical component of CPI.)130
In a population study of stroke costs within 30 days of an acute event, 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).131
Inpatient hospital costs for an acute stroke event account for 70% of the first-year post-stroke costs.130
The largest components of acute care costs were room charges (50%), medical management (21%) and diagnostic costs (19%).132
Mortality within 7 days, subarachnoid hemorrhage, and stroke while hospitalized for another condition are associated with higher costs in the first year. Conversely, lower costs are associated with mild cerebral infarctions or residence in a nursing home prior to the stroke.131
Demographic variables (age, sex and insurance status) are not associated with stroke cost. Severe strokes (NIHSS score greater than 20) cost twice as much as mild strokes, despite similar diagnostic testing. Co-morbidities such as ischemic heart disease and AF predict higher costs.132,133
Operations and Procedures
In 2003, an estimated 117 000 inpatient endarterectomy procedures were performed in the United States. Carotid endarterectomy is the most frequently performed surgical procedure to prevent stroke.
Stroke in Children
Stroke in children has a peak in the perinatal period. In the National Hospital Discharge Survey from 1980–98, the rate of stroke for infants less than 30 days old (per 100 000 live births per year) was 26.4, with rates of 6.7 for hemorrhagic stroke and 17.8 for ischemic stroke.134
A history of infertility, preeclampsia, prolonged rupture of membranes, and chorioamnionitis were found to be independent risk factors for radiologically confirmed perinatal arterial ischemic stroke in the Kaiser Permanente Medical Care Program. The risk of perinatal stroke increased approximately 25-fold with an absolute risk of 1 per 200 deliveries when 3 or more of the following antenatally determined risk factors were present: infertility, preeclampsia, chorioamnionitis, prolonged rupture of membranes, primiparity, oligohydramnios, decreased fetal movement, prolonged second stage of labor, and fetal heart rate abnormalities.135
The Greater Cincinnati/Northern Kentucky Stroke Study found the stroke rate per 100 000 for children ages 1–14 was 2.7. The rate of ischemic stroke and intracerebral hemorrhage is similar in this age group.136,137
Stroke in childhood and young adulthood has a disproportionate impact on the affected patients, their family and society, compared to stroke at older ages. Outcome of childhood stroke was a moderate or severe deficit in 42% of cases.138
Compared to the stroke risk of white children, black children have a higher relative risk of 2.12, Hispanics have a lower relative risk of 0.76, and Asians have a similar risk. Boys have a 1.28-fold higher risk of stroke than girls. There are no ethnic differences in stroke severity or case-fatality, but boys have a higher case-fatality rate for ischemic stroke. 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.139
Despite current treatment, 1 out of 10 children with ischemic stroke will have a recurrence within 5 years.140
Cerebrovascular disorders are among the top 10 causes of death in children, with rates highest in the first year of life. Stroke mortality in children under 1 year of age has remained the same over the last 40 years.134
From 1979–98 in the United States, childhood mortality from stroke declined by 58% overall, with reductions in all major subtypes.141
–Ischemic stroke decreased by 19%, subarachnoid hemorrhage by 79%, and intracerebral hemorrhage by 54%.
–Black ethnicity was a risk factor for mortality from all stroke types.
–Male sex was a risk factor for mortality from subarachnoid hemorrhage and intracerebral hemorrhage but not from ischemic stroke.
Sickle cell disease is the most important cause of ischemic stroke among African-American children. The Stroke Prevention Trial in Sickle Cell Anemia (STOP) demonstrated the efficacy of blood transfusions for primary stroke prevention in high-risk children with sickle cell disease in 1998. First admission rates for stroke in California among persons under age 20 with sickle cell disease showed a dramatic decline subsequent to the publication of the STOP study. For the study years 1991–98, 93 children with sickle cell disease were admitted to California hospitals with a first stroke; 92.5% were ischemic and 7.5% were hemorrhagic. The first-stroke rate was 0.88 per 100 person-years during 1991–98, compared to 0.50 in 1999 and 0.17 in 2000 (P<0.005 for trend).142
5. High Blood Pressure
(ICD/9 401–404) (ICD/10 I10–I15). See Table 5A.
|Population Group||Prevalence 2003||Mortality 2003#||Hospital Discharges 2003||Cost 2006|
|Note: (…) = data not available. NH = non-Hispanic.|
|*These percentages represent the portion of total HBP mortality that is for males vs. females.|
|Sources: Prevalence: NHANES (1999–2002), Fields et al,145 and NHLBI; data are age-adjusted for age 20 and older. Estimates from NHANES 1999–2002 applied to 2003 population estimates.|
|**NHIS (2003), CDC/NCHS; data are estimates for Americans age 18 and older. Mortality: CDC/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, CDC/NCHS; data include people discharged alive and dead. Cost: NHLBI; data include estimated direct and indirect costs for 2006.|
|Total||65 000 000 (32.3%)||52 602||520 000||$63.5 billion|
|Total males||29 400 000 (31.5%)||21 537 (40.9%)*||221 000||…|
|Total females||35 600 000 (32.8%)||31 065 (59.1%)*||299 000||…|
|NH white males||30.6%||15 565||…||…|
|NH white females||31.0%||23 920||…||…|
|NH black males||41.8%||5441||…||…|
|NH black females||45.4%||6490||…||…|
|Hispanic or Latino**||19.0%||…||…||…|
|American Indians/Alaska Natives**||23.9%||…||…||…|
HBP is defined as:
–systolic pressure of 140 mm Hg or higher, or diastolic pressure of 90 mm Hg or higher
–taking antihypertensive medicine
–being told at least twice by a physician or other health professional that you have HBP
“Prehypertension” is systolic pressure of 120–139 mm Hg, or diastolic pressure of 80–89 mm Hg, and both not taking antihypertensive medication, or not being told on 2 occasions by a doctor or other health professional that you have hypertension.
Nearly 1 in 3 adults has HBP.145
About 28% of American adults age 18 and older, or about 59 million people, have “prehypertension” (NHANES 1999–2002, CDC/NCHS, NHLBI).
In a study conducted in 1999–2000, 39% of persons were normotensive, 31% were prehypertensive, and 29% were hypertensive. The age-adjusted prevalence of prehypertension was greater in men (39%) than in women (23.1%). African Americans ages 20–39 had a higher prevalence of prehypertension (37.4%) than whites (32.2%) and Mexican Americans (30.9%), but their prevalence was lower at older ages because of a higher prevalence of hypertension.146
A higher percentage of men than women have HBP until age 45. From ages 45–54, the percentage of women is slightly higher. After that a much higher percentage of women have HBP than men do ( CDC/NCHS).
HBP is 2–3 times more common in women taking oral contraceptives, especially in obese and older women, than in women not taking them (JNC 5 and 6).
Data from the BRFSS study of the CDC showed that in 2003, 24.8% of respondents had been told they had HBP (CDC Web site).
Race/Ethnicity and HBP
The prevalence of hypertension in blacks in the United States is among the highest in the world. Compared with whites, blacks develop HBP earlier in life and their average blood pressures 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 heart disease death and a 4.2-times greater rate of end-stage kidney disease (JNC 5 and 6).
Within the African-American community, rates of hypertension vary substantially.147
–Those with the highest rates are more likely to be middle aged or older, less educated, overweight or obese, physically inactive, and to have diabetes.
–Those with the lowest rates are more likely to be younger, but also overweight or obese.
–Those with uncontrolled HBP who are not on antihypertensive medication tend to be male, younger and have infrequent contact with a physician.
Compared with white women, black women have an 85% higher rate of ambulatory medical care visits for HBP.148
A study from 1988–94 to 1999–2000, of children and adolescents ages 8–17 showed that among NH blacks, mean systolic BP levels increased 1.6 mm Hg among girls and 2.9 mm Hg among boys, when compared with NH whites. Among Mexican Americans, girls’ systolic BP increased 1.0 mm Hg and boys’ increased 2.7 mm Hg when compared with NH whites.149
Data from the 1999–2003 NHIS study of the CDC/NCHS showed that American Indian or Alaska Native adults age 18 and older were less likely (29.7%) than black adults (33.9%) and more likely than white adults (22.8%) and Asian adults (19.3%) to ever have been told they had hypertension.150
The prevalence of HBP among blacks and whites in the southeastern United States is greater and death rates from stroke are higher than among those in other regions (JNC 5 and 6).
HBP was listed as a primary or contributing cause of death in about 277 000 of over 2 440 000 US deaths in 2003.
From 1993–2003, the age-adjusted death rate from HBP increased 29.3%, and the actual number of deaths rose 56.1%.
The 2003 overall death rate from HBP was 18.1. Death rates were 14.9 for white males, 49.7 for black males, 14.5 for white females and 40.8 for black females.
As many as 30% of all deaths in hypertensive black men and 20% of all deaths in hypertensive black women may be due to HBP (JNC 5 and 6).
In NHANES 1999–2000, rates of control were lower in Mexican Americans (17.7%) compared with NH whites (33.4%) and NH blacks (28.1%).151
The awareness, treatment and control of HBP among those in the CHS age 65 and older improved during the 1990s. The percentages who were aware of and treated for HBP were higher among blacks than among whites. Prevalences with HBP under control were similar. For both groups combined, the control of BP to lower than 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 increasing the proportion of the CHS population treated for hypertension from 34.5% to 51.1%.152
Data from the FHS study of the NHLBI show that in Americans age 80 and older, only 38% of men and 23% of women had BP that met targets set forth in the National High Blood Pressure Education Program’s clinical guidelines.153
About 69% of people who have a first heart attack, 77% who have a first stroke, and 74% who have CHF have BP higher than 140/90 mm Hg (NHLBI unpublished estimates from ARIC, CHS and FHS Cohort and Offspring Studies).
People with systolic BP of 160 mm Hg or higher and/or diastolic BP of 95 mm Hg or higher have a RR for stroke about 4 times greater than for those with normal BP.154
Hypertension precedes the development of CHF in 91% of cases. HBP is associated with a 2–3 times higher risk for developing CHF (FHS, NHLBI, Levy et al155).
Data from Ambulatory Care Visits to Physician Offices, Hospital Outpatient Departments, and Emergency Departments: U.S., 1999–2000, showed the number of visits for essential hypertension was 37.5 million.56
Data from NHANES 1999–2002 showed that of those with hypertension, 63.4% were aware of their condition, 45.3% were under current treatment, 29.3% had it under control, and 70.7% did not have it controlled.158
The estimated direct and indirect cost of HBP for 2006 is $63.5 billion.
End-Stage Renal Disease (ESRD)
ESRD (also called end-stage kidney disease) is a condition closely related to high blood pressure, and occurs when the kidneys can no longer function normally on their own. When this happens, patients are required to undergo treatment such as kidney dialysis or a kidney transplant. ESRD morbidity rates vary dramatically among different age, race, ethnicity and sex population groups. Morbidity rates tend to increase with age, then fall off for the oldest age group. The age group with the highest incidence rate is ages 75–79; for prevalence rates, it’s ages 70–74. Chronic kidney disease (categorized in stages by level of estimated glomerular filtration rate and urine proteins), which eventually progresses to ESRD, is also a substantial public health burden in the United States. The excess CVD risk in people with chronic renal disease is caused, in part, by a higher prevalence of CVD risk factors in this group than in the general population. The main factors include older age, HBP, high blood cholesterol and lipids, diabetes and physical inactivity. An independent, graded association was observed between a reduced estimated glomerular filtration rate (GFR, an indicator of kidney function) and the risk of death, cardiovascular events and hospitalization in a large, community-based population of over 1 million men and women.159
The incidence of reported ESRD has almost doubled in the past 10 years (NHLBI from usrds.org Web site).
In 2003, 102 567 new cases of ESRD were reported.
Nearly 453 000 patients were being treated for ESRD by the end of 2003.
82 588 patients died from ESRD in 2003.
More than 15 700 kidney transplants were performed in 2003.
Diabetes continues to be the most common reported cause of ESRD.
An estimated 11%, or 19.2 million American adults, have between stage 1–4 chronic kidney disease.160
Between 1996 and 1997, 3.2% of the Medicare population had a diagnosis of chronic kidney disease, representing 63.6% of persons who progressed to ESRD after 1 year.161
Age, Sex, Race and Ethnicity
The average incidence rates for pediatric ESRD are more than twice as high among children ages 15–19 as for children ages 10–14. The rates are more than 3 times higher than those for children ages 0–4 and 5–9.
Children with pediatric ESRD have high transplantation rates. More than 44% of children starting therapy received a transplant during the first year of therapy, compared with 10% of patients ages 20–64 at ESRD incidence.
The median age of the prevalent population is 58.1 years (59.2 for whites, 56.1 for blacks, 56.7 for Hispanics, 58.9 for Asians and 57.5 for Native Americans) (USRDS 2004 Annual Data Report. NIH, NIDDK).
Treatment of ESRD is more common in men than in women.
Blacks and Native Americans have much higher rates of ESRD than whites and Asians. Blacks represent 29% of treated ESRD patients.
Without treatment, ESRD is fatal. Even with dialysis treatment, 20% of ESRD patients die yearly (2004 National Healthcare Disparities Report, AHRQ, USDHHS).
Expenditures for ESRD totaled almost $23 billion in 2001 (2004 National Healthcare Disparities Report, AHRQ, USDHHS).
Performance for urea reduction ratio of 65 or greater in hemodialysis patients increased from 74% in 1996 to 90% in 2002 (2004 National Healthcare Disparities Report, AHRQ, USDHHS).
In both 2001 and 2002, the proportion of adult hemodialysis patients who received adequate dialysis was lower among blacks and higher among Asians compared with whites. The proportion who received adequate dialysis was similar among Hispanics and NH whites.
6. Congenital Cardiovascular Defects
(ICD/9 745–747) (ICD/10 Q20–Q28). See Table 6A.
|Population Group||Mortality 2002||Hospital Discharges 2003|
|Note: (…) = data not available.|
|*These percentages represent the portion of total congenital CV mortality that is males vs. females.|
|Sources: Mortality: CDC/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, CDC/NCHS; data include people discharged alive and dead.|
|Total males||2201 (52.7%)*||30 000|
|Total females||1977 (47.3%)*||31 000|
Congenital cardiovascular defects, also known as congenital heart defects, are structural problems arising from abnormal formation of the heart or major blood vessels. At least 15 distinct types of congenital defects are recognized, with many additional anatomic variations.
Defects range in severity from tiny pinholes between chambers that are nearly irrelevant and often resolve spontaneously, to major malformations that result in fetal loss or death in infancy or childhood. Common complex defects include:
tetralogy of Fallot (9–14%)
transposition of the great arteries (10–11%)
atrioventricular septal defects (4–10%)
coarctation of the aorta (8–11%)
hypoplastic left heart syndrome (4–8%)
ventricular septal defects (VSDs), the most common defect. Many close spontaneously, but VSDs still account for 14–16% of defects requiring an invasive procedure within the first year of life.162
About 1 million Americans, or 3.4 per 1000, reported being told by a physician that they had a congenital cardiovascular defect, according to a national interview survey in 1993–95. The current prevalence is likely to be higher, since both diagnosis and treatment for all types of defects have improved substantially over the past decade, and since some patients may have been unaware of their diagnosis at the time of the survey (CDC/NCHS, HIS Survey, 1993–95. Unpublished data).
Major defects are usually apparent in the neonatal period, but minor defects may not be detected until adulthood. Thus, true measures of incidence for congenital heart disease would need to record new cases of defects presenting anytime in fetal life through adulthood. However, estimates are only available for new cases detected between birth and 30 days of life, known as birth prevalence, or as new cases detected in the first year of life only. Both of 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 undergo an invasive procedure or result in death within the first year of life. Despite the absence of true incidence figures, some data are available, and are shown in Table 6B.
|Type of Presentation||Rate per 1000 Live Births||Number|
|*Includes stillbirths and pregnancy termination at less than 20 weeks gestation; includes some defects that resolve spontaneously or don’t require treatment.|
|Invasive procedure during the first year||2.3||9200|
|Detected during first year*||9.0||36 000|
|Bicommisural aortic valve||13.7||54 800|
|Other defects detected after first year||Unknown||Unknown|
According to the CDC, 1 in every 110 babies in the metropolitan Atlanta area was born with a congenital heart defect, including some infants with tiny defects that resolved without treatment. Some defects occur more commonly in males or females, or in whites or blacks.163
Nine (9.0) defects per 1000 live births are expected, or 36 000 babies per year in the United States. Of these, several studies suggest that 9200, or 2.3 per 1000 live births, require invasive treatment or result in death in the first year of life.164
Estimates are also available for bicommisural aortic valves, occurring in 13.7 per 1000 people; these defects may not require treatment in infancy, but can cause problems later in adulthood.165,166
Some studies suggest that as many as 5% of newborns, or 200 000 per year, are born with tiny muscular ventricular septal defects, almost all of which close spontaneously.167,168 These defects nearly never require treatment, so they aren’t included in Table 6B.
As an underlying or contributing cause of death—6110.
Congenital cardiovascular disease is the most common cause of infant death from birth defects; 1 in 3 infants who die from a birth defect have a heart defect (NVSS Final Data for 2000).
The 2002 overall death rate for congenital cardiovascular defects was 1.4. Death rates were 1.5 for white males, 1.9 for black males, 1.3 for white females and 1.6 for black females. Crude infant death rates (under 1 year) were 41.5 for white babies and 51.7 for black babies.
In 2000, 213 000 life years were lost before age 65 due to deaths from congenital cardiovascular disease. This is nearly equivalent to the life years lost from leukemia, prostate cancer and Alzheimer’s disease combined (CDC/NCHS; NHLBI).
In 2000, over 25 000 cardiovascular operations for congenital heart disease were performed on children less than 20 years of age. Inpatient mortality after all types of cardiac surgery was 4.7%. However, mortality risk varies substantially for different defect types, from 0.3% for atrial septal defect repair to 20.1% for first stage palliation for hypoplastic left heart syndrome. Of these operations, 54% were performed in males. In unadjusted analyses, mortality after cardiac surgery was somewhat higher for females than for males (4.8% versus 4.6%) (Healthcare Cost and Utilization Project, HCUP KID2000).
Mortality from congenital defects has been declining. From 1979–97, age-adjusted death rates from all defects declined 39%, and deaths tended to occur at progressively older ages. However, 43% of deaths still occurred in infants of less than 1 year of age. Mortality varies considerably according to type of defect.169
From 1992–2002, death rates for congenital cardiovascular defects declined 25.0%, while the actual number of deaths declined 24.1%.
In 2000, over 130 000 hospitalizations, as a primary or secondary diagnosis, were for infants or children with congenital cardiovascular disease; hospital charges were $6.5 billion (HCUPKID2000).
7. Heart Failure
(ICD/9 428) (ICD/10 I50). See Table 7A.
|Population Group||Prevalence 2003||Incidence (New Cases)||Mortality 2003#||Hospital Discharges 2003||Cost 2006|
|Note: (…) = data not available. NH = non-Hispanic.|
|*These percentages represent the portion of total HF mortality that is for males vs. females.|
|Sources: Prevalence: NHANES (1999–2002), CDC/NCHS and NHLBI; percentages are age-adjusted for Americans age 20 and older. These data are based on self reports. Estimates from NHANES 1999–2002 applied to 2003 population estimates. Incidence: FHS, NHLBI. Mortality: CDC/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, CDC/NCHS; data include people discharged alive and dead. Cost: NHLBI; data include estimated direct and indirect costs for 2006.|
|Total||5 000 000 (2.3%)||550 000||57 218||1 093 000||$29.6 billion|
|Total males||2 400 000 (2.6%)||…||22 313 (39.0%)*||496 000||…|
|Total females||2 600 000 (2.1%)||…||34 905 (61.0%)*||597 000||…|
|NH white males||2.5%||…||18 894||…||…|
|NH white females||1.9%||…||33 381||…||…|
|NH black males||3.1%||…||2138||…||…|
|NH black females||3.5%||…||3159||…||…|
In a study conducted in Minnesota, 20.8% of the population had mild diastolic dysfunction, 6.6% had moderate diastolic dysfunction, 0.7% had severe diastolic dysfunction, and 5.6% had moderate or severe diastolic dysfunction with normal ejection fraction (EF). The prevalence of any systolic dysfunction was 6.0% and moderate or severe systolic dysfunction was 2.0%. CHF was much more common among those with systolic or diastolic dysfunction than in those with normal ventricular function. Even among those with moderate or severe diastolic or systolic dysfunction, less than half had recognized CHF. Mild diastolic dysfunction and moderate or severe diastolic dysfunction were predictive of all-cause mortality.170
Based on the 44-year follow-up of the NHLBI’s FHS2…
–HF incidence approaches 10 per 1000 population after age 65.
–Seventy-five percent of HF cases have antecedent hypertension.
–About 22% of male and 46% of female heart attack (MI) victims will be disabled with HF within 6 years.
Based on 1971–96 data from the NHLBI’s FHS171…
–At age 40, the lifetime risk of developing CHF for both men and women is 1 in 5.
–At age 40, the lifetime risk of CHF occurring without antecedent MI is 1 in 9 for men and 1 in 6 for women.
–The lifetime risk doubles for people with BP greater than 160/90 mm Hg versus those with BP less than 140/90 mm Hg.
The annual rates per 1000 population of new and recurrent HF events for non-black men are 21.5 for ages 65–74, 43.3 for ages 75–84, and 73.1 for age 85 and older. For non-black women in the same age groups the rates are 11.2, 26.3 and 64.9, respectively. For black men the rates are 21.1, 52.0 and 66.7, and for black women the rates are 18.9, 33.5 and 48.4, respectively (CHS, NHLBI).
A community-based cohort study conducted in Olmsted County, Minn., showed that the incidence of HF (ICD9/428) has not declined during 2 decades, but survival after onset has increased overall, with less improvement among women and elderly persons.172
A study of the predictors of HF among women with CHD found that diabetes was the strongest risk factor. Diabetic women with elevated body mass index (BMI) or depressed creatinine clearance were at highest risk with annual incidence rates of 7% and 13% respectively. Among nondiabetic women with no risk factors, the annual incidence rate was 0.4%. The rate increases with each additional risk factor, and nondiabetic women with 3 or more risk factors had an annual incidence of 3.4%. Among diabetic participants with no additional risk factors, the annual incidence of HF was 3.0% compared with 8.2% among diabetics with at least 3 additional risk factors. Diabetics with fasting glucose >300 mg/dL had a 3-fold adjusted risk of developing HF, compared with diabetics with controlled fasting blood sugar levels.173
As an underlying or contributing cause of death—286 700.
Based on the 44-year follow-up of the NHLBI’s FHS…
–Eighty percent of men and 70% of women under age 65 who have HF will die within 8 years.
–After HF is diagnosed, survival is poorer in men than in women, but fewer than 15% of women survive more than 8–12 years. The 1-year mortality rate is high, with 1 in 5 dying.
–In people diagnosed with HF, sudden cardiac death occurs at 6–9 times the rate of the general population.
From 1993–2003, deaths from HF (ICD 428) increased 20.5%. In the same time period, the death rate declined 2.0%.
The 2003 overall death rate for HF was 19.7. Death rates were 20.5 for white males, 23.4 for black males, 18.4 for white females and 20.4 for black females.
Hospital discharges for HF rose from 399 000 in 1979 to 1 093 000 in 2003, an increase of 174% (National Hospital Discharge Survey, CDC/NCHS).
Data from Ambulatory Care Visits to Physician Offices, Hospital Outpatient Departments, and Emergency Departments: US, 1999–2000, showed the number of visits for CHF was 3.4 million.56
The estimated direct and indirect cost of HF in the United States for 2006 is $29.6 billion.
In 2001, $4.0 billion ($5912 per discharge) was paid to Medicare beneficiaries for CHF.35
8. Other Cardiovascular Diseases
Mortality, prevalence and death rate data in this section are for 2002 or 2003. Mortality for 2003 is preliminary. Mortality as an underlying or contributing cause of death is for 2002. Hospital discharge data for 2003 are based on ICD/9 codes.
Arrhythmias (Disorders of Heart Rhythm)
(ICD/9 426, 427) (ICD/10 I46–I49)
Mortality—38 698. Mortality as an underlying or contributing cause of death—479 700 of over 2 440 000 US deaths. Hospital discharges—856 000. In 2001, $2.7 billion ($6634 per discharge) was paid to Medicare beneficiaries for cardiac dysrhythmias.35
Atrial fibrillation and flutter (ICD/9 427.3) (ICD/10 I48). Mortality—10 089. Mortality as an underlying or contributing cause of death—77 800. Prevalence—>2 200 000. Incidence—>75 000.174 Hospital discharges—470 000.
In the FHS study, the lifetime risk for development of AF is 1 in 4 for men and women 40 years of age and older. Lifetime risks for AF are high (1 in 6), even in the absence of antecedent CHF or MI.175
Data from the National Hospital Discharge Survey (1996–2001) on cases that included AF as a primary discharge diagnosis found that176:
–About 44.8% of patients were men.
–The mean age for men was 66.8 years versus 74.6 for women.
–The racial breakdown for admissions was 71.2% white, 5.6% black, 2.0% other races (20.8% were not specified).
–African-American patients were much younger than patients of other races.
–The incidence in men ranged from 20.58/100 000 persons per year for patients ages 15–44 to 1077.39/100 000 persons per year for patients age 85 and older. In women, the incidence ranged from 6.64/100 000 persons per year for patients ages 15–44 to 1 203.7/100 000 persons per year for those age 85 and older.
–From 1996–2001, hospitalizations with AF as the first-listed diagnosis increased 34%.
Age-adjusted death rates for AF were highest among whites (25.7) and blacks (16.4) and higher for men (34.7) than women (22.8).177
The most common diseases listed as the primary diagnosis for persons hospitalized with AF were CHF (11.8%), followed by AF (10.9%), CHD (9.9%), and stroke (4.9%).177
AF is an independent risk factor for stroke, increasing risk about 5-fold. The risk for stroke attributable to AF increases with age.93
AF is responsible for about 15–20% of all strokes.178
AF is also an independent risk factor for stroke recurrence and stroke severity. A recent report showed people who had AF and were not treated with anticoagulants had a 2.1-fold increase in risk for recurrent stroke and a 2.4-fold increase in risk for recurrent severe stroke.179
People who have strokes caused by AF have been reported as 2.23 times more likely to be bedridden compared to those who have strokes from other causes.180
Participants in the FHS Offspring Study of the NHLBI were examined between 1984 and 1987 and monitored for 10 years. Data show that symptoms of anger and hostility were predictive of 10-year incidence of AF in men.181
Participants in the FHS study of the NHLBI were followed from 1968–99. At age 40, lifetime risks for AF were 26.0% for men and 23.0% for women. At 80 years, lifetime risks for AF were 22.7% for men and 21.6% for women. In further analysis, counting only those who had development of AF without prior or concurrent CHF or MI, lifetime risk for AF was approximately 16%.175
Tachycardia (ICD/9 427.0,1,2) (ICD/10 I47.0,1,2,9). Mortality—610. Mortality as an underlying or contributing cause of death—7200. Hospital discharges—84 000.
Paroxysmal supraventricular tachycardia (ICD/9 427.0) (ICD/10 I47.1). Mortality—151. Mortality as an underlying or contributing cause of death—1454. Hospital discharges—28 000.
Ventricular fibrillation (ICD/9 427.4) (ICD/10 I49.0). Mortality—1264. Mortality as an underlying or contributing cause of death—13 100. Hospital discharges—8000. Ventricular fibrillation is listed as the cause of relatively few deaths, but the overwhelming number of sudden cardiac deaths from coronary disease (estimated at about 330 000 per year) are thought to be from ventricular fibrillation.
Arteries, Diseases of
(ICD/9 440–448) (ICD/10 I70–I79) (Includes peripheral arterial disease)
Mortality—37 647. Mortality as an underlying or contributing cause of death—115 400. Hospital discharges—262 000.
Aortic aneurysm (ICD/9 441) (ICD/10 I71). Mortality—14 751. Mortality as an underlying or contributing cause of death—20 800. Hospital discharges—53 000.
Atherosclerosis (ICD/9 440) (ICD/10 I70) is a process that leads to a group of diseases characterized by a thickening of artery walls. Preliminary mortality (2003)—13 030. Mortality as an underlying or contributing cause of death—66 000. Hospital discharges—118 000. Atherosclerosis causes many deaths from heart attack and stroke and accounts for nearly three-fourths of all deaths from CVD (FHS, NHLBI).
In 1999 US community hospitals billed $26.2 billion for coronary atherosclerosis, more than for any other condition (AHRQ Electronic Newsletter, June 14, 2002).
Other diseases of arteries (ICD/9 442–448) (ICD/10 I72–I78). Preliminary mortality (2003)—9867. Mortality as an underlying or contributing cause of death—10 109. Hospital discharges—91 000.
Kawasaki disease (ICD/9 446.1) (ICD/10 M30.3). Mortality—9. Mortality as an underlying or contributing cause of death—14. Hospital discharges—5000, primary plus secondary diagnoses.
–About 76% of Kawasaki disease patients are under age 5.182
–Up to 2500 cases of Kawasaki disease are diagnosed yearly. Kawasaki disease occurs more often among boys (63%) and among those of Asian ancestry.183
–The highest incidence in the United States is in Hawaii. A hospitalization rate of 47.7 per 100 000 children under age 5 was reported during the mid-1990s. In the continental United States, the estimated incidence is from 9–19 per 100 000 children.184
Peripheral arterial disease (PAD) affects about 8 million Americans and is associated with significant morbidity and mortality.185,186
A study from the NHANES 1999–2000 data found that PAD affects about 5 million adults. Prevalence increases dramatically with age and disproportionately affects blacks.187 However, the measurement of systolic BP utilizing the right arm only and the omission of queries for surgical procedures to correct PAD in this study led to an underestimate of the true PAD prevalence. Experts in the field generally agree that PAD affects approximately 8 million Americans.185,186
PAD affects 12–20% of Americans age 65 and older. Despite its prevalence and cardiovascular risk implications, only 25% of PAD patients are undergoing treatment.188
In the general population, only about 10% of persons with PAD have the classic symptoms of intermittent claudication (IC). About 40% do not complain of leg pain, while the remaining 50% have a variety of leg symptoms different from classic claudication.185,189 However, in an older, disabled, population of women, as many as two-thirds of individuals with PAD had no exertional leg symptoms.190
The risk factors for PAD are similar to those for CHD, although diabetes and cigarette smoking are particularly strong risk factors for PAD.191
Persons with PAD have impaired function and quality of life. This is true even for persons who do not report leg symptoms. Furthermore, PAD patients, including those who are asymptomatic, experience significant decline in lower extremity functioning over time.192,193
PAD is a marker for systemic atherosclerotic disease. Persons with PAD, compared to those without, have 4–5 times the risk of dying of a CVD event, resulting in 2–3 times higher total mortality risk.186,194
In the Framingham Heart Study (FHS), the incidence of PAD was based on symptoms of IC in subjects ages 29–62. Annual incidence of IC per 10 000 subjects at risk rose from 6 in men and 3 in women ages 30–44 to 61 in men and 54 in women ages 65–74.195 IC incidence has declined since 1950, but mortality has remained high and unchanged.196
Several studies have evaluated both symptomatic and asymptomatic PAD using the ankle brachial index. The prevalence of asymptomatic PAD was 25.5% among 1537 participants of the Systolic Hypertension in the Elderly Program (SHEP).195
In the FHS, the annual mortality rate was almost 4 times greater in subjects with IC. In a major cohort study, investigators observed a risk for all-cause mortality in these subjects that was 3.1 times higher than that for patients without PAD. In addition, PAD patients had a 5.9-times higher risk for death from CVD complications and a 6.6-times higher risk for death from CHD specifically.186,195
African-American ethnicity was a strong and independent risk factor for PAD, and was not explained by higher levels of diabetes, hypertension, and BMI. African Americans had a higher PAD prevalence than NH whites (OR= 2.3). There was no evidence of a greater susceptibility of African Americans to CVD risk factors as a reason for their higher PAD prevalence.197
Data from NHANES 1999–2000 (CDC/NCHS), show that even low blood levels of lead and cadmium may increase the risk of PAD. Exposure to these 2 metals is possible through cigarette smoke. The risk was 2.8 for high levels of cadmium and 2.9 for high levels of lead. The odds ratio of PAD for current smokers was 4.13 compared to people who had never smoked.198 Results from the NHANES 1999–2000 survey of the CDC/NCHS showed a remarkably high prevalence of PAD among patients with renal insufficiency. Accurate identification of patients with renal insufficiency combined with routine ABI measurement in this group would greatly enhance efforts to detect subclinical PAD.199
(ICD/9 421.0) (ICD/10 I33.0)
Mortality as an underlying or contributing cause of death—2370. Hospital discharges—29 000, primary plus secondary diagnoses.
(ICD/9 425) (ICD/10 I42)
Mortality—27 728. Mortality as an underlying or contributing cause of death—54 700. Hospital discharges—39 000.
Eighty-seven percent of cases are congestive or dilated cardiomyopathy. Of patients with dilated cardiomyopathy, 50% are alive 5 years after their initial diagnosis and 25% are alive 10 years after the diagnosis (Facts About Cardiomyopathy, NIH, NHLBI, 1995).
Mortality from cardiomyopathy is highest in older persons, men and blacks (FHS, NHLBI).
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.200
Since 1996, the NHLBI’s Pediatric Cardiomyopathy Registry has collected data on all children with newly diagnosed cardiomyopathy in New England and the Central Southwest (Texas, Oklahoma and Arkansas).201
–The overall incidence of cardiomyopathy is 1.13 cases per 100 000 in children younger than age 18.
–In children under 1 year of age, the incidence is 8.34 and in children ages 1–18 it’s 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).
Studies show that 36% of young athletes who die suddenly have probable or definite hypertrophic cardiomyopathy.202
Rheumatic Fever/Rheumatic Heart Disease
(ICD/9 390–398) (ICD/10 I00–I09). See Table 8A.
|Population Group||Mortality 2003#||Hospital Discharges 2003|
|Note: (…) = data not available.|
|*These percentages represent the portion of total mortality that is for males vs. females.|
|Sources: Mortality: CDC/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, CDC/NCHS; data include people discharged alive and dead.|
|Total males||1152 (32.4%)*||15 000|
|Total females||2402 (67.6%)*||28 000|
Many operations on heart valves are related to rheumatic heart disease (RHD).
The incidence of rheumatic fever (RF) remains higher in African Americans, Puerto Ricans, Mexican Americans and American Indians.2
Mortality as an underlying or contributing cause of death—7440.
In 1950, about 15 000 Americans (adjusted for changes in ICD codes) died of RF/RHD compared with about 3500 today.
From 1993–2003 the death rate from RF/RHD fell 36.8%, while actual deaths declined 24.6%.
The 2003 overall death rate for RF/RHD was 1.2. Death rates were 1.0 for white males and 0.9 for black males, 1.4 for white females and 1.2 for black females.
Valvular Heart Disease
(ICD/9 424) (ICD/10 I34–I38)
Mortality—19 989. Mortality as an underlying or contributing cause of death—42 590. Hospital discharges—95 000.
Aortic valve disorders (ICD/9 424.1) (ICD/10 I35). Mortality—12 471. Mortality as an underlying or contributing cause of death—about 26 336. Hospital discharges—48 000.
Mitral valve disorders (ICD/9 424.0) (ICD/10 I34). Mortality—2759. Mortality as an underlying or contributing cause of death—about 6600. Hospital discharges—43 000.
–The NHLBI’s FHS reports that among people ages 26–84, prevalence is about 1–2% and equal between women and men.
Pulmonary valve disorders (ICD/9 424.3) (ICD/10 I37). Mortality—11. Mortality as an underlying or contributing cause of death—35.
Tricuspid valve disorders (ICD/9 424.2) (ICD/10 I36). Mortality—16. Mortality as an underlying or contributing cause of death—69.
Operations and Procedures
In 2003, an estimated 95 000 inpatient valve procedures were performed in the United States.
Venous thromboembolism (VTE) occurs for the first time in about 100 persons per 100 000 each year in the United States. About one-third of patients with symptomatic VTE manifest pulmonary embolism (PE), whereas two-thirds manifest deep vein thrombosis (DVT) alone.203
Caucasians and African Americans have a significantly higher incidence than Hispanics and Asians or Pacific Islanders.203
In studies conducted in Worcester, Mass., and Olmsted County, Minn., the incidence of VTE was about 1 in 1000. In both studies, VTE was more common in men; for each 10-year increase in age, the incidence doubled. By extrapolation, it’s estimated that more than 250 000 patients are hospitalized annually with VTE.204
The crude incidence rate per 1000 person-years was 0.80 in the ARIC study, 2.15 in the CHS and 1.08 in the combined cohort. Half of the participants who developed incident VTE were women and 72% were white.205
Over 200 000 new cases of VTE occur annually. Of these, 30% die within 30 days, one-fifth suffer sudden death due to PE, and about 30% develop recurrent VTE within 10 years. Independent predictors for recurrence include increasing age, obesity, malignant neoplasm and extremity paresis.206
Data from the ARIC study of the NHLBI showed the 28-day fatality from DVT is 9%; from PE, 15%; from idiopathic DVT or PE, 5%; from secondary non-cancer-related DVT or PE, 7%; and secondary cancer-related DVT or PE, 25%.207
Deep vein thrombosis (ICD/9 451.1) (ICD/10 I80.2). Mortality—2809. Mortality as an underlying or contributing cause of death—10 530. Hospital discharges—9000.
A review of 9 studies conducted in the United States and Sweden showed that the mean incidence of first DVT in the general population was 5.04 per 10 000 person-years. The incidence was similar in males and females and increased dramatically with age from about 2–3 per 10 000 person-years at ages 30–49 to 20 at ages 70–79.208
Death occurs in about 6% of DVT cases within 1 month of diagnosis.203
Pulmonary embolism (ICD/9 415.1) (ICD/10 I26). Mortality—8620. Mortality as an underlying or contributing cause of death—26 600. Hospital discharges —124 000.
In the Nurses’ Health Study, nurses age 60 or older in the highest BMI quintile had the highest rates of pulmonary embolism. Heavy cigarette smoking and high blood pressure were also identified as risk factors for PE.204
Death occurs in about 12% of PE cases within 1 month of diagnosis.203
A study of Medicare recipients age 65 and older reported 30-day case fatality rates in patients with PE. Overall, men had higher fatality rates than women (13.7% versus 12.8%), and blacks had higher fatality rates than whites (16.1% versus 12.9%).204
In the International Cooperative Pulmonary Embolism Registry, the 3-month mortality rate was 17.5%. In contrast, the overall 3-month mortality rate in the Prospective Investigation of Pulmonary Embolism Diagnosis was 15%, but only 10% of deaths during 1 year of follow-up were ascribed to PE.204
The age-adjusted rate of deaths from pulmonary thromboembolism (PTE) decreased from 191 per million in 1979 to 94 per million in 1998 overall, decreasing 56% for men and 46% for women. During this time, the age-adjusted mortality rates for blacks were consistently 50% higher than those for whites, and those for whites were 50% higher than those for people of other races (Asian, American Indian, etc.). Within racial strata, mortality rates were consistently 20–30% higher among men than among women.209
9. Risk Factors
|Population Group||Prevalence 2004#||Cost* 1997 to 2001|
|NH = non-Hispanic.|
|#Data are for 2004 for Americans age 18 and older. NHIS percents applied to 2003 population estimates. MMWR.210|
|Total||44 300 000 (20.9%)||$167 billion per year|
|Total males||24 100 000 (23.4%)||…|
|Total females||20 200 000 (18.5%)||…|
|NH white males||24.1%||…|
|NH white females||20.4%||…|
|NH black males||23.9%||…|
|NH black or females||17.2%||…|
|Asian only males||17.8%||…|
|Asian only females||4.8%||…|
|American Indian/Alaska Native males||37.3%||…|
|American Indian/Alaska Native females||33.4%||…|
|Population Group||Ages 12 to 17||Age 18 and Older|
|Note: (…) = data not available; NR = data considered unreliable.|
|Source: percentage of persons ages 12–17 and age 18 and older reporting cigarette use during the preceding month, by race/ethnicity and sex (National Survey on Drug Use and Health212).|
|Central or South American||9.9%||9.3%||26.3%||16.9%|
|American Indian/Alaska Native||29.5%||26.3%||40.9%||40.0%|
|Hawaiian/Other Pacific Islander||7.0%||NR||NR||NR|
In 2003, for grades 9–12, 30.3% of male students and 24.6% of female students reported current tobacco use; 19.9% of males and 9.4% of females reported current cigar use; and 11.0% of males and 2.2% of females reported current smokeless tobacco use.213
White youths ages 18–24 from families with lower educational attainment report substantially higher smoking rates than black and Mexican-American youths from families with similar educational attainment. Seventy-seven percent of young white men and 61% of young white women are smokers compared with 35% of minority youth.214
From 1980–2003, the percentage of high school seniors who smoked in the past month decreased 20%. This percentage decreased by 2.2% in males, 23.7% in females, 9% in whites and 64.3% in blacks or African Americans (Health, United States, 2004, CDC/NCHS).
An estimated 150 000–300 000 children younger than 18 months of age have respiratory tract infections because of exposure to secondhand smoke (CDC/NCHS).
Children’s exposure to secondhand smoke, as indicated by cotinine levels, dropped between 1988–94 and 1999–2002. Overall, 59% of children ages 4–11 had cotinine in their blood in 1999–2002, down from 88% in 1988–94. In 1999–2002, 84% of NH black children ages 4–11 had cotinine in their blood compared to 58% of NH white children and 47% of Mexican-American children. The percentage of homes with children under age 7 in which someone smokes on a regular basis decreased from 29% in 1994 to 11% in 2003.215
Since 1965 smoking in the United States has declined by 47% among people age 18 and older (Health, United States, 2004, CDC/NCHS).
Among Americans age 18 and older, 23.4% of men and 18.5% of women are smokers, putting them at increased risk of heart attack and stroke.210
Use of any tobacco product in 2002 was 32.0% for white only, 28.8% for black or African-American only, 44.3% for American Indian or Alaska Native only, 28.8% for Native Hawaiian or other Pacific Islander only, 18.6% for Asian only and 25.2% for Hispanic or Latino, any race (Health, United States, 2004, CDC).
Smoking prevalence is higher among those with 9–11 years of education (34.0%) compared with those with more than 16 years of education (8.0%). It’s highest among persons living below the poverty level (29.1%) compared with other income groups.213
Compared with results from 1988–91, median cotinine levels measured from 1999–2002 in nonsmokers have decreased 68% in children, 69% in adolescents, and about 75% in adults. NH blacks have levels more than twice as high as those of NH whites and Mexican Americans. Children’s levels are more than twice those of adults.216
Data from the BRFSS study of the CDC show that more than one-third of white men and women ages 18–24 smoked, the highest rate among all the groups covered in the survey in 2000. Those young people and Hispanic women the same age had the largest increases in smoking rates from 1990–2000. More than half of men and women ages 18–24 from all ethnic groups failed to quit smoking in 2000. Younger white women and men ages 18–44 had higher overall risk levels for noncommunicable diseases, probably due to increased smoking and obesity.23
According to the World Health Organization (WHO), 1 year after quitting, the risk of CHD decreases by 50%. Within 15 years, the relative risk of dying from CHD for an ex-smoker approaches that of a long-time (lifetime) nonsmoker (World No-Tobacco Day 1998, www.who.ch/ntday/ntday98).
Data from the 2004 NHIS study of the CDC/NCHS showed that American Indian or Alaska Native adults age 18 and older were more likely (33.4%) to be current smokers than NH white adults (22.2%), black adults (20.2%) and Asian adults (11.3%).210
A survey conducted in 2002 found that an estimated 1.4 million Americans began smoking cigarettes daily in 2001. This translates to close to 4000 new regular smokers per day, including more than 2000 youths under age 18 (National Survey on Drug Use and Health, samhsa.gov).
About 80% of people who use tobacco begin before age 18. The most common age of initiation is 14–15.220
Information from the CDC Health Effects of Cigarette Smoking Fact Sheet, February 2004:
–Cigarette smokers are 2–4 times more likely to develop CHD than nonsmokers.
–Cigarette smoking approximately doubles a person’s risk for stroke.
–Cigarette smokers are more than 10 times as likely as nonsmokers to develop peripheral vascular disease.
From 1997–2001, an estimated 437 902 Americans died each year of smoking-related illnesses, and 34.7% of these deaths were cardiovascular-related.221
On average, male smokers die 13.2 years earlier than male nonsmokers, and female smokers die 14.5 years earlier than female nonsmokers.222
From 1997–2001, smoking caused 3.3 million years of potential life lost for men and 2.2 million years for women annually.223
From 1997–2001, smoking during pregnancy resulted in an estimated 523 male and 387 female infant deaths annually.221
Current cigarette smoking is a powerful independent predictor of sudden cardiac death in patients with CHD.224
Cigarette smoking results in a 2–3-fold risk of dying from CHD.225
After up to 14.5 years of follow-up of participants in the Lung Health Study (LHS) of the NHLBI, all-cause mortality was significantly lower (15%) compared to those who received usual care.226
An estimated 35 052 nonsmokers die from CHD each year as a result of exposure to environmental tobacco smoke (MMWR, Vol. 54, No. 25, 2005, CDC).
Data from The Health Consequences of Smoking, 2004—A Report of the Surgeon General (CDC/NCHS): A study of women younger than 44 years of age found there was a strong dose-relationship for MI, with a risk of 2.5 for those smoking 1–5 cigarettes per day, rising to 74.6 for those smoking more than 40 cigarettes per day, compared with nonsmokers.
—Another study on female smokers found the highest risk (6.8) for MI was in women younger than 55 years of age.
—One-third of those who receive percutaneous coronary artery vascularization are current smokers, and 50–60% continue to smoke after the procedure.
—Cigarette smoking remains a major cause of stroke in the United States. The evidence is sufficient to infer a causal relationship between smoking and subclinical atherosclerosis.
—The 2004 Health Consequences of Smoking Report of the Surgeon General states that the risk of stroke decreases steadily after smoking cessation. Former smokers have the same risk as nonsmokers after 5–15 years.227
About 5 million American men and women use chewing tobacco (NHANES III [1988–94], CDC/NCHS).
–Rates are highest in the South and rural areas.
–Men use chewing tobacco at 10 times the rate for women. For men, the percentages who use chewing tobacco are 6.8 for whites, 3.1 for blacks, 1.5 for Hispanics, 1.2 for Asians or Pacific Islanders and 7.8 for American Indians or Alaska Natives.
–For women, the percentages are 0.3 for whites, 2.9 for blacks, 0.1 for Hispanics, almost none for Asians or Pacific Islanders and 1.2 for American Indians or Alaska Natives.
–Use rates increase as years of education decrease for both men and women.
Direct medical costs ($75.5 billion) and lost productivity costs associated with smoking ($92 billion) total an estimated $167 billion per year.221
High Blood Cholesterol and Other Lipids
|Population Group||Prevalence of Total Cholesterol 200 mg/dL or Higher 2003||Prevalence of Total Cholesterol 240 mg/dL or Higher 2003||Prevalence of LDL Cholesterol 130 mg/dL or Higher 2003||Prevalence of HDL Cholesterol Less Than 40 mg/dL 2003|
|Note: mg/dL = milligrams per deciliter of blood. Prevalence of total cholesterol 200 mg/dL or higher includes people with total cholesterol of 240 mg/dL or higher. In adults, levels of 200–239 mg/dL are considered borderline-high cholesterol. Levels of 240 mg/dL or higher are considered high cholesterol.|
|(…) = data not available. NH = non-Hispanic.|
|*Total data for total cholesterol are for Americans age 20 and older. Data for LDL cholesterol, HDL cholesterol and all racial/ethnic groups are age-adjusted for age 20 and older.|
|#BRFSS (1997), MMWR230; data are for Americans age 18 and older.|
|Source for total cholesterol 200 mg/dL or higher; 240 mg/dL or higher; LDL and HDL: NHANES (1999–2002), CDC/NCHS and NHLBI. Estimates from NHANES 1999–2002 applied to 2003 population estimates.|
|Total*||99 900 000 (49.8%)||34 500 000 (17.3%)||76 100 000 (39.5%)||46 000 000 (22.6%)|
|Total males*||48 400 000 (48.9%)||16 400 000 (16.3%)||39 100 000 (43.1%)||33 200 000 (33.6%)|
|Total females*||51 500 000 (50.2%)||18 100 000 (17.8%)||37 000 000 (35.8%)||12 800 000 (12.6%)|
|NH white males||48.9%||16.5%||43.8%||34.5%|
|NH white females||52.1%||18.4%||36.9%||12.4%|
|NH black males||41.6%||12.2%||36.0%||22.7%|
|NH black females||46.8%||17.4%||34.5%||11.3%|
|Total Asian/Pacific Islanders#||…||27.3%||…||…|
|Total American Indians/Alaska Natives, Alaska#||…||26.0%||…||…|
|Total American Indians/Alaska Natives, Oklahoma#||…||28.6%||…||…|
|Total American Indians/Alaska Natives, Washington#||…||26.5%||…||…|
For information on dietary cholesterol, total fat, saturated fat and other factors that affect blood cholesterol levels, see Nutrition section.
Among children and adolescents ages 4–19 (NHANES III [1988–94], CDC):
–Females have significantly higher average total cholesterol and low-density lipoprotein (LDL) cholesterol (bad cholesterol) than do males.
–NH black children and adolescents have significantly higher mean total cholesterol, LDL (bad) cholesterol and HDL (good) cholesterol levels when compared with NH white and Mexican-American children and adolescents.
Among children and adolescents ages 4–19, the mean total blood cholesterol level is 165 mg/dL. For boys, it’s 163 mg/dL and for girls, it’s 167 mg/dL. The racial/ethnic breakdown is (NHANES III [1988–94], CDC/NCHS):
–For NH whites, 162 mg/dL for boys and 166 mg/dL for girls.
–For NH blacks, 168 mg/dL for boys and 171 mg/dL for girls.
–For Mexican Americans, 163 mg/dL for boys and 165 mg/dL for girls.
About 10% of adolescents ages 12–19 have total cholesterol levels exceeding 200 mg/dL (NHANES III [1988–94], CDC/NCHS).
BRFSS data from 1991–2003 showed the prevalence of cholesterol screening during the preceding 5 years increased from 67.3% in 1991 to 73.1% in 2003. The age-standardized prevalence of high blood cholesterol awareness among persons screened increased from 25.3% in 1991 to 31.1% in 2003.231
A 10% decrease in total cholesterol levels (population-wide) may result in an estimated 30% reduction in the incidence of CHD.232
Data from NHANES 1999–2002 showed that overall, 63.3% of participants whose test results indicated high blood choleserol or who were taking a cholesterol-lowering medication had been told by a professional that they had high cholesterol. Women were less likely than men to be aware of their condition; blacks and Mexican Americans were less likely to be aware of their condition than whites. Less than half of Mexican Americans with high cholesterol were aware of their condition.233
Between 1988–94 and 1999–2002, the age-adjusted mean total serum cholesterol level of adults age 20 and over decreased from 206 mg/dL to 203 mg/dL and LDL cholesterol levels decreased from 129 mg/dL to 123 mg/dL.234
Based on data from the Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults235:
Less than half of persons who qualify for any kind of lipid-modifying treatment for CHD risk reduction are receiving it.
Less than half of even the highest-risk persons, those who have symptomatic CHD, are receiving lipid-lowering treatment.
Only about a third of treated patients are achieving their LDL goal; less than 20% of CHD patients are at their LDL goal.
LDL (Bad) Cholesterol
Mean LDL cholesterol levels among children and adolescents ages 12–19 are (NHANES III [1988–94], CDC/NCHS):
–Among NH whites, 91 mg/dL for boys and 100 mg/dL for girls.
–Among NH blacks, 99 mg/dL for boys and 102 mg/dL for girls.
–Among Mexican Americans, 93 mg/dL for boys and 92 mg/dL for girls.
The mean level of LDL cholesterol for American adults age 20 and older is 123 mg/dL. Levels of 130–159 mg/dL are considered borderline high. Levels of 160–189 mg/dL are classified as high, and levels of 190 mg/dL and higher are very high.234
According to NHANES 1999–2002
— Among NH whites, the mean LDL cholesterol level was 126 mg/dL for men and 121 mg/dL for women.
— Among NH blacks, the mean LDL cholesterol level was 121 mg/dL for both men and women.
— Among Mexican Americans, the mean LDL cholesterol level was 125 mg/dL for men and 117 mg/dL for women.
HDL (Good) Cholesterol
The higher a person’s HDL cholesterol level is, the better. A level of less than 40 mg/dL in adults is considered low HDL cholesterol, which is a risk factor for heart disease and stroke.
Mean HDL cholesterol levels among children and adolescents ages 4–19 are (NHANES III [1988–94], CDC/NCHS):
–Among NH whites, 48 mg/dL for boys and 50 mg/dL for girls.
–Among NH blacks, 55 mg/dL for boys and 56 mg/dL for girls.
–Among Mexican Americans, 51 mg/dL for boys and 52 mg/dL for girls.
The mean level of HDL cholesterol for American adults age 20 and older is 51.3 mg/dL.234
According to NHANES 1999–2002
— Among NH whites, the mean HDL cholesterol level was 45.5 mg/dL for men and 52.9 for women.
— Among NH blacks, the mean HDL cholesterol level was 51.0 mg/dL for men and 57.3 for women.
— Among Mexican Americans, the mean HDL cholesterol level was 45.0 mg/dL for men and 52.9 for women.
See Tables 9D and 9E.
|Population Group||Prevalence 2004|
|Note: Regular leisure-time physical activity is defined as light–moderate activity for ≥30 minutes, ≥5 times per week or vigorous activity for ≥20 minutes, ≥3 times per week. (Early Release of Selected Estimates on Data from the 2004 NHIS, CDC/NCHS.)|
|Data are age-adjusted for adults age 18+. NH = non-Hispanic or non-Latino.|
|Source: NHIS 2004 (Personal communication, Susan Jack, CDC/NCHS.)|
|NH white only males||33.4%|
|NH white only females||31.8%|
|NH black only males||29.5%|
|NH black only females||19.6%|
|Hispanic or Latino males||24.9%|
|Hispanic or Latino females||21.8%|
|Population Group||Prevalence 2004||2000 Cost**|
|Note: Prevalence is the percentage of population who report no leisure-time physical activity.|
|NH = non-Hispanic.|
|Source: BRFSS (2004), CDC; data are age-adjusted for Americans age 18 and older. MMWR, Vol.54/No.39. Oct. 7, 2005.|
|NH white males||18.4%||…|
|NH white females||21.6%||…|
|NH black males||27.0%||…|
|NH black females||33.9%||…|
|American Indian/Alaska Native males||23.8%||…|
|American Indian/Alaska Native females||31.8%||…|
|Asian/Pacific Islander males||20.4%||…|
|Asian/Pacific Islander females||24.0%||…|
In 2003, 58.5% of male and 52.8% of female high school students, grades 9–12, were enrolled in physical education (PE) classes. Among these students, 30.5% of males and 26.4% of females attended classes daily and 84.5% of males and 75.3% of females exercised or played sports during an average PE class.237
2002 data from the Youth Media Campaign Longitudinal Study (YMCLS) of the CDC showed that 61.5% of children ages 9–13 don’t participate in any organized physical activity (PA) during their nonschool hours and that 22.6% don’t engage in any free-time PA. NH black and Hispanic children are significantly less likely than NH white children to report involvement in organized activities, as are children with parents who have lower incomes and education levels.239
By the age of 16 or 17, 31% of white girls and 56% of black girls report no habitual leisure-time activity.240
–Lower levels of parental education are associated with greater decline in activity for white girls at both younger and older ages. For black girls, this association is seen only at the older ages.
–Cigarette smoking is associated with decline in activity among white girls. Pregnancy is associated with decline in activity among black girls but not among white girls.
–A higher BMI is associated with greater decline in activity among girls of both races.
2001–2003 data from the BRFSS study of the CDC showed that among Asians and Native Hawaiians or Other Pacific Islanders, 21.2% of men and 27.0% of women reported no leisure-time PA. Of these, 21.5% were overweight (BMI 25.0–29.9) and 23.8% were obese (BMI 30.0 and over).241
2004 data from the BRFSS study of the CDC showed that 77.1% of respondents had participated in any PA in the past month. Of these, the median percentage that were male was 79.2, and 74.8% were female; 79.7% were white, 66.1% were black, and 61.5% were Hispanic (CDC Web site).
Based on data from the 1999–2001 NHIS survey of the CDC/NCHS242…
–31.3% of US adults age 18 and older engage in any regular leisure-time PA.
–Men (64.2 %) were more likely than women (59.0%) to engage in at least some leisure-time PA.
–Engaging in any PA declined steadily with age from 39.7% of adults ages 18–24 to 15.6% age 75 and older.
–Engaging in any regular leisure-time PA was more prevalent among white adults (32.7%) than among Asian adults (27.8%) and black adults (23.9%).
–NH white adults (65.7%) were more likely than NH black adults (49.3%) and Hispanic adults (45.0%) to engage in at least some leisure-time PA.
–Adults with a graduate degree (80.6%) were about twice as likely as adults with less than a high school diploma (41.0%) to engage in at least some leisure-time PA.
–Adults who had incomes 4 times the poverty level or more (39.9%) were about twice as likely as adults with incomes below the poverty level (22.6%) to engage in any regular PA.
–Widowed adults (23.6%) were less likely than never-married adults (33.0%), married adults (31.1%), and divorced or separated adults (29.1%) to engage in regular PA.
–Adults living in the West (65.3%) were more likely than adults living in the South (56.4%) to engage in at least some leisure-time PA.
The relative risk of CHD associated with physical inactivity ranges from 1.5–2.4, an increase in risk comparable to that observed for high blood cholesterol, HBP or cigarette smoking.243
A study of over 72 000 female nurses indicates that moderate-intensity PA such as walking is associated with a substantial reduction in risk of total and ischemic stroke.98
The prevalence of physical inactivity during leisure time among Mexican Americans is higher than in the general population.244
–The prevalence of physical inactivity among those whose main language is English is 15% of men and 28% of women. This is similar to that of the general population (17% of men and 27% of women).
–Those whose main language is Spanish have the highest prevalence of physical inactivity (38% of men and 58% of women).
Data from the 1999–2003 NHIS study of the CDC/NCHS showed that American-Indian or Alaska Native (AIAN) adults, age 18 and older, were as likely (50.3%) as black adults (49.9%) and more likely than Asian adults (38.1%) and white adults (36.6%) to never engage in any leisure-time PA.150
The annual estimated direct medical cost of physical inactivity in 2000 was $76.6 billion (www.cdc.gov).
Overweight and Obesity
See Table 9F.
|Population Group||Prevalence of Overweight and Obesity in Adults 2003||Prevalence of Obesity in Adults 2003||Prevalence of Overweight in Children Ages 6–11 2003||Prevalence of Overweight in Adolescents Ages 12–19 2003||Cost** 2001|
|Note: BMI (body mass index) = weight in kilograms divided by height in meters squared (kg/m2).|
|Data for white, black or African-American, and Asian or Pacific Islander males and females are for non-Hispanics.|
|(…) = data not available. NH = non-Hispanic.|
|Overweight and obesity in adults is BMI 25 and higher. Obesity in adults is BMI 30.0 or higher. Overweight in children and adolescents was defined as being at or above the 95th percentile of the sex-specific BMI-for-age CDC 2000 growth chart.|
|*NHIS (2003), CDC/NCHS; data are crude percent distributions for Americans age 18 and older.|
|Sources: NHANES (1999–2002), (Hedley et al245); CDC/NCHS data in adults are for age 20 and older. Estimates from NHANES 1999–2002 applied to 2003 population estimates.|
|Total||136 500 000 (65.1%)||64 000 000 (30.4%)||3 840 000 (15.8%)||5 330 000 (16.1%)||$117 billion|
|Total males||69 600 000 (68.8%)||27 900 000 (27.6%)||2 100 000 (16.9%)||2 840 000 (16.7%)||…|
|Total females||66 900 000 (61.6%)||36 100 000 (33.2%)||1 740 000 (14.7%)||2 490 000 (15.4%)||…|
|NH white males||69.4%||28.2%||14.0%||14.6%||…|
|NH white females||57.2%||30.7%||13.1%||12.7%||…|
|NH black males||62.9%||27.9%||17.0%||18.7%||…|
|NH black females||77.2%||49.0%||22.8%||23.6%||…|
|Hispanic or Latino*||38.9%||24.7%||…||…||…|
|American Indian/Alaska Native*||33.5%||32.9%||…||…||…|
An estimated 9.2 million children and adolescents ages 6–19 are considered overweight or obese, based on the 95th percentile or higher of BMI values in the 2000 CDC growth chart for the United States (NHANES [1999–2002], CDC/NCHS).
Based on data from NHANES (1999–2002), the prevalence of overweight in children ages 6–11 increased from 4.2% to 15.8% compared with data from 1963–65. The prevalence of overweight in adolescents ages 12–19 increased from 4.6% to 16.1% (CDC/NCHS).
Over 10% of preschool children ages 2–5 are overweight, up from 7% in 1994.245
–Among preschool children, the following are overweight: 8.6% of NH whites, 8.8% of NH blacks and 13.1% of Mexican Americans.
–Among children ages 6–11, the following are overweight: 13.5% of NH whites, 19.8% of NH blacks and 21.8% of Mexican Americans.
–Among adolescents ages 12–19, the following are overweight: 13.7% of NH whites, 21.1% of NH blacks and 22.5% of Mexican Americans.
–In addition, the data show that another 31% of children and teens ages 6–19 are considered at risk of becoming overweight (BMI from the 85th–95th percentile).
43% of adolescents watch more than 2 hours of television each day. Overweight adolescents have a 70% chance of becoming overweight adults. This increases to 80% if 1 or both parents are overweight or obese (www.surgeongeneral.gov).
Data from the YRBS 2003 survey showed that the prevalence of being overweight was higher among black (16.2%) and Hispanic (16.4%) than white (10.4%) students; higher among black female (14.2%) and Hispanic female (11.5%) than white female (6.5%) students; and higher among black male (18.2%) and Hispanic male (21.3%) than white male (14.0%) students. The prevalence of being at risk for overweight was higher among black (18.2%) and Hispanic (17.4%) than white (13.3%) students; higher among black female (21.2%) than white female (12.4%) and Hispanic female (15.7%) students; and higher among Hispanic male (19.1%) and black male (15.1%) than white male (14.0%) students.246
Among all overweight children and teens ages 2–19 (or their parents), 36.7% reported ever having been told by a doctor or healthcare professional that they were overweight. For ages 2–5, 17.4%; for ages 6–11, 32.6%; for ages 12–15, 39.6%; and for ages 16–19, 51.6% were told that they were overweight. Similar trends were seen for males and females. Among racial/ethnic populations, overweight NH black females were significantly more likely to be told that they were overweight than NH white females (47.4% versus 31.0%). Among those informed of overweight status, 39% of NH black females were severely overweight compared with 17% of NH white females.247
Analysis of the FHS, 1971–2001, showed the 4-year rates of developing overweight varied from 14–19% in women and 26–30% in men. Four-year rates of developing obesity were from 5–7% in women and 7–9% in men. The 30-year risk was similar for both sexes; with some variation by age. Overall, the 30-year risk exceeded 1 in 2 persons for “overweight or more,” 1 in 4 for obesity, and 1 in 10 for stage II obesity (BMI ≥30), across different age groups. The 30-year estimates correspond to the lifetime risk for overweight or more or obesity for participants 50 years of age.248
The age-adjusted prevalence of overweight increased from 55.9% in NHANES III (1988–94) to 65.1% in NHANES (1999–2002). The prevalence of obesity also increased during this period from 22.9% to 30.4%. Extreme obesity (BMI of 40.0 or higher) increased from 2.9% to 4.9%.245
Since 1993, the prevalence of those who are obese increased over 61%. Among states in 2002, West Virginia had the highest rate of obesity and Colorado had the lowest (www.cdc.gov/brfss).
Data from the BRFSS study of the CDC showed that in participants ages 18–24, studied from 1990–2000, obesity increased among every ethnic group, especially in black women. Almost 20% of black women were obese by ages 18–24, increasing to over 35% by ages 25–44. Between one-third and one-half of those surveyed ate fewer than 3 servings of fruits and vegetables a day, although older black men and older Hispanic men and women improved dramatically in that regard between 1990 and 2000.23
Abdominal obesity is an independent risk factor for ischemic stroke in all race/ethnic groups with an odds ratio (OR) about 3 times greater when comparing the first and fourth quartiles. This effect was larger for those under age 65 (OR=4.4) than over age 65 (OR=2.2). (NOMASS).249
A recent comparison of risk factors in both the HHP and FHS showed a BMI increase of around 3 kg/m2 raised the risk of hospitalized thromboembolic stroke by 10–30%.251
In 1998–99, surveys of people in 8 states and the District of Columbia by the BRFSS study of the CDC indicated that obesity rates are significantly higher among people with disabilities, especially blacks and those ages 45–64.252
Data from the FHS showed that overweight and obesity were associated with large decreases in life expectancy. Forty-year-old female nonsmokers lost 3.3 years and 40-year-old male nonsmokers lost 3.1 years of life expectancy because of overweight. In 40-year-old nonsmokers, females lost 7.1 years and males lost 5.8 years due to obesity. Obese female smokers lost 7.2 years and obese male smokers lost 6.7 years when compared to normal-weight nonsmokers.253
Data from the 1999–2003 NHIS study of the CDC/NCHS showed that American Indian or Alaska Native (AIAN) adults, age 18 and older, were as likely (30.4%) as black adults (30.8%) and less likely than white adults (40.9%) and Asian adults (62.8%) to be at a healthy weight.150
Data from the 1999–2003 NHIS study of the CDC/NCHS showed that American Indian or Alaska Native (AIAN) women, age 18 and older, were less likely (29.4%) than black women (36.6%) and more likely than white women (20.3%) and Asian women (5.8%) to be obese.150
According to the WHO, the number of overweight and obese people worldwide is set to increase to 1.5 billion by 2015 if current trends continue. Excessive weight and obesity are major risk factors for CVD, the No. 1 cause of death worldwide, claiming more than 17 million lives a year.254
Obesity was associated with nearly 112 000 excess deaths (95% confidence interval [CI], 53 754–170 064) and underweight with nearly 34 000 excess deaths (95% CI, 15 726–51 766).255
Among people diagnosed with type 2 diabetes, 67% have a BMI ≥27 and 46% have a BMI ≥30. An estimated 70% of diabetes risk in the United States can be attributed to excess weight (win.niddk.nih.gov).
The age-adjusted prevalence of hypertension in overweight US adults is 22.1% for men with BMI >25 and <27; 27.0% for men with BMI ≥27 and <30; 27.7% for women with BMI ≥25 and <27; and 32.7% for women with BMI ≥27 and <30. In comparison, the prevalence in adults who are obese (BMI ≥30) is 41.9% for men and 37.8% for women (win.niddk.nih.gov/statistics).
The age-adjusted prevalence of high blood cholesterol (≥240 mg/dL) in overweight US adults is 19.1% for men with BMI ≥25 and <27; 21.6% for men with BMI ≥27 and <30; 30.5% for women with BMI ≥25 and <27; and 29.6% for women with BMI ≥27 and <30. In comparison, the prevalence of high cholesterol in adults who are not overweight (BMI <25) is 13.0% for men and 13.4% for women. The prevalence for adults who are obese (BMI ≥30) is 22.0% for men and 27.0% for women (win.niddk.nih.gov/statistics).
Among children and adolescents, annual hospital costs related to obesity were $127 million during 1997–99. (CDC. “Preventing Obesity and Chronic Diseases Through Good Nutrition and Physical Activity”256)
The estimated cost of overweight and obesity, in 2001 dollars, is $117 billion. Direct cost is $61 billion and the indirect cost is $56 billion. The direct cost of heart disease related to overweight and obesity, independent of stroke, is $8.8 billion. For type 2 diabetes, it’s $98 billion. For hypertension, it’s $4.1 billion. The cost of lost productivity related to obesity (BMI >30) among Americans ages 17–64 is $3.9 billion (www.win.niddk.nih.gov).
(ICD/9 250) (ICD/10 E10–E14). See Table 9G.
|Population Group||Prevalence of Physician-Diagnosed Diabetes 2003||Prevalence of Undiagnosed Diabetes 2003||Prevalence of Pre-Diabetes 2003||Incidence of Diagnosed Diabetes||Mortality (Diabetes) 2003#||Hospital Discharges 2003||Cost 2002++|
|Note: Undiagnosed diabetes is defined here for those whose fasting glucose is 126 mg/dL or higher but who did not report being told they had diabetes by a health care provider. Pre-diabetes is a fasting blood glucose of 100 to less than 126 mg/dL (impaired fasting glucose). Pre-diabetes also includes impaired glucose tolerance.|
|(…) = data not available. NH = non-Hispanic.|
|*These percentages represent the portion of total DM mortality that is males vs. females.|
|**NHIS (2003), CDC/NCHS; data are estimates for Americans age 18 and older.|
|Sources: Prevalence: NHANES (1999–2002), CDC/NCHS and NHLBI; percentages for racial/ethnic groups are age-adjusted for Americans age 20 and older. Estimates from NHANES 1999–2002 applied to 2003 population estimates. Incidence: NIDDK estimates. Mortality: CDC/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, CDC/NCHS; data include people discharged alive and dead.|
|Total||14 100 0000 (6.7%)||6 000 000 (2.9%)||14 700 000 (7.0%)||1 500 000||73 965||597 000||$132 billion|
|Total males||7 000 000 (7.2%)||3 000 000 (3.0%)||8 600 000 (8.9%)||…||35 257 (47.7%)*||286 000||…|
|Total females||7 100 000 (6.3%)||3 000 000 (2.7%)||6 100 000 (5.4%)||…||38 748 (52.4%)*||314 000||…|
|NH white males||6.2%||3.0%||8.6%||…||28 765||…||…|
|NH white females||4.7%||2.7%||4.6%||…||30 189||…||…|
|NH black males||10.3%||1.3%||8.3%||…||5 401||…||…|
|NH black females||12.6%||6.1%||5.9%||…||7 419||…||…|
|Hispanic or Latino**||8.6%||…||…||…||…||…||…|
|American Indians/Alaska Natives**||12.2%||…||…||…||…||…||…|
The prevalence of diabetes increased by 8.2% from 2000–01. Since 1990, the prevalence of those diagnosed with diabetes increased 61%. In 2001, Alabama had the highest rate of diagnosed diabetes (10.5%) and Minnesota had the lowest (5.0%).257
From 1994–2002, the age-adjusted prevalence of diabetes increased 54.0% for US adults (from 4.8% to 7.3%), and increased 33.2% (from 11.5% to 15.3%) among American Indian or Alaska Native adults. The overall age-adjusted prevalence for American Indian or Alaska Native adults was more than twice that of US adults overall.258
Based on data from the NHANES studies of the CDC/NCHS, in 1976–80, total diabetes prevalence in African Americans ages 40–74 was 8.9%; in 1988–94 the rate was 18.2%, a doubling of the rate in just 12 years. In 1988–94, among people ages 40–74, the prevalence rate was 18.2% for African Americans compared to 11.2% for whites.259
Data from the NHANES (1999–2000) study of the CDC/NCHS showed a disproportionately high prevalence of diabetes in NH blacks and Mexican Americans when compared to NH whites. For previously diagnosed diabetes the percentage was 11.7 for NH blacks and 9.6 for Mexican Americans compared to 4.8 for NH whites. For undiagnosed diabetes the percentages were 3.2, 2.4 and 2.6, respectively. For impaired fasting glucose the percentages were 6.3, 6.7 and 5.7, respectively.260
BRFSS data in selected areas, 1998–2002, showed that diabetes disproportionately affects Hispanics in the United States and Puerto Rico. Hispanics were twice as likely to have diabetes as NH whites of similar age (9.8% versus 5.0%). This disparity, however, varied by geographic location—it was lowest in Florida and higher in California, Texas, and Puerto Rico. Among Hispanic adults in California, Florida, Illinois, New York/New Jersey, Puerto Rico and Texas, the overall prevalence of diabetes was 7.4%; it ranged from 6.2% in Illinois and New York/New Jersey to 9.3% in Puerto Rico.261
About 15% of American Indians or Alaska Natives who receive care from the Indian Health Service have been diagnosed with diabetes. On average, American Indians or Alaska Natives are 2.6 times as likely to have diagnosed diabetes as NH whites of the same age (niddk.nih.gov, 2004).
The prevalence of diabetes for all age groups worldwide was estimated to be 2.8% in 2000 and a projected 4.4% in 2030. The total number of people with diabetes is projected to rise from 171 million in 2000 to 366 million in 2030.262
Type 2 diabetes may account for 90–95% of all diagnosed cases of diabetes (niddk.nih.gov, 2004).
In April 2004, the USDHHS announced that about 40% of US adults ages 40–74, or 41 million, currently have pre-diabetes, a condition that raises a person’s risk of developing type 2 diabetes, heart disease and stroke. Many don’t know that they are at risk or that they have pre-diabetes.263
In the United States each year, over 13 000 children are diagnosed with type 1 diabetes. Increasingly, healthcare providers are finding more and more children and teens with type 2 diabetes. Some clinics report that one-third to one-half of all new cases of childhood diabetes are now type 2. African-American, Hispanic or Latino and American Indian children who are obese and have a family history of type 2 diabetes are at especially high risk for this type of diabetes (niddk.nih.gov, 2004).
Mortality as an underlying or contributing cause of death—224 100.
The 2003 overall death rate from diabetes was 25.2. Death rates were 26.8 for white males, 50.5 for black males, 20.0 for white females and 47.3 for black females.
At least 65% of people with diabetes mellitus die of some form of heart or blood vessel disease.264
Heart disease death rates among adults with diabetes are 2–4 times higher than the rates for adults without diabetes (diabetes.niddk.nih.gov).
Death rates for people with diabetes are 27% higher for African Americans compared with whites (niddk.nih.gov, 2004).
The age-adjusted prevalence of major CVD for women with diabetes is twice that for women without diabetes, and the age-adjusted major CVD hospital discharge rate for women with diabetes is almost 4 times the rate for women without diabetes.265
A population-based study of over 13 000 men and women in Denmark showed that in people with type 2 diabetes, the RR of first, incident and admission for MI was increased 1.5–4.5-fold in women and 1.5–2-fold in men. The RR of first, incident and admission for stroke was increased 2–6.5-fold in women and 1.5–2-fold in men, with a significant difference between the sexes. In both men and women the RR of death was increased 1.5–2 times.266
Diabetes increases the risk of stroke, with the RR ranging from 1.8 to almost 6.0.267
Ischemic stroke patients with diabetes are younger, more likely to be African American and more likely to have hypertension, MI, and high cholesterol than nondiabetic patients. Diabetes increases ischemic stroke incidence at all ages, but this risk is most prominent before age 55 in African Americans and before age 65 in whites.95
Compared with white women, black women have a 138% higher rate of ambulatory medical care visits for diabetes.268
Based on data from the CDC Diabetes Surveillance System, 1997–2000:
–In 2000, the age-standardized prevalence of any self-reported cardiovascular condition among persons with diabetes age 35 and older was 37.5% for white men, 32.2% for white women, 31.4% for black men, 34.0% for black women, 23.9% for Hispanic men and 22.9% for Hispanic women.
–In 2000, the self-reported prevalence of any cardiovascular condition was 28.8 per 100 diabetic population among persons ages 35–64, 45.7 per 100 diabetic population among persons ages 65–74, and 53.5 per 100 diabetic population among persons age 75 and older.
–In 2000, among persons with diabetes age 35 and older, 37.2% reported being diagnosed with a cardiovascular condition, (ie, CHD, stroke or other cardiovascular condition).
–In 2000, among persons with diabetes age 35 and older, the age-standardized prevalence of self-reported CHD, angina or heart attack, was almost 3 times that of self-reported stroke (22.1% versus 8.0%).
–In 2000, 4.4 million persons age 35 and older with diabetes reported being diagnosed with a cardiovascular condition, 2.9 million were diagnosed with CHD (ie, self-reported CHD, angina or heart attack) and 1.1 million reported being diagnosed with a stroke.
–Approximately one-third of adults with diabetes received all 5 interventions recommended for comprehensive diabetes care in 2001. The proportion receiving all 5 interventions was lower among blacks compared with whites and among Hispanics compared with NH whites (2004 National Healthcare Disparities Report, AHRQ, USDHHS).
–The difference in hospital admissions for long-term complications between men and women is highly significant, with women 22% less likely than men to be admitted (2004 National Healthcare Disparities Report, AHRQ, USDHHS).
–In multivariate models controlling for age, gender, income, education, insurance and residence location, blacks were 38% less likely, and Hispanics were 33% less likely than their respective comparison groups to receive all services in 2001 (2004 National Healthcare Disparities Report, AHRQ, USDHHS).
Among US adults with diabetes, data from the NHANES surveys from 1971–74 to 1999–2000 showed that mean total cholesterol declined from 5.95 mmol/liter to 5.48 mmol/liter. The proportion with high cholesterol decreased from 72% to 55%. Mean blood pressure declined from 146/86 mm Hg to 134/72 mm Hg. The proportion with HBP decreased from 64% to 37%, and smoking prevalence decreased from 32% to 17%. Although these trends are encouraging, still 1 of 2 people with diabetes had high cholesterol, 1 of 3 had HBP, and 1 of 6 was a smoker.269
Data from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the NIH stated:
–Heart disease is the leading cause of diabetes-related death. Adults with diabetes have heart disease death rates about 2–4 times higher than adults without diabetes.
–The risk for stroke is 2–4 times higher among people with diabetes.
–About 73% of adults with diabetes have BP greater than or equal to 130/80 mm Hg or use prescription medication for hypertension.
–An estimated 49–69 million adults in the United States may have insulin resistance (personal communication with Earl Ford, MD, CDC/NCHS, 2003), and 1 in 4 of them will develop type 2 diabetes (ndep.nih.gov).
In 2002, the direct and indirect cost of diabetes was $132 billion.270
10. Metabolic Syndrome
The prevalence of metabolic syndrome (MetS) among 12–19-year-old US adolescents was estimated in an analysis of NHANES III data, by applying a modification of the ATP III definition (Third Report of the National Cholesterol Education Program [NCEP] Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults [ATP III, NHLBI]) for adults. MetS during adolescence was defined as 3 or more of the following abnormalities:
—Serum triglyceride level of 110 mg/dL or higher.
—High-density lipoprotein (HDL) cholesterol level of 40 mg/dL or lower.
—Elevated fasting glucose of 110 mg/dL or higher.
—Blood pressure at or above the 90th percentile for age, sex and height.
—Waist circumference at or above the 90th percentile for age and sex (NHANES III data set)
An estimated 1 million 12–19-year-old adolescents in the United States have MetS, or 4.2% overall (6.1% of males and 2.1% of females).272
–Of adolescents with MetS, 73.9% were overweight and 25.2% were at risk of overweight.
–The mean BMI of adolescents with the MetS (30.1%) was just above the 95th percentile of the CDC Growth Chart; thus they are likely to represent a fairly common clinical problem in pediatrics.
–MetS was present in 28.7% of overweight adolescents (BMI 95th percentile of CDC Growth Chart) compared with 6.8% of at-risk-of-overweight adolescents, and 0.1% of those with BMI below the 85th percentile (P<0.001).
–Among adolescents with MetS, 40.9% had 1 criterion; 14.2% had 2 criteria; 4.2% had 3 criteria and 0.9% had 4 criteria for MetS. For overweight adolescents, 88.5% had 1 criterion; 54.4% had 2 criteria; 28.7% had 3 criteria and 5.8% had 4 criteria for MetS.
Among more than 3400 children examined in 1 study, 1 in 10 had MetS.273
Using a sample of adolescents from NHANES III, the overall prevalence of MetS was 38.7% in moderately obese subjects and 49.7% in severely obese subjects. The prevalence of MetS in severely obese black subjects was 39%.274
People with MetS are at increased risk for developing diabetes and cardiovascular disease as well as increased mortality from CVD and all causes. Unless otherwise stated, the following data are based on the definition of the metabolic syndrome as determined in the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III, NHLBI).
An estimated 47 million US residents have MetS.275
The age-adjusted prevalence of MetS for adults is 23.7%.275
–The prevalence ranges from 6.7% among people ages 20–29 to 43.5% for ages 60–69 and 42.0% for those age 70 and older.
–The age-adjusted prevalence is similar for men (24.0%) and women (23.4%).
–Mexican Americans have the highest age-adjusted prevalence of MetS (31.9%). The lowest prevalence is among whites (23.8%), African Americans (21.6%) and people reporting an “other” race or ethnicity (20.3%).
–Among African Americans, women had about a 57% higher prevalence than men. Among Mexican Americans, women had a 26% higher prevalence than men did.
The prevalences of people with MetS are 24.3%, 13.9% and 20.8 % for white, black and Mexican-American men, respectively. For women the percentages are 22.9, 20.9 and 27.2, respectively.276
In a study of over 15 000 men and women, ages 45–64, in the ARIC study, MetS prevalence was 30% and 27% using ATP III and modified WHO definitions with substantial variation across race and gender subgroups. CHD prevalence was greater in those with than without MetS (ATP III 7.4% versus 3.6%; WHO 7.8% versus 3.6%, both P<0.0001). Using either definition, subjects with MetS were about 2 times more likely to have prevalent CHD than those without the syndrome after adjustment for established risk factors. Among individuals free of CVD, the average age, sex, and race/center-adjusted intima-media thickness (IMT) was greater among individuals with the syndrome (ATP III 747 versus 704, WHO 750 versus 705 micrometers, both P<0.0001). These data suggest that MetS was significantly associated with the presence of CHD and carotid IMT.277
See Table 11A.
|Mean Dietary Intake of Energy and 10 Key Nutrients for Public Health||Total Population||Males||Females|
|Source: NHANES (1999–2000), CDC/NCHS, 2003. (Advance Data, Vital and Health Statistics, No. 334, April 17, 2003).|
|Protein, % of calories||14.7%||14.9%||14.6%|
|Carbohydrate, % of calories||51.9%||50.9%||52.8%|
|Total fat, % of calories||32.7%||32.7%||32.6%|
|Saturated fat, % of calories||11.2%||11.2%||11.1%|
The Economic Research Service of the USDA suggests that the average daily calorie consumption in the United States increased by 12% between 1985 and 2000, or roughly 300 calories. Of that increase, grains (mainly refined grains) accounted for 46%, added fats 24%, added sugars 23%, fruits and vegetables 8%, and the meat and dairy groups together declined 1%. Per capita availability of total dietary fat, after remaining steady from 1985–99, jumped 6% in 2000. American diets tend to be low in whole grains and other nutritious foods.279
Between 1965 and 1991, among US adults age 18 and older, total daily calories declined from 2049 to 1807, but then rebounded to 2000 calories in 1996. This contributed to the marked increase in obesity levels in the past decade.280
In 1999–2000, among children ages 2–6, 20% had a good diet, 74% had a diet that needed improvement, and 6% had a poor diet. For those ages 7–12, 8% had a good diet, 79% had a diet that needed improvement, and 13% had a poor diet.281
Between 1988–94 and 1999–2000, the median caloric intake rose in boys ages 8–11 and 12–19. It rose a small amount in girls ages 6–11 and basically remained constant in girls ages 12–19.282
Between 1977 and 1996, portion sizes for key food groups grew markedly in the United States, not only at fast-food outlets but also in homes and at conventional restaurants. One study of portion sizes for typical items showed that:
–Salty snacks increased from 132 calories to 225 calories.
–Soft drinks increased from 144 calories to 193 calories.
–French fries increased from 188 calories to 256 calories.
–Hamburgers increased from 389 calories to 486 calories.283
Between 1965 and 1996 among adults, total fat as a proportion of daily calorie intake fell steadily from 39.1% to 33.1%. Saturated fat fell from 14.4% to 11.0%. However, total calorie intake increased between 1991 and 1996. Over the same period daily total fat consumption rose from 70.9 grams (g) to 74.8 g.280
The average daily intake of total fat in the United States is 81.4 grams (96.5 g for males and 67.3 g for females) (NHANES III [1988–94], CDC/NCHS).
–For NH whites the average is 82.7 g (99.0 g for males and 67.4 g for females).
–For NH blacks the average is 82.0 g (94.6 g for males and 71.2 g for females).
–For Mexican Americans the average is 77.6 g (88.0 g for males and 66.5 g for females).
The average daily intake of saturated fat in the United States is 27.9 g (33.1 g for males and 23.0 g for females) (NHANES III [1988–94], CDC/NCHS).
–For NH whites the average is 28.4 g (34.1 g for males and 23.1 g for females).
–For NH blacks the average is 27.5 g (31.7 g for males and 23.8 g for females).
–For Mexican Americans the average is 26.7 g (30.1 g for males and 23.1 g for females).
The proportion of fat calories from beef, pork, dairy products and eggs fell from 50% in 1965 to 33% in 1994–96. The proportion of fat calories from poultry increased from 4% to 7%. Calories from fruits and vegetables rose from 8% to 13%.280
In 1994–96, pizza, Mexican food, Chinese food, hamburgers, French fries and cheeseburgers accounted for 10.8% of total fat intake. These 6 foods accounted for only 1.9% of fat intake in 1965.280
The major sources of saturated fat in the diet are red meat, butter, whole milk and eggs. Intake of these foods has fallen markedly since 1965. The decline in whole milk consumption from 21.3 gallons in 1972–76 to 8.2 gallons in 1997 accounts for most of the reduction in saturated fat.280
According to USDA data, in 2001 total meat consumption (red meat, poultry and fish) amounted to 194 pounds per person, 16 pounds above the level in 1970. Each American consumed an average of 21 pounds less red meat (mostly beef) than in 1970, 34 pounds more poultry and 3.4 pounds more fish.279
The average daily intake of dietary cholesterol in the United States is 269.6 milligrams (mg). For males it’s 323.5 mg and for females it’s 218.9 mg (NHANES III [1988–94], CDC/NCHS).
–For NH whites the average is 259.3 mg (312.6 mg for males and 209.1 mg for females).
–For NH blacks the average is 297.9 mg (358.8 mg for males and 245.6 mg for females).
–For Mexican Americans the average is 316.2 mg (365.9 mg for males and 263.8 mg for females).
The recommended daily intake of dietary fiber is 25 g or more. Americans consume a daily average of 15.6 g of dietary fiber (17.8 g for males and 13.6 g for females) (NHANES III [1988–94], CDC/NCHS).
–For NH whites the average is 15.8 g (18.1 g for males and 13.7 g for females).
–For NH blacks the average is 13.4 g (15.0 g for males and 12.0 g for females).
–For Mexican Americans the average is 18.5 g (21.0 g for males and 15.9 g for females).
Analysis of participants in the Cardiovascular Health Study (CHS) showed that cereal fiber consumption late in life was associated with lower risk of incident CVD, supporting recommendations for elderly people to increase consumption of dietary cereal fiber.284
Despite USDA Food Pyramid recommendations to consume several daily servings of whole grains, in 1994–96, intake of whole grains for children was 1 serving or less.285
Most Americans consume less than 1 serving of whole grains a day, but between the early 1980s and 2000, consumption of refined grains increased. (Refined grains include white, whole wheat and durum flour, all of which have less nutritional value than whole grains).282
In 2000, 81% of men and 73% of women reported eating fewer than 5 servings of fruits and vegetables a day. More than 60% of young people eat too much fat, and less than 20% eat the recommended 5 or more servings of fruits and vegetables each day (CDC, BRFSS, 2000).
Only 22.7% of adults consumed fruits and vegetables at least 5 times a day in 1996. This was an increase from 19.0% in 1990 (BRFSS [1990–96], CDC).
The highest proportion of adults who consumed fruits and vegetables at least 5 times a day were those age 65 and older, whites, college graduates, those actively engaged in leisure-time physical activity, and nonsmokers.280
The percentage of males who consumed fruits and vegetables at least 5 times a day was 17.7 in 2003. For females the percentage was 27.0 (BRFSS 2003, CDC).
From 1990–96, the percentage of obese adults who consumed at least 5 servings of fruits and vegetables a day dropped from 16.8% to 15.4%.280
Recent studies support the intake of up to 9 servings of fruits and vegetables per day.286
In 2003, the percentage of students in grades 9–12 who reported eating fruits and vegetables 5 or more times per day was 23.6% for males and 20.3% for females.287
–Black students (24.5%) were more likely than white students (20.2%) to have eaten 5 or more servings per day. This racial/ethnic difference was significantly higher for male students.
From 1994–96 for children ages 6–19, only 14% met then-current USDA Food Pyramid recommendations for daily fruit intake (2–4 servings per day). Only 20% got enough vegetables (3–5 servings per day).288
In 1980, about 50% of high school seniors reported eating green vegetables “nearly every day or more.” By 2003, that figure had dropped to about 30%.289
Each year over $33 billion in medical costs and $9 billion in lost productivity due to heart disease, cancer, stroke and diabetes are attributed to diet (CDC).
12. Quality of Care
The Institute of Medicine defines quality of care as “the degree to which health services for individuals and populations increase the likelihood of desired health outcomes and are consistent with current professional knowledge.”290
This section of the Update highlights national data on quality of care for several cardiovascular conditions. It is intended to serve as a benchmark for current care and to stimulate efforts to improve the quality of cardiovascular care nationally. Where possible, data is reported from standardized quality indicators (ie, those consistent with the methods for quality performance measures endorsed by the American College of Cardiology and American Heart Association291 Additional data on aspects of quality of care such as compliance with ACC/AHA clinical practice guidelines is also included to provide a spectrum of quality-of-care data.
Nearly 3800 patient medical records from 38 US hospitals showed that among patients with AF and at high risk for stroke, only 54.7% received warfarin sodium, and 20.6% received neither aspirin nor warfarin. Of patients with AMI, only 75.5% received aspirin on hospital arrival. After orthopedic surgery procedures, only 85.6% received prophylaxis with a parenteral anticoagulant agent or warfarin. In 49.4% of patients with DVT, PE, or both, unfractionated or low-molecular-weight heparin use was discontinued before an international normalized ratio of 2.0 or greater was achieved for 2 consecutive days. Patients with DVT or PE were rarely discharged from the hospital with bridge therapy (an injectable anticoagulant agent plus warfarin), although the length of hospitalization was significantly shorter than if discharged taking warfarin alone.294
During the 7-year study period of data from all managed care plans administered by Medicare, clinical performance improved on all measures for both white and black enrollees. However, racial disparities did not decrease for glucose control among patients with diabetes or for cholesterol control among patients with cardiovascular disorders.295
Using Medicare data from 1992–2001, the rates of receipt for 9 surgical procedures previously shown to have disparities in the rates at which they were performed in white and black patients, was examined. The rates of receipt for all 9 procedures were higher among whites than blacks. The difference between the rates among whites and blacks increased significantly between 1992 and 2001 for 5 of the 9 procedures, remained unchanged for 3 procedures, and narrowed significantly for 1 procedure. Rates of CABG, carotid endarterectomy and total hip replacement in 158 hospital-referral regions were examined. In the early 1990s, whites had higher rates for these procedures than blacks in every hospital-referral region. By 2001, the disparity in the rates of these procedures narrowed significantly in 22 hospital-referral regions, widened significantly in 42, and was not significantly changed in the remaining regions. At the end of the study period, no hospital-referral region was found in which the difference in rates between whites and blacks was eliminated for men or women with regard to any of those 3 procedures.296
Using data from 1994–2002 from the National Registry of Myocardial Infarction (NRMI), sex and racial differences in the treatment of patients deemed to be “ideal candidates” for particular treatments, and differences in deaths among 598 911 patients hospitalized with MI were examined. It was found that rates of reperfusion therapy, coronary angiography, and in-hospital death after MI, but not the use of aspirin and beta-blockers, vary according to race and sex, with no evidence that the differences have narrowed in recent years.297
Based on data from the American Board of Psychiatry and Neurology (ABPN), there are 240 board-certified vascular neurologists (August 2005).
In 2002, there were 16 989 doctors of medicine with a specialty of cardiovascular diseases (Health, United States, 2004. CDC/NCHS).
As of Sept. 28, 2005, there were 175 total certified primary stroke centers by JCAHO standards.
13. Medical Procedures
From 1979–2003, the total number of inpatient cardiovascular operations and procedures increased 470%.
From 1979–2003, the number of cardiac catheterizations increased 373%.
An estimated 1 414 000 inpatient cardiac catheterizations were performed in 2003.
The mean charge for patients hospitalized for diagnostic cardiac catheterization increased from $11 611 in 1993 to $24 893 in 2003. The total number of patients increased from 628 962 to 728 786, while the average length of stay decreased from 4.9 days to 3.7 days.298
Coronary Artery Bypass Surgery
In the United States in 2003, the NCHS estimates that 467 000 of these procedures were performed on 268 000 patients.
Compared with Canadian patients, US patients were older, more likely to be female, and discharged from the hospital sooner. In-hospital costs of treatment were substantially higher in the United States than in Canada. After controlling for demographic and clinical differences, length of stay in Canada was 16.8% longer than in the United States; there was no difference in in-hospital mortality; and the cost in the United States was 82.5% higher than in Canada.299
In 2004, 2016 heart transplants were performed in the United States. There are 309 organ transplant centers in the United States, 186 of which perform heart transplants.
In the United States, 72.6% of heart transplant patients are male, 70.4% are white, 20.0% are ages 35–49, and 46.1% are ages 50–64.
As of July 15, 2005, the 1-year survival rate for males was 86.4% and for females it was 84.6%; the 3-year rate was 78.9% for males and 76.1% for females, and the 5-year rate was 72.2% for males and 68.5% for females.
As of July 15, 2005, there were 3142 heart patients on the transplant waiting list.
Percutaneous Coronary Intervention (PCI, previously referred to as PTCA)
An estimated 664 000 PCI procedures were performed on 652 000 patients in 2003 in the United States. From 1987–2003, the number of procedures increased 326%.
In 2003, 65% of PCI procedures were performed on men, and 52% were performed on people age 65 and older.
The rate of coronary stent insertion increased 147% between 1996 and 2000. Among the elderly, this procedure increased 168% during the same period. The rate of stent insertion also more than doubled for the population 45–64 years of age, increasing from 157 to 318 per 100 000.300
In 2003, approximately 84% of 660 000 hospitalized patients who underwent a coronary angioplasty received a stent. Black and white patients were equally likely to receive a stent. However, white patients were more likely than black patients to receive a drug-eluting stent.301
14. Economic Cost of Cardiovascular Diseases
The cost of cardiovascular diseases and stroke in the United States for 2006 is estimated at $403.1 billion. This figure includes health expenditures (direct costs, which include the cost of physicians and other professionals, hospital and nursing home services, the cost of medications, home health care and other medical durables) and lost productivity resulting from morbidity and mortality (indirect costs). By comparison, in 2004 the estimated cost of all cancers was $190 billion ($69 billion in direct costs, $17 billion in morbidity indirect costs and $104 billion in mortality indirect costs). In 1999, the estimated cost of HIV infections was $28.9 billion ($13.4 billion direct and $15.5 billion indirect).
|Heart Diseases**||Coronary Heart Disease||Stroke||Hypertensive Disease||Heart Failure||Total Cardiovascular Disease*|
|Note: N/A = data not available.|
|*Totals do not add up due to rounding and overlap.|
|**This category includes coronary heart disease, congestive heart failure, part of hypertensive disease, cardiac dysrhythmias, rheumatic heart disease, cardiomyopathy, pulmonary heart disease, and other or ill-defined “heart” diseases.|
|#Tom Hodgson and Liming Cai (Medical Care 2001) estimated that healthcare expenditures attributed to hypertension that could be allocated to cardiovascular complications and other diagnoses totaled $108 billion in 1997.|
|##Lost future earnings of persons who will die in 2006, discounted at 3%.|
|Sources: Hodgson and Cohen.302|
|National Health Expenditures Amounts, and Average Annual Percent Change, by Type of Expenditure: Selected Calendar Years 1990–2013.303|
|Rice et al.304|
|Historic Income Tables — People (census.gov).|
|Deaths for 358 Selected Causes by 5-Year Age Groups, Race, and Sex, United States, 2002.305|
|Rice, Max, Michel, and Sung. Present Value of Lifetime Earnings, U.S. 2003 Unpublished tables, Institute for Health and Aging, University of California, San Francisco, 2005.|
|All estimates prepared by Thomas Thom, NHLBI.|
|Home health care||$5.2||$1.6||$3.1||$1.7||$2.4||$11.8|
15. At-a-Glance Summary Tables
|Diseases and Risk Factors||Total||Total Males||White Males||Black Males||Mexican-American Males|
|Note: AP = angina pectoris (chest pain); BMI = body mass index; CHD = coronary heart disease; includes heart attack, angina pectoris (chest pain) or both; CVD = cardiovascular disease; K = thousands; M = millions; MI = myocardial infarction (heart attack); mg/dL = milligrams per deciliter; (…) = data not available.|
|*New and recurrent heart attacks and fatal CHD.|
|††Regular leisure-time physical activity.|
|Sources: See summary tables for each chapter in this update. For data on men in other ethnic groups, see other chapters and Statistical Fact Sheets (http://www.americanheart.org/presenter.jhtml?identifier=2007).|
|Prevalence 2003||71.3 M (34.2%)||33.1 M (34.4%)||34.3%||41.1%||29.2%|
|Mortality 2003#||910.6 K||426.8 K||368.2 K||49.0 K||…|
|Coronary heart disease|
|Prevalence 2003 CHD||13.2 M (6.9%)||7.2 M (8.4%)||8.9%||7.4%||5.6%|
|Prevalence 2003 MI||7.2 M (3.5%)||4.2 M (5.0%)||5.1%||4.5%||3.4%|
|Prevalence 2003 AP||6.5 M (3.8%)||3.2 M (4.2%)||4.5%||3.1%||2.4%|
|New and recurrent CHD*||1.2 M||715.0 K||650.0 K||65.0 K||…|
|New and recurrent MI||865.0 K||520.0 K||…||…||…|
|Incidence AP (stable angina)||400.0 K||…||…||…||…|
|Mortality 2003 CHD#||479.3 K||245.4 K||216.2 K||24.0 K||…|
|Mortality 2003 MI#||171.0 K||89.7 K||79.4 K||8.4 K||…|
|Prevalence 2003||5.5 M (2.6%)||2.4 M (2.5%)||2.3%||4.0%||2.6%|
|New and recurrent strokes||700.0 K||327.0 K||277.0 K||50.0 K||…|
|Mortality 2003#||157.8 K||61.6 K||51.8 K||7.8 K||…|
|High blood pressure|
|Prevalence 2003||65.0 M (32.3%)||29.4 M||30.6%||41.8%||27.8%|
|Mortality 2003#||52.6 K||21.5 K||15.6 K||5.4 K||…|
|Prevalence 2003||5.0 M (2.3%)||2.4 M (2.6%)||2.5%||3.1%||2.7%|
|Mortality 2003#||57.2 K||22.3 K||18.9 K||2.1 K||…|
|Prevalence 2004||44.3 M (20.9%)||24.1 M (23.4%)||24.1%||23.9%||18.9%†|
|Total cholesterol 200 mg/dL+||99.9 M (49.8%)||48.4 M (48.9%)||48.9%||41.6%||51.9%|
|Total cholesterol 240 mg/dL+||34.5 M (17.3%)||16.4 M (16.3%)||16.5%||12.2%||16.7%|
|LDL cholesterol 130 mg/dL+||76.1 M (39.5%)||39.1 M (43.1%)||43.8%||36.0%||43.7%|
|HDL cholesterol <40 mg/dL||46.0 M (22.6%)||33.2 M (33.6%)||34.5%||22.7%||34.4%|
|Overweight and obesity|
|Overweight BMI 25.0 or higher||136.5 M (65.1%)||69.6 M (68.8%)||69.4%||62.9%||73.1%|
|Obesity BMI 30.0 or higher||64.0 M (30.4%)||27.9 M (27.6%)||28.2%||27.9%||27.3%|
|Physician-diagnosed diabetes||14.1 M (6.7%)||7.0 M (7.2%)||6.2%||10.3%||10.4%|
|Undiagnosed diabetes||6.0 M (2.9%)||3.0 M (3.0%)||3.0%||1.3%||3.5%|
|Pre-diabetes||14.7 M (7.0%)||8.6 M (8.9%)||8.6%||8.3%||8.7%|
|Mortality 2003#||74.0 K||35.3 K||28.8 K||5.4 K||…|
|Diseases and Risk Factors||Total||Total Females||White Females||Black Females||Mexican-American Females|
|Note: AP = angina pectoris (chest pain); BMI = body mass index; CHD = coronary heart disease; includes heart attack, angina pectoris (chest pain) or both; CVD = cardiovascular disease; K = thousands; M = millions; MI = myocardial infarction (heart attack); mg/dL = milligrams per deciliter; (…) = data not available.|
|*New and recurrent heart attacks and fatal CHD.|
|††Regular leisure-time physical activity.|
|Sources: See summary tables for each chapter in this update. For data on women in other ethnic groups, see other chapters and Statistical Fact Sheets (http://www.americanheart.org/presenter.jhtml?identifier=2007).|
|Prevalence 2003||71.3 M (34.2%)||38.2 M (33.9%)||32.4%||44.7%||29.3%|
|Mortality 2003#||910.6 K||483.8 K||419.2 K||55.8 K||…|
|Coronary heart disease|
|Prevalence 2003 CHD||13.2 M (6.9%)||6.0 M (5.6%)||5.4%||7.5%||4.3%|
|Prevalence 2003 MI||7.2 M (3.5%)||3.0 M (2.3%)||2.4%||2.7%||1.6%|
|Prevalence 2003 AP||6.5 M (3.8%)||3.3 M (3.6%)||3.5%||4.7%||2.2%|
|New and recurrent CHD*||1.2 M||485.0 K||425.0 K||60.0 K||…|
|New and recurrent MI||865.0 K||345.0 K||…||…||…|
|Incidence AP (stable angina)||400.0 K||…||…||…||…|
|Mortality 2003 CHD#||479.3 K||233.9 K||205.0 K||24.9 K||…|
|Mortality 2003 MI#||171.0 K||81.3 K||71.1 K||8.9 K||…|
|Prevalence 2003||5.5 M (2.6%)||3.1 M (2.6%)||2.6%||3.9%||1.8%|
|New and recurrent strokes||700.0 K||373.0 K||312.0 K||61.0 K||…|
|Mortality 2003#||157.8 K||96.2 K||83.2 K||10.8 K||…|
|High blood pressure|
|Prevalence 2003||65.0 M (32.3%)||35.6 M||31.0%||45.4%||28.7%|
|Mortality 2003#||52.6 K||31.1 K||23.9 K||6.5 K||…|
|Prevalence 2003||5.0 M (2.3%)||2.6 M (2.1%)||1.9%||3.5%||1.6%|
|Mortality 2003#||57.2 K||34.9 K||33.4 K||3.2 K||…|
|Prevalence 2004||44.3 M (20.9%)||20.2 M (18.5%)||20.4%||20.2%||10.9%†|
|Total cholesterol 200 mg/dL+||99.9 M (49.8%)||51.5 M (50.2%)||52.1%||46.8%||44.8%|
|Total cholesterol 240 mg/dL+||34.5 M (17.3%)||18.1 M (17.8%)||18.4%||17.4%||13.6%|
|LDL cholesterol 130 mg/dL+||76.1 M (39.5%)||37.0 M (35.8%)||36.9%||34.5%||31.3%|
|HDL cholesterol <40 mg/dL||46.0 M (22.6%)||12.8 M (12.6%)||12.4%||11.3%||15.4%|
|Overweight and obesity|
|Overweight BMI 25.0 or higher||136.5 M (65.1%)||66.9 M (61.6%)||57.2%||77.2%||71.7%|
|Obesity BMI 30.0 or higher||64.0 M (30.4%)||36.1 M (33.2%)||30.7%||49.0%||38.4%|
|Physician-diagnosed diabetes||14.1 M (6.7%)||7.1 M (6.3%)||4.7%||12.6%||11.3%|
|Undiagnosed diabetes||6.0 M (2.9%)||3.0 M (2.7%)||2.7%||6.1%||1.8%|
|Pre-diabetes||14.7 M (7.0%)||6.1 M (5.4%)||4.6%||5.9%||7.2%|
|Mortality 2003#||74.0 K||38.7 K||30.2 K||7.4 K||…|
|Diseases and Risk Factors||Total||Whites||Blacks||Mexican Americans||Hispanics/Latinos|
|Note: AP = angina pectoris (chest pain); BMI = body mass index; CHD = coronary heart disease; includes heart attack, angina pectoris (chest pain) or both; CVD = cardiovascular disease; K = thousands; M = millions; MI = myocardial infarction (heart attack); mg/dL = milligrams per deciliter; (…) = data not available.|
|*New and recurrent heart attacks and fatal CHD.|
|†BRFSS (1997). MMWR, Vol. 49, No. SS-2, March 24, 2000.|
|††Regular leisure-time physical activity.|
|Sources: See summary tables for each chapter in this update. For data on other ethnic groups, see other chapters and Statistical Fact Sheets (http://www.americanheart.org/presenter.jhtml?identifier=2007).|
|Prevalence 2003||71.3 M (34.2%)||34.3%||32.4%||41.1%||44.7%||29.2%||29.3%||…||…|
|Mortality 2003#||910.6 K||368.2 K||419.2 K||49.0 K||55.8 K||…||…||…||…|
|Coronary heart disease|
|Prevalence 2003 CHD||13.2 M (6.9%)||8.9%||5.4%||7.4%||7.5%||5.6%||4.3%||4.5%|
|Prevalence 2003 MI||7.2 M (3.5%)||5.1%||2.4%||4.5%||2.7%||3.4%||1.6%||…||…|
|Prevalence 2003 AP||6.5 M (3.8%)||4.5%||3.5%||3.1%||4.7%||2.4%||2.2%||…||…|
|New and recurrent CHD*||1.2 M||650.0 K||425.0 K||65.0 K||60.0 K||…||…||…||…|
|Mortality 2003 CHD#||479.3 K||216.2 K||205.0 K||24.0 K||24.9 K||…||…||…||…|
|Mortality 2003 MI#||171.0 K||79.4 K||71.1 K||8.4 K||8.9 K||…||…||…||…|
|Prevalence 2003||5.5 M (2.6%)||2.3%||2.6%||4.0%||3.9%||2.6%||1.8%||2.2%|
|New and recurrent strokes||700.0 K||277.0 K||312.0 K||50.0 K||61.0 K||…||…||…||…|
|Mortality 2003#||157.8 K||51.8 K||83.2 K||7.8 K||10.8 K||…||…||…||…|
|High blood pressure|
|Prevalence 2003||65.0 M (32.3%)||30.6%||31.0%||41.8%||45.4%||27.8%||28.7%||19.0%|
|Mortality 2003#||52.6 K||15.6 K||23.9 K||5.4 K||6.5 K||…||…||…||…|
|Prevalence 2003||5.0 M (2.3%)||2.5%||1.9%||3.1%||3.5%||2.7%||1.6%||…||…|
|Mortality 2003#||57.2 K||18.9 K||33.4 K||2.1 K||3.2 K||…||…||…||…|
|Prevalence 2004||44.3 M (20.9%)||24.1%||20.4%||23.9%||20.2%||…||…||18.9%||10.9%|
|Total cholesterol 200 mg/dL+||99.9 M (49.8%)||48.9%||52.1%||41.6%||46.8%||51.9%||44.8%||…||…|
|Total cholesterol 240 mg/dL+||34.5 M (17.3%)||16.5%||18.4%||12.2%||17.4%||16.7%||13.6%||25.6%†|
|LDL cholesterol 130 mg/dL+||76.1 M (39.5%)||43.8%||36.9%||36.0%||34.5%||43.7%||31.3%||…||…|
|HDL cholesterol <40 mg/dL||46.0 M (22.6%)||34.5%||12.4%||22.7%||11.3%||34.4%||15.4%||…||…|
|Overweight and obesity|
|Overweight BMI 25.0 or higher||136.5 M (65.1%)||69.4%||57.2%||62.9%||77.2%||73.1%||71.7%||38.9%|
|Obesity BMI 30.0 or higher||64.0 M (30.4%)||28.2%||30.7%||27.9%||49.0%||27.3%||38.4%||24.7%|
|Physician-diagnosed diabetes||14.1 M (6.7%)||6.2%||4.7%||10.3%||12.6%||10.4%||11.3%||8.6%|
|Undiagnosed diabetes||6.0 M (2.9%)||3.0%||2.7%||1.3%||6.1%||3.5%||1.8%||…||…|
|Pre-diabetes||14.7 M (7.0%)||8.6%||4.6%||8.3%||5.9%||8.7%||7.2%||…||…|
|Mortality 2003#||74.0 K||28.8 K||30.2 K||5.4 K||7.4 K||…||…||…||…|
|Diseases and Risk Factors||Total||Total Males||Total Females||Whites||Blacks||Mexican Americans|
|Note: K = thousands; M = millions; mg/dL = milligrams per deciliter; overweight in children is body mass index (BMI) 95th percentile of the CDC 2000 growth chart; (…) = data not available.|
|†Regular leisure-time physical activity.|
|Sources: See summary tables for related chapters in this update. For more data on congenital defects, see Chapter 6, and our Statistical Fact Sheet, Congenital Cardiovascular Defects (http://www.americanheart.org/presenter.jhtml?identifier=3020898).|
|Congenital CV defects|
|Mortality 2002 (all ages)||4.2 K||2.2 K||2.0 K||1.7 K||1.6 K||0.4 K||0.3 K||…||…|
|Mortality 2002 (< age 15)||2.1 K||1.2 K||0.9 K||0.9 K||0.7 K||0.2 K||0.2 K||…||…|
|Prevalence ages 12–17:|
|Current cigarette use 1999–2001||…||13.3%||14.2%||14.9%||17.2%||8.2%||5.9%||11.4%||10.6%|
|High school students grades 9–12:|
|Current cigarette smoking 2003||…||21.8%||21.9%||23.3%||26.6%||19.3%||10.8%||19.1%*||17.7%*|
|Current cigar smoking 2003||…||19.9%||9.4%||21.3%||8.6%||19.5%||10.3%||14.9%*||12.2%*|
|Smokeless tobacco use 2003||…||11.0%||2.2%||13.2%||1.6%||4.1%||2.0%||6.1%*||3.3%*|
|Mean total cholesterol mg/dL||165||163||167||162||166||168||171||163||165|
|Mean HDL cholesterol mg/dL||…||…||…||48||50||55||56||51||52|
|Mean LDL cholesterol mg/dL||…||…||…||91||100||99||102||93||92|
|Prevalence 2003 grades 9–12:|
|Vigorous activity last 7 days||62.6%||70.0%||55.0%||71.9%||58.1%||65.0%||44.9%||66.7%*||51.8%*|
|Moderate activity last 7 days||24.7%||27.2%||22.1%||28.9%||23.3%||25.8%||17.5%||23.3%*||20.6%*|
|Preschool children ages 2–5††||>10%||…||…||8.6%||8.8%||13.1%|
|Children ages 6–11||3.8 M (15.8%)||2.1 M (16.9%)||1.7 M (14.7%)||14.0%||13.1%||17.0%||22.8%||26.5%||17.1%|
|Adolescents ages 12–19||5.3 M (16.1%)||2.8 M (16.7%)||2.5 M (15.4%)||14.6%||12.7%||18.7%||23.6%||24.7%||19.9%|
|Students grades 9–12||13.5%||17.4%||9.4%||16.2%||7.8%||19.5%||15.6%||21.7%*||11.8%*|
Age-Adjusted Rates—Used mainly to compare the rates of two or more communities, population groups or the nation as a whole, over time. The American Heart Association uses a standard population (2000), so that these rates aren’t affected by changes or differences in the age composition of the population.
AHRQ—Agency for Healthcare Research and Quality—A part of the US Department of Health and Human Services, this is the lead agency charged with supporting research designed to improve the quality of healthcare, reduce its cost, improve patient safety, decrease medical errors, and broaden access to essential services. AHRQ sponsors and conducts research that provides evidence-based information on healthcare outcomes; quality; and cost, use, and access. The information helps healthcare decisionmakers—patients and clinicians, health system leaders, and policymakers—make more informed decisions and improve the quality of healthcare services.
Bacterial Endocarditis—An infection of the heart’s inner lining (endocardium) or the heart valves. The bacteria that most often cause endocarditis are streptococci, staphylococci, and enterococci.
Body Mass Index (BMI)—A mathematical formula to assess body weight relative to height. The measure correlates highly with body fat. Calculated as weight in kilograms divided by the square of the height in meters (kg/m2).
Centers for Disease Control and Prevention/National Center for Health Statistics (CDC/NCHS)—An agency within the US Department of Health and Human Services (USDHHS). The CDC conducts the:
–Behavioral Risk Factor Surveillance System (BRFSS), an ongoing study.
The NCHS conducted the:
–National Ambulatory Medical Care Survey (NAMCS).
–National Health Examination Survey (NHES).
–National Health and Nutrition Examination Survey I (NHANES I, 1971–74).
–National Health and Nutrition Examination Survey II (NHANES II,1976–80).
–National Health and Nutrition Examination Survey III (NHANES III, 1988–94). Prevalence estimates for coronary heart disease, stroke and congestive heart failure are based on the self-reported questionnaire portion of this study. Exam-based estimates are being developed.
–National Health and Nutrition Examination Survey (NHANES, 1999–2002).
The NCHS also conducts these ongoing studies (among others):
–National Health Interview Survey (NHIS)
–National Hospital Ambulatory Medical Care Survey
–National Home and Hospice Care Survey
–National Hospital Discharge Survey
Centers for Medicare and Medicaid Services (CMS), formerly Health Care Financing Administration (HCFA)—The federal agency that administers the Medicare, Medicaid and Child Health Insurance Programs, which provide health insurance for more than 74 million Americans.
Comparability Ratio—Provided by the NCHS to allow time-trend analysis from one ICD revision to another. It compensates for the “shifting” of deaths from one causal code number to another. Its application to mortality based on one ICD revision means that mortality is “comparability-modified” to be more comparable to mortality coded to the other ICD revision.
Coronary Heart Disease (ICD/10 codes I20–I25)—This category includes acute myocardial infarction (I21–I22); other acute ischemic (coronary) heart disease (I24); angina pectoris (I20); atherosclerotic cardiovascular disease (I25.0); and all other forms of chronic ischemic heart disease (I25.1–I25.9).
Death Rate—The relative frequency with which death occurs within some specified interval of time in a population. National death rates are computed per 100 000 population. Dividing the mortality by the population gives a crude death rate. It’s restricted because it doesn’t reflect a population’s composition with respect to such characteristics as age, sex, race or ethnicity. Thus rates calculated within specific subgroups, such as age-specific or sex-specific rates, are often more meaningful and informative. They allow well-defined subgroups of the total population to be examined.
Diseases of the Circulatory System—ICD codes (I00–I99); included as part of what the American Heart Association calls “Cardiovascular Disease.” Mortality data for states can be obtained from cdc.gov/nchs, by direct communication with the CDC/NCHS, or from our National Center Biostatistics Program Coordinator on request. (See “Total Cardiovascular Disease” in this Glossary.)
Diseases of the Heart—Classification the NCHS uses in compiling the leading causes of death. Includes acute rheumatic fever/chronic rheumatic heart diseases (I00–I09); hypertensive heart disease (I11) and hypertensive heart and renal disease (I13); coronary heart disease (I20–I25); pulmonary heart disease and diseases of pulmonary circulation (I26–I28); heart failure (I50); and other forms of heart disease (I29–I49, I50.1–I51). “Diseases of the Heart” is not equivalent to “Total Cardiovascular Disease,” which the American Heart Association prefers to use to describe the leading causes of death. “Diseases of the Heart” represents about three-fourths of “Total Cardiovascular Disease” mortality.
Health Care Financing Administration (HCFA)—See Centers for Medicare and Medicaid Services (CMS).
Hispanic Origin—In US government statistics, “Hispanic” includes persons who trace their ancestry to Mexico, Puerto Rico, Cuba, Spain, the Spanish-speaking countries of Central or South America, the Dominican Republic or other Spanish cultures, regardless of race. It doesn’t include people from Brazil, Guyana, Suriname, Trinidad, Belize and Portugal because Spanish is not the first language in those countries. Much of our data are for Mexican Americans or Mexicans, as reported by government agencies or specific studies. In many cases, data for all Hispanics are more difficult to obtain.
Hospital Discharges—The number of inpatients discharged from short-stay hospitals where some type of disease was the first listed diagnosis. Discharges include people discharged alive and dead.
ICD Codes—A classification system in standard use in the United States. The “International Classification of Diseases” (ICD) is published by the World Health Organization. This system is reviewed and revised about every 10 to 20 years to ensure its continued flexibility and feasibility. The tenth revision (ICD/10) began with the release of 1999 final mortality data. The ICD revisions can cause considerable change in the number of deaths reported for a given disease. The NCHS provides “comparability ratios” to compensate for the “shifting” of deaths from one ICD code to another. In this update the reported mortality is used for one year’s data. To compare the number or rate of deaths with that of an earlier year, the “comparability-modified” number or rate is used.
Incidence—An estimate of the number of new cases of a disease that develop in a population in a one-year period. For some statistics, new and recurrent attacks or cases are combined. The incidence of a specific disease is estimated by multiplying the incidence rates reported in community- or hospital-based studies by the US population. The rates change only when new data are available; they are not computed annually.
Major Cardiovascular Diseases—Disease classification commonly reported by the NCHS; represents ICD codes I00–I78. The American Heart Association doesn’t use “Major CVD” for any calculations. See “Total Cardiovascular Disease” in this Glossary.
Metabolic Syndrome*—The metabolic syndrome is defined as having any 3 of the following 5 diagnostic measures: elevated waist circumference (≥102 cm. in men or ≥88 cm. in women); elevated triglycerides (≥150 mg/dL [1.7 mmol/L] or drug treatment for elevated triglycerides); reduced HDL (high density lipoprotein) cholesterol (<40 mg/dL [0.9 mmol/L] in men or <50 mg/dL [1.1 mmol/L] in women or drug treatment for reduced HDL cholesterol); elevated blood pressure (≥130 mm Hg systolic blood pressure or ≥85 mm Hg diastolic blood pressure or drug treatment for hypertension); elevated fasting glucose (≥100 mg/dL or drug treatment for elevated glucose). *According to criteria established by the American Heart Association/National Heart, Lung, and Blood Institute, in “Diagnosis and Management of the Metabolic Syndrome: An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement,” published in Circulation. (2005, Vol. 112, pages 2735-2752)
Morbidity—Incidence and prevalence rates are both measures of morbidity, that is, measures of various effects of disease on a population.
Mortality—The total number of deaths from a given disease in a population during a specific interval of time, usually a year. These data are compiled from death certificates and sent by state health agencies to the NCHS. The process of verifying and tabulating the data takes about two years. For example, 2002 mortality statistics, the latest available, didn’t become available until late 2004. Mortality is “hard” data, so it’s possible to do time-trend analysis and compute % changes over time.
National Heart, Lung, and Blood Institute (NHLBI)—An institute in the National Institutes of Health in the US Department of Health and Human Services. The NHLBI conducts such studies as the:
–Framingham Heart Study (FHS) (1948 to date).
–Honolulu Heart Program (HHP) (1965–97).
–Cardiovascular Health Study (CHS) (1988 to date).
–Atherosclerosis Risk in Communities (ARIC) study (1985 to date).
–Strong Heart Study (SHS) (1989–92; 1991–98).
The NHLBI also publishes: The reports of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. JNC 7 is the most recent. The report of the National Cholesterol Education Program, Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III, or ATP III).
National Institute of Neurological Disorders and Stroke (NINDS)—An institute in the National Institutes of Health in the US Department of Health and Human Services. The NINDS sponsors and conducts research studies such as these:
–Greater Cincinnati/Northern Kentucky Stroke Study (GCNKSS)
–Rochester (Minnesota) Stroke Epidemiology Project
–Northern Manhattan Stroke Study (NOMASS)
–Brain Attack Surveillance in Corpus Christi (BASIC) Project
Prevalence—An estimate of the total number of cases of a disease existing in a population at a specific point in time. Prevalence is sometimes expressed as a percentage of population. Rates for specific diseases are calculated from periodic health examination surveys that government agencies conduct. Annual changes in prevalence as reported in this booklet only reflect changes in the population; rates do not change until there’s a new survey.
NOTE: In the data tables which precede the different disease and risk factor categories, if the percentages shown are age-adjusted, they will not add to the total.
Race and Hispanic Origin—Race and Hispanic origin are reported separately on death certificates. In this publication, unless otherwise specified, deaths of Hispanic origin are included in the totals for whites, blacks, American Indians or Alaska Natives and Asian or Pacific Islanders, according to the race listed on the decedent’s death certificate. Data for Hispanic persons include all persons of Hispanic origin of any race. See “Hispanic Origin” in this Glossary.
Stroke (ICD/10 codes I60–I69)—This category includes subarachnoid hemorrhage (I60); intracerebral hemorrhage (I61); other nontraumatic intracranial hemorrhage (I62); cerebral infarction (I63); stroke, not specified as hemorrhage or infarction (I64); occlusion and stenosis of precerebral arteries, not resulting in cerebral infarction (I65); occlusion and stenosis of cerebral arteries, not resulting in cerebral infarction (I66); other cerebrovascular diseases (I67); cerebrovascular disorders in diseases classified elsewhere (I68) and sequalae of cerebrovascular disease (I69).
Total Cardiovascular Disease (ICD/10 codes I00–I99, Q20–Q28)—This category includes rheumatic fever/rheumatic heart disease (I00–I09); hypertensive diseases (I10–I15); ischemic (coronary) heart disease (I20–I25); pulmonary heart disease and diseases of pulmonary circulation (I26–I28); other forms of heart disease (I30–I52); cerebrovascular disease (stroke) (I60–I69); atherosclerosis (I70); other diseases of arteries, arterioles and capillaries (I71–I79); diseases of veins, lymphatics and lymph nodes, not classified elsewhere (I80–I89); and other and unspecified disorders of the circulatory system (I95–I99). When data are available, we include congenital cardiovascular defects (Q20–Q28).
ACS—acute coronary syndrome
ADHERE—Acute Decompensated HEart Failure National REgistry
AED—automated external defibrillator
AHA—American Heart Association
AHRQ—Agency for Healthcare Research and Quality
AIDS—acquired immune deficiency syndrome
AJC—American Journal of Cardiology
ARIC—Atherosclerosis Risk in Communities
ATP—Adult Treatment Panel
BMI—body mass index
BRFSS—Behavioral Risk Factor Surveillance System
BWIS—Baltimore-Washington Infant Study
CAD—coronary artery disease
CDC—Centers for Disease Control and Prevention
CHD—coronary heart disease
CHS—Cardiovascular Health Study
CMS—Centers for Medicare and Medicaid Services
COPD—Chronic obstructive pulmonary disease
CPI—Consumer Price Index
DVT—deep vein thrombosis
EMS—emergency medical services
ESRD—end-stage renal disease
FHS—Framingham Heart Study
GCNKSS—Greater Cincinnati/Northern Kentucky Stroke Study
GWTG—Get With The GuidelinesSM
HBP—high blood pressure
HCFA—Health Care Financing Administration
HCUP—Healthcare Cost and Utilization Project
HHP—Honolulu Heart Program
HIV—human immunodeficiency virus
ICD—International Classification of Diseases
ICDA—International Classification of Diseases, Adapted
JACC—Journal of the American College of Cardiology
JAMA—Journal of the American Medical Association
JCAHO—Joint Commission on Accreditation of Health Care Organizations
JNC—Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure
LVEF—left ventricular ejection fraction
MACDP—Metropolitan Atlanta Congenital Defects Program
mg/dL—milligrams per deciliter
mm Hg—millimeters of mercury
MMWR—Morbidity and Mortality Weekly Report
NCEP—National Cholesterol Education Program
NCHS—National Center for Health Statistics
NCQA—National Committee for Quality Assurance
NEJM—New England Journal of Medicine
NHANES—National Health and Nutrition Examination Survey
NHES—National Health Examination Survey
NHIS—National Health Interview Survey
NHLBI—National Heart, Lung, and Blood Institute
NIDDK—National Institute of Diabetes and Digestive and Kidney Diseases
NIHSS—National Institutes of Health Stroke Scale
NINDS—National Institute of Neurological Disorders and Stroke
NOMASS—Northern Manhattan Stroke Study
NRMI—National Registry of Myocardial Infarction
NVSS—National Vital Statistics System
PAD—peripheral arterial disease
PTCA—percutaneous transluminal coronary angioplasty
PVD—peripheral vascular disease
RHD—rheumatic heart disease
SCD—sudden cardiac death
SHS—Strong Heart Study
STEMI—ST elevation myocardial infarction
TIA—transient ischemic attack
UNOS—United Network for Organ Sharing
USDA—United States Department of Agriculture
USDHHS—United States Department of Health and Human Services
VSD—ventricular septal defect
WHO—World Health Organization
YLL—years of life lost
YMCLS—Youth Media Campaign Longitudinal Study
|Percent of Inpatients/Time|
|Mean rates for rate-based measures are based on aggregate calculations (dividing all patients who met the criterion by the total number of patients. Mean values for continuous variables are based on aggregated mean rates for each participating hospital weighted by the total number of patients included by each hospital. The average number of patients per hospital per quarter on which the summary data above were based ranged from 4 (for mean time to thrombolysis for acute MI) to 69 (for assessment of LV function for heart failure).|
|Acute myocardial infarction|
|Aspirin at admission||95%|
|Aspirin at discharge||95%|
|ACE inhibitor for LV systolic dysfunction||80%|
|Smoking cessation counseling||84%|
|β-Blocker at admission||91%|
|β-Blocker at discharge||93%|
|Mean time to thrombolysis||54 min|
|Mean time to PCI||293 min|
|Assessment of LV function||88%|
|ACE inhibitor for LV systolic dysfunction||77%|
|Smoking cessation counseling||72%|
|Percent of Inpatients|
|Plus-minus values are mean±standard deviation. Measures based on discharge data from at least 25 patients (per hospital) were defined as stable.|
|Acute myocardial infarction|
|Aspirin at admission||92 ±12|
|Aspirin at discharge||87 ±19|
|ACE inhibitor for LV systolic dysfunction||75 ±26|
|β-Blocker at admission||85 ±20|
|β-Blocker at discharge||84 ±19|
|Assessment of LV function||80 ±18|
|ACE-inhibitor for LV dysfunction||74 ±20|
|Percent of Inpatients|
|Acute myocardial infarction|
|Aspirin within 24 hours of admission||97%|
|Aspirin at discharge||98%|
|β-Blocker within 24 hours of admission||96%|
|β-Blocker at discharge||98%|
|ACE inhibitor for patients with LVEF <40%||93%|
|Smoking cessation advice given||93%|
|Documentation of LVEF||99%|
|ACE inhibitor for patients with LVEF <40%||93%|
|Complete discharge instructions||83%|
|Smoking cessation advice given||88%|
|Blood pressure at goal (<140/90)||72%|
|Cholesterol screening in all patients||94%|
|Cholesterol measured after acute MI||96%|
|LDL cholesterol <100 mg/dL after acute MI||60%|
|Performance Indicator||Percent of Inpatients|
|These data demonstrate the treatment gaps for each of the quality-of-care indicators. GWTG aims to bridge these gaps in care. Information on GWTG can be found on the American Heart Association Web site, www.americanheart.org.|
|Aspirin at discharge||92%|
|β-Blocker at discharge||86%|
|ACE inhibitor at discharge||67%|
|ACE inhibitor at discharge for AMI patients||71%|
|Lipid therapy at discharge||71%|
|Lipid therapy at discharge if LDL >100 mg/dL||79%|
|Blood pressure control (to <160/90) at discharge||74%|
|Smoking cessation counseling||82%|
|Referral to cardiac rehabilitation||64%|
|Performance Indicator||Percent of Inpatients|
|* indicates the 7 key performance measures targeted in GWTG–Stroke.|
|**A smaller denominator for IV tPA measures in the study population.|
|IV tPA in patients who arrived <2 hr after symptom onset*||45%|
|IV tPA in patients who arrived <3 hr after symptom onset||36%|
|Documentation of ineligibility (why no tPA)||87%|
|Symptomatic intracranial hemorrhage after IV tPA**||5%|
|Antithrombotics <48 hr*||95%|
|DVT prophylaxis <48 hr||78%|
|Antithrombotics at discharge*||97%|
|Anticoagulation for atrial fibrillation at discharge*||97%|
|Therapy at discharge if LDL >100 mg/dL or on therapy at admit*||76%|
|Counseling for smoking cessation*||60%|
|Lifestyle changes recommended for BMI >25 kg/m2||30%|
|Performance Indicator||Percent of Inpatients|
|1Excludes TIA patients.|
|2Includes patients who were discharged alive with final diagnosis of ischemic stroke or TIA.|
|3Includes patients who were discharged alive who were current smokers.|
|4Includes patients who were discharged alive with no physician-documented contraindication to treatment, and who had final diagnosis of ischemic stroke or TIA.|
|5Includes patients who had atrial fibrillation during hospitalization, who were discharged alive, who had no physician-documented contraindication to treatment, and who had final diagnosis of ischemic stroke or TIA.|
|Screening for dysphagia1||44%|
|Lipid profile checked2||40%|
|Smoking cessation counseling3||23%|
|Antithrombotic medication at discharge4||94%|
|Anticoagulation medication at discharge5||79%|
|Percent of Inpatients|
|These patients were hospitalized with a primary diagnosis of heart failure. The mean age was 72.3 years and 51% of them were female. Fifty-nine percent of HF patients had a medical history of coronary artery disease. Of patients with LV function measured (n=31 454), 50.3% had LVEF < 40% or showed moderate-to-severe impairment. Mechanical ventilation was required in 3.7% of patients. In-hospital mortality was 3.4% and mean length of hospital stay was 5.6 days (median 4.2 days).|
|Further information on the ADHERE registry can be found at adhereregistry.com.|
|JCAHO performance indicators|
|HF-1: Complete set of discharge instructions||61%|
|HF-2: Measure of LV function||89%|
|HF-3: ACE inhibitor at discharge for patients with LVSD, no contraindications to ACE inhibitors||74%|
|HF-4: Smoking cessation counseling, current smokers||67%|
|ACE inhibitor or ARB at discharge for patients with LVSD, no contraindications to ACE inhibitors||83%|
|β-Blockers at discharge for patients with LVEF <40%, no contraindications||77%|
|Overall||“Leading” Centers (Top 25%)||“Lagging” Centers (Bottom 25%)|
|*Excluding patients with contraindications to these therapies.|
|**Excluding patients with contraindications, transfers out, and deaths.|
|#Including only patients with history of hypertension, diabetes, CHF, and LVEF <40%.|
|+Including only patients with history of hyperlipidemia or LDL >100mg/dL.|
|***Excluding patients with contraindications to cardiac catheterization.|
|Note that not all of the treatment measures reported above are established quality indicators. Further information on the CRUSADE registry can be found at its Web site (www.CRUSADEQI.com).|
|Acute Medications* (Within 24 Hours)|
|Glycoprotein IIb/IIIa inhibitor, any||41%||57%||21%|
|ACE-I, among recommended#||62%||71%||48%|
|Lipid-lowering agent, overall||71%||81%||50%|
|Lipid-lowering agent, recommended+||83%||88%||67%|
|Cardiac catheterization, overall||73%||84%||43%|
|Cardiac catheterization, within 48 hours of presentation||52%||64%||26%|
|Diagnostic Cardiac Catheterization||Overall||“Leading” Centers (Mean Top 25%)||“Lagging” Centers (Mean Bottom 25%)|
|1Mortality in lab.|
|2,3Cerebrovascular accident, myocardial infarction, congestive heart failure, cardiac tamponade, renal failure.|
|4Bleeding, vessel occlusion, loss of distal pulse, dissection, psuedoaneurysm, arteriovenous fistula.|
|5Percentage of patients receiving antiplatelet therapy such as clopidogrel (Plavix) or ticlopidine (Ticlid) during admission.|
|6Percentage of PCI patients requiring emergency or coronary artery bypass surgery within same admission for: ischemic dysfunction including rest angina despite maximal medical therapy and/or intraaortic balloon pump; acute evolving MI within 24 hours before intervention; pulmonary edema requiring intubation; or shock with or without circulatory support.|
|7Often called “door-to-balloon time” or DBT, this is the elapsed time between entry to facility and reperfusion of the affected coronary vessel for patients with acute myocardial infarction treated with primary percutaneous coronary intervention (primary PCI).|
|8Percentage of Primary PCI patients with coronary reperfusion within 90 minutes of entry to facility.|
|9Percentage of Primary PCI patients with coronary reperfusion within 120 minutes of entry to facility.|
|10In-hospital mortality rate adjusted by ACC–NCDR Risk Adjustment Algorithm. This includes mortality for any reason whether or not related to the procedure.|
|PCI (percutaneous coronary intervention)|
|Antiplatelet drug administration5||94.14%||97.03%||98.59%||93.81%|
|DBT (door-to-balloon time)7||123.84 min||95.00 min||71.00 min||133.00 min|
|Pct. patients with DBT <90 minutes8||44.79%||44.44%||60.00%||29.81%|
|Pct. patients with DBT <120 minutes9||67.75%||70.83%||82.05%||57.03%|
|In-hospital risk-adjusted mortality10||1.13%||1.01%||0.71%||1.44%|
|Procedure||Mean Charges||In-Hospital Death Rate|
|Coronary artery bypass graft||$83 919||2.2%|
|Diagnostic cardiac catheterization||$24 893||1.0%|
|Cardiac pacemaker||$41 075||1.1%|
|Implantable defibrillator||$103 680||1.0%|
|Operations/Procedures/Patients (ICD/9 Code)||Total||Sex||Age||Region#|
|Note: (…) = data not available.|
|*Breakdowns are not available for some procedures, so entries for some categories don’t add to totals. These data include codes where the estimated number of procedures is fewer than 5000. Categories of such small numbers are considered unreliable by CDC/NCHS and in some cases may have been omitted.|
|**Totals include procedures not shown here.|
|#Regions: Northeast — Connecticut, Maine, Massachusetts, New Hampshire, New Jersey, New York, Pennsylvania, Rhode Island, Vermont; Midwest — Illinois, Indiana, Iowa, Kansas, Michigan, Minnesota, Missouri, Nebraska, North Dakota, Ohio, South Dakota, Wisconsin; South — Alabama, Arkansas, Delaware, District of Columbia, Florida, Georgia, Kentucky, Louisiana, Maryland, Mississippi, North Carolina, Oklahoma, South Carolina, Tennessee, Texas, Virginia, West Virginia; West — Alaska, Arizona, California, Colorado, Hawaii, Idaho, Montana, Nevada, New Mexico, Oregon, Utah, Washington, Wyoming.|
|(a) Does not include procedures in the outpatient or other non-hospitalized setting; thus, excludes some cardiac catheterizations and PCIs.|
|(b) Because one or more procedure codes are required to describe the specific bypass procedure performed, it’s impossible from this (mixed) data to determine the average number of grafts per patient.|
|(c) Includes valves, bypass and 104 000 “other” open-heart procedures (Codes 35 [less 35.1–35.2, 35.4, 35.96, 35.99]; 36 [less 36.0–36.1]; 37.1, 37.3–37.5).|
|(d) There are additional insertions, revisions and replacements of pacemaker leads, including those associated with temporary (external) pacemakers.|
|(e) Open heart valvuloplasty without replacement; replacement of heart valve; other operations on heart valves.|
|(f) Previously referred to as PTCA.|
|(g) 36.06: insertion of non–drug-eluting stents; 36.07: insertion of drug-eluting stents.|
|Source: Hospital Care Statistics Branch, CDC/NCHS. Estimates are based on a sample of inpatient records from short-stay hospitals in the United States (National Hospital Discharge Survey).|
|Note: These data do not reflect any procedures performed on an outpatient basis. Many more procedures are being performed on an outpatient basis. Some of the lower numbers in the table probably reflect this trend. Outpatient procedure data are not available at this time.|
|PCI (36.01, .02, .05) (a) (f)||Procedures||664||430||220||…||33||278||342||106||187||240||122|
|Stenting (36.06, .07) (g)||Procedures||574||378||196||…||34||244||296||93||160||210||111|
|Cardiac revascularization (bypass)|
|Diagnostic cardiac catheterizations|
|Implantable defibrillators (37.94–.99)||Procedures||64||50||11||…||…||18||32||12||13||22||8|
|Open-heart surgery (c)||Procedures||666||460||208||30||33||250||348||141||140||252||122|
|Pacemakers (37.8) (d)||Procedures||197||89||107||…||…||23||169||48||41||71||37|
|Valves (35.1, .2, .99) (e)||Procedures||95||54||42||…||6||27||53||20||14||33||24|
|Total vascular and cardiac surgery and Procedures (35–39)**||6821||3929||2892||229||647||2414||3530||1323||1508||2640||1350|
|mm Hg = millimeters of mercury. mg/dL = milligrams per deciliter of blood.|
|Blood pressure, mm Hg||120/80||140/90||140/90||140/90|
|Total cholesterol, mg/dL||200||240||240||240|
|HDL cholesterol, mg/dL||50||50||40||40|
|*Blood pressures are in millimeters of mercury (mm Hg).|
|Prior atrial fibrillation||No||No||No||No||Yes||Yes|
*The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention.
**In addition to these writing group members.
The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.
A single reprint is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Ave, Dallas, TX 75231-4596. Ask for reprint No. 71-0354. To purchase additional reprints: up to 999 copies, call 800-611-6083 (US only) or fax 413-665-2671; 1000 or more copies, call 410-528-4121, fax 410-528-4264, or e-mail [email protected] To make photocopies for personal or educational use, call the Copyright Clearance Center, 978-750-8400.
We wish to thank Drs. Joseph Broderick, Hong Chang, Michael Criqui, Brian Eigel, Gregg Fonarow, Mary Fran Hazinski, Kathy Jenkins, Alice Liechtenstein, Mary McDermott, Graham Nicole, Jerry Potts, Kathryn Taubert, and Christine Williams for their valuable comments and contributions. We would like to acknowledge Tim Anderson and Tom Schneider for their editorial assistance.
|Writing Group Member Name||Employment||Research Grant||Speakers Bureau/Honoraria||Stock Ownership||Consultant/Advisory Board||Other|
|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.|
|Nancy Haase||American Heart Association||None||None||None||None||None|
|Virginia J. Howard||University of Alabama at Birmingham||NIH, NINDS||None||None||None||Amgen|
|John Rumsfeld||University of Colorado at Denver and Health Sciences||None||None||None||Pfizer, Inc, CV Therapeutics, Inc., United Healthcare||None|
|Steven Kittner||University of Maryland School of Medicine||None||None||None||None||None|
|Donald M. Lloyd-Jones||Northwestern University Feinberg School of Medicine||None||Pfizer||None||Pfizer, Novartis||None|
|David Goff||Wake Forest University||None||Pfizer||None||Pfizer||None|
|Yuling Hong||American Heart Association||None||None||None||None||None|
- 1 CDC/NCHS, Vital Health Stat 10. July 2005; No. 225.Google Scholar
- 2 Hurst W. The Heart, Arteries and Veins. 10th ed. New York, NY: McGraw-Hill; 2002.Google Scholar
- 3 Strong Heart Study Data Book. Washington, DC: NIH, NHLBI; 2001.Google Scholar
- 4 U.S. Decennial Life Tables for 1989–91, Volume 1, No. 4. September 1999.Google Scholar
- 5 Centers for Disease Control and Prevention (CDC). Disparities in premature deaths from heart disease: 50 states and the District of Columbia, 2001. MMWR Morb Mortal Wkly Rep. 2004; 53: 121–125.MedlineGoogle Scholar
- 6 Healthy People 2000. Atlanta, Ga: CDC/NCHS, Jan. 2002. Statistical Notes No. 23.Google Scholar
- 6A Jacobs I, Nadkarni V, Bahr J, Berg RA, Billi JE, Bossaert L, Cassan P, Coovadia A, D’Este K, Finn J, Halperin H, Handley A, Herlitz J, Hickey R, Idris A, Kloeck W, Larkin GL, Mancini ME, Mason P, Mears G, Monsieurs K, Montgomery W, Morley P, Nichol G, Nolan J, Okada K, Perlman J, Shuster M, Steen PA, Sterz F, Tibballs J, Timerman S, Truitt T, Zideman D; International Liaison Committee on Resuscitation; American Heart Association; European Resuscitation Council; Australian Resuscitation Council; New Zealand Resuscitation Council; Heart and Stroke Foundation of Canada; InterAmerican Heart Foundation; Resuscitation Councils of Southern Africa; ILCOR Task Force on Cardiac Arrest and Cardiopulmonary Resuscitation Outcomes. Cardiac arrest and cardiopulmonary resuscitation outcome reports: update and simplification of the Utstein templates for resuscitation registries: a statement for healthcare professionals from a task force of the International Liaison Committee on Resuscitation (American Heart Association, European Resuscitation Council, Australian Resuscitation Council, New Zealand Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Councils of Southern Africa). Circulation. 2004; 110: 3385–3397.LinkGoogle Scholar
- 6B Fox CS, Evans JC, Larson MG, Lloyd-Jones DM, O’Donnell CJ, Sorlie PD, Manolio TA, Kannel WB, Levy D. A comparison of death certificate out-of-hospital coronary heart disease death with physician-adjudicated sudden cardiac death. Am J Cardiol. 2005; 95: 856–859.CrossrefMedlineGoogle Scholar
- 7 Zheng ZJ, Croft JB, Giles WH, Mensah GA. Sudden cardiac death in the United States, 1989 to 1998. Circulation. 2001; 104: 2158–2163.CrossrefMedlineGoogle Scholar
- 8 Vaillancourt C, Stiell IG, for the Canadian Cardiac Outcomes Research Team. Cardiac arrest care and emergency medical services in Canada. Can J Cardiol. 2004; 20: 1081–1090.MedlineGoogle Scholar
- 9 Rea TD, Eisenberg MS, Sinibaldi G, White RD. Incidence of EMS-treated out-of-hospital cardiac arrest in the United States. Resuscitation. 2004; 63: 17–24.CrossrefMedlineGoogle Scholar
- 10 Monthly Postcensal Resident Population (8/1/2005): U.S. Census data. Available at: http://www.census.gov. Accessed October 19 2005.Google Scholar
- 11 Myerburg RJ, Kessler KM, Castellanos A. Sudden cardiac death: epidemiology, transient risk, and intervention assessment. Ann Intern Med. 1993; 119: 1187–1197.CrossrefMedlineGoogle Scholar
- 12 Chugh SS, Jui J, Gunson K, Stecker EC, John BT, Thompson B, Ilias N, Vickers C, Dogra V, Daya M, Kron J, Zheng ZJ, Mensah G, McAnulty J. Current burden of sudden cardiac death: multiple source surveillance versus retrospective death certificate-based review in a large U.S. community. J Am Coll Cardiol. 2004; 44: 1268–1275.CrossrefMedlineGoogle Scholar
- 13 Cobb LA, Fahrenbruch CE, Olsufka M, Copass MK. Changing incidence of out-of-hospital ventricular fibrillation, 1980–2000. JAMA. 2002; 288: 3008–3013.CrossrefMedlineGoogle Scholar
- 14 Nichol G, Stiell IG, Laupacis A, Pham B, De Maio V, Wells GA. A cumulative meta-analysis of the effectiveness of defibrillator-capable emergency medical services for victims of out-of-hospital cardiac arrest. Ann Emerg Med. 1999; 34: 517–525.CrossrefGoogle Scholar
- 15 Culley LL, Rea TD, Murray JA, Welles B, Fahrenbruch CE, Olsufka M, Eisenberg MS, Copass MK. Public access defibrillation in out-of-hospital cardiac arrest: a community-based study. Circulation. 2004; 109: 1859–1863.LinkGoogle Scholar
- 16 Young KD, Gausche-Hill M, McClung CD, Lewis RJ. A prospective, population-based study of the epidemiology and outcome of out-of-hospital pediatric cardiopulmonary arrest. Pediatrics. 2004; 114: 157–164.CrossrefMedlineGoogle Scholar
- 17 Mogayzel C, Quan L, Graves JR, Teidman D, Fahrenbruch C, Herndon P. Out-of-hospital ventricular fibrillation in children and adolescents: causes and outcomes. Ann Emerg Med. 1995; 25: 484–491.CrossrefMedlineGoogle Scholar
- 18 Donoghue A, Nadkarni V, Berg RA, Osmond MH, Wells GA, Nesbitt L, et al. Out-of-hospital pediatric cardiac arrest: an epidemiologic review and assessment of current knowledge. Ann Emerg Med. 2005; 46: 512–522.CrossrefMedlineGoogle Scholar
- 19 Luckstead EF, Patel DR. Catastrophic pediatric sports injuries. Pediatr Clin North Am. 2002; 49: 581–591.CrossrefMedlineGoogle Scholar
- 20 Maron BJ, Gohman TE, Aeppli D. Prevalence of sudden cardiac death during competitive sports activities in Minnesota high school athletes. J Am Coll Cardiol. 1998; 32: 1881–1884.CrossrefMedlineGoogle Scholar
- 21 Winkleby MA, Kraemer HC, Ahn DK, Varady AN. Ethnic and socioeconomic differences in cardiovascular disease risk factors: findings for women from the Third National Health and Nutrition Examination Survey, 1988–1994. JAMA. 1998; 280: 356–362.CrossrefMedlineGoogle Scholar
- 22 Centers for Disease Control and Prevention (CDC). Racial/ethnic and socioeconomic disparities in multiple risk factors for heart disease and stroke: United States, 2003. MMWR. 2005; 54: 113–117.MedlineGoogle Scholar
- 23 Winkleby MA, Cubbin C. Changing patterns in health behaviors and risk factors related to chronic disease, 1999–2000. Am J Health Promot. 2004; 19: 19–27.CrossrefMedlineGoogle Scholar
- 24 Daviglus ML, Stamler J, Pirzada A, Yan LL, Garside DB, Liu K, Wang R, Dyer AR, Lloyd-Jones DM, Greenland P. Favorable cardiovascular risk profile in young women and long-term risk of cardiovascular and all-cause mortality. JAMA. 2004; 292: 1588–1592.CrossrefMedlineGoogle Scholar
- 25 Stamler J, Stamler R, Neaton JD, Wentworth D, Daviglus ML, Garside D, Dyer AR, Liu K, Greenland P. Low risk-factor profile and long-term cardiovascular and noncardiovascular mortality and life expectancy: findings for 5 large cohorts of young adult and middle-aged men and women. JAMA. 1999; 282: 2012–2018.CrossrefMedlineGoogle Scholar
- 26 Mensah GA, Mokdad AH, Ford ES, Greenlund KJ, Croft JB. State of disparities in cardiovascular health in the United States. Circulation. 2005; 111: 1233–1241.LinkGoogle Scholar
- 27 Reeves MJ, Rafferty AP. Healthy lifestyle characteristics among adults in the United States, 2000. Arch Intern Med. 2005; 165: 854–857.CrossrefMedlineGoogle Scholar
- 27A Briefel, RR, Johnson CL. Secular trends in dietary intake in the United States. Annu Rev Nutr. 2004; 24: 401–431.CrossrefMedlineGoogle Scholar
- 28 Gregg EW, Cheng YJ, Cadwell BL, Imperatore G, Williams DE, Flegal KM, Narayan KM, Williamson DF. Secular trends in cardiovascular disease risk factors according to body mass index in US adults. JAMA. 2005; 293: 1868–1874.CrossrefMedlineGoogle Scholar
- 29 Bonow RO, Smaha LA, Smith SC Jr, Mensah GA, Lenfant C. World Heart Day 2002: the international burden of cardiovascular disease: responding to the emerging global epidemic. Circulation. 2002; 106: 1602–1605.LinkGoogle Scholar
- 30 National Hospital Discharge Survey. 2001. Annual Summary With Detailed Diagnosis and Procedure Data. NCHS. Vital and Health Statistics. 13 (156). 2004.Google Scholar
- 31 National Ambulatory Medical Care Survey: 2003 Summary. Advanced Data from Vital and Health Ststistics; No. 365. Hyattsville, MD: NCHS 2005.Google Scholar
- 32 National Hospital Ambulatory Medical Care Survey: Emergency Department Summary. 2003. Advance Data from Vital and Health Ststistics; No.358. Hyattsville, MD: NCHS. 2005.Google Scholar
- 33 1999 National Nursing Home Survey. June 2002. http://www.cdc.gov/nchs/data/series/sr_13/sr13_152.pdfGoogle Scholar
- 34 National Hospital Ambulatory Medical Care Survey: 2002 Outpatient Department Summary. Vital and Health Statistics. NCHS. http://www.cdc.gov/nchs/data/ad/ad345.pdfGoogle Scholar
- 35 Health Care Financing Review, 2003 Medicare and Medicaid Statistical Supplement. (www.cms.hhs.gov/review/supp/2003)Google Scholar
- 36 Thorpe KE, Florence CS, Howard DH, Joski P. The impact of obesity on rising medical spending. Health Aff (Millwood). 2004;suppl web exclusives:W4-480-6.Google Scholar
- 37 Deleted in proof.Google Scholar
- 38 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.MedlineGoogle Scholar
- 39 Atherosclerosis Risk in Communities (ARIC, 1987–2000), NHLBI.Google Scholar
- 40 Lloyd-Jones DM, Larson MG, Beiser A, Levy D. Lifetime risk for developing coronary heart disease. Lancet. 1999; 353: 89–92.CrossrefMedlineGoogle Scholar
- 41 Jones DW, Chambless LE, Folsom AR, Heiss G, Hutchinson RG, Sharrett AR, Szklo M, Taylor HA Jr. Risk factors for coronary heart disease in African Americans: the Atherosclerotic Risk in Communities Study, 1987–1997. Arch Intern Med. 2002; 162: 2565–2571.CrossrefMedlineGoogle Scholar
- 42 Kannel WB, Hjortland MC, McNamara PM, Gordon T. Menopause and risk of cardiovascular disease: the Framingham study. Ann Intern Med. 1976; 85: 447–452.CrossrefMedlineGoogle Scholar
- 43 Rea TD, Pearce RM, Raghunathan TE, Lemaitre RN, Sotoodehnia N, Jouven X, Siscovick DS. Incidence of out-of-hospital cardiac arrest. Am J Cardiol. 2004; 93: 1455–1460.CrossrefMedlineGoogle Scholar
- 44 Fox CS, Evans JC, Larson MG, Kannel WB, Levy D. Temporal trends in coronary heart disease mortality and sudden cardiac death from 1950–1999: the Framingham Heart Study. Circulation. 2004; 110: 522–527.LinkGoogle Scholar
- 45 NRMI. Available at: www.nrmi.org/nrmi_data.html.Google Scholar
- 46 Rogers WJ, Canto JG, Lambrew CT, Tiefenbrunn AJ, Kinkaid B, Shoultz DA, Frederick PD, Every N. Temporal trends in the treatment of over 1.5 million patients with myocardial infarction in the US from 1990 through 1999: the National Registry of Myocardial Infarction 1, 2 and 3. J Am Coll Cardiol. 2000; 36: 2056–2063.CrossrefMedlineGoogle Scholar
- 47 French WJ. Trends in acute myocardial management: use of the National Registry of Myocardial Infarction in quality improvement. Am J Cardiol. 2000; 85: 5B–9B.CrossrefMedlineGoogle Scholar
- 48 Vaccarino V, Parsons L, Every NR, Barron HV, Krumholz HM. Sex-based differences in early mortality after myocardial infarction: National Registry of Myocardial Infarction 2 participants. N Engl J Med. 1999; 341: 217–225.CrossrefMedlineGoogle Scholar
- 49 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.CrossrefMedlineGoogle Scholar
- 50 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.CrossrefMedlineGoogle Scholar
- 51 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.LinkGoogle Scholar
- 52 Manolio TA, et al. U.S. trends in prevalence of low coronary risk: National Health and Nutrition Examination Surveys. Circulation. 2004; 109: 32. Abstract.Google Scholar
- 53 Ford ES, Giles WH, Mokdad AH. The distribution of 10-year risk for coronary heart disease among US adults: findings from the National Health and Nutrition Survey III. J Am Coll Cardiol. 2004; 43: 1791–1796.CrossrefMedlineGoogle Scholar
- 54 Vasan RS, Sullivan LM, Wilson PW, Sempos CT, Sundstrom J, Kannel WB, Levy D, D’Agostino RB. Relative importance of borderline and elevated levels of coronary heart disease risk factors. Ann Intern Med. 2005; 142: 393–402.CrossrefMedlineGoogle Scholar
- 55 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.CrossrefMedlineGoogle Scholar
- 56 NCHS. Vital Health Stat. 2004; 13 (157).Google Scholar
- 57 Mosca L, Ferris A, Fabunmi R, Robertson RM; American Heart Association. Tracking women’s awareness of heart disease: an American Heart Association national study. Circulation. 2004; 109: 573–579.LinkGoogle Scholar
- 58 Mosca L, Jones WK, King KB, Ouyang P, Redberg RF, Hill MN. Awareness, perception, and knowledge of heart disease risk and prevention among women in the United States: American Heart Association Women’s Heart Disease and Stroke Campaign Task Force. Arch Fam Med. 2000; 9: 506–515.CrossrefMedlineGoogle Scholar
- 59 Biswas MS, Calhoun PS, Bosworth HB, Bastian LA. Are women worrying about heart disease? Womens Health Issues. 2002; 12: 204–211.CrossrefMedlineGoogle Scholar
- 60 Greenlund KJ, Keenan NL, Giles WH, Zheng ZJ, Neff LJ, Croft JB, Mensah GA. Public recognition of major signs and symptoms of heart attack: seventeen states and the US Virgin Islands, 2001. Am Heart J. 2004; 147: 1010–1016.CrossrefMedlineGoogle Scholar
- 61 Gans KM, Assmann SF, Sallar A, Lasater TM. Knowledge of cardiovascular disease prevention: an analysis from two New England communities. Prev Med. 1999; 29: 229–237.CrossrefMedlineGoogle Scholar
- 62 Davis SK, Winkleby MA, Farquhar JW. Increasing disparity in knowledge of cardiovascular disease risk factors and risk-reduction strategies by socioeconomic status: implications for policymakers. Am J Prev Med. 1995; 11: 318–323.CrossrefMedlineGoogle Scholar
- 63 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.LinkGoogle Scholar
- 64 McGinn AP, Rosamond WD, Goff DC Jr, 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.CrossrefMedlineGoogle Scholar
- 65 Morrow DA, et al. Performance of the Thrombolysis in Myocardial Infarction Risk Index for Early Acute Coronary Syndrome in the National Registry of Myocardial Infarction: a simple risk index predicts mortality in both ST and non-ST elevation myocardial infarction. J Am Coll Cardiol. 2003; 41 (suppl A): 365A–366A.Google Scholar
- 66 Moriel M, Behar S, Tzivoni D, Hod H, Boyko V, Gottlieb S. Management and outcomes of elderly women and men with acute coronary syndromes in 2000 and 2002. Arch Intern Med. 2005; 165: 1521–1526.CrossrefMedlineGoogle Scholar
- 67 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.CrossrefMedlineGoogle Scholar
- 68 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.CrossrefMedlineGoogle Scholar
- 69 Muntner P, Garrett E, Klag MJ, Coresh J. Trends in stroke prevalence between 1973 and 1991 in the US population 25 to 74 years of age. Stroke. 2002; 33: 1209–1213.LinkGoogle Scholar
- 70 Advance data from Vital and Health Statistics. No. 356. April 27, 2005.Google Scholar
- 71 Centers for Disease Control and Prevention (CDC). Disparities in deaths from stroke among persons <75 years: United States, 2002. MMWR Morb Mortal Wkly Rep. 2005; 54: 477–481.MedlineGoogle Scholar
- 71A Howard G, Wagenknecht LE, Cai J, Cooper L, Kraut MA, Toole JF. Cigarette smoking and other risk factors for silent cerebral infarction in the general population. Stroke. 1998; 29: 913–917.CrossrefMedlineGoogle Scholar
- 71B Bryan RN, Wells SW, Miller TJ, Elster AD, Jungreis CA, Poirier VC, Lind BK, Manolio TA. Infarctlike lesions in the brain: prevalence and anatomic characteristics at MR imaging of the elderly: data from the Cardiovascular Health Study. Radiology. 1997; 202: 47–54.CrossrefMedlineGoogle Scholar
- 72 Price TR, Psaty B, O’Leary D, Burke G, Gardin J. Assessment of cerebrovascular disease in the Cardiovascular Health Study. Ann Epidemiol. 1993; 3: 504–5077.CrossrefMedlineGoogle Scholar
- 73 Hankey et al. Impact of people with transient ischemic attack on stroke incidence and public health. Cerebrovasc Dis. 1996; 6 (suppl 1): 26–33.CrossrefGoogle Scholar
- 74 Ovbiagele B, Kidwell CS, Saver JL. Epidemiological impact in the United States of a tissue-based definition of transient ischemic attack. Stroke. 2003; 34: 919–924.LinkGoogle Scholar
- 75 Hill MD, Yiannakoulias N, Jeerakathil T, Tu JV, Svenson LW, Schopflocher DP. The high risk of stroke immediately after transient ischemic attack: a population-based study. Neurology. 2004; 62: 2015–2020.CrossrefMedlineGoogle Scholar
- 76 Kleindorfer D, Panagos P, Pancioli A, Khoury J, Kissela B, Woo D, Schneider A, Alwell K, Jauch E, Miller R, Moomaw C, Shukla R, Broderick JP. Incidence and short-term prognosis of transient ischemic attack in a population-based study. Stroke. 2005; 36: 720–723.LinkGoogle Scholar
- 77 Johnston SC, Fayad PB, Gorelick PB, Hanley DF, Shwayder P, van Husen D, Weiskopf T. Prevalence and knowledge of transient ischemic attack among US adults. Neurology. 2003; 60: 1429–1434.CrossrefMedlineGoogle Scholar
- 78 Dennis MS, Bamford JM, Sandercock PA, Warlow CP. Incidence of transient ischemic attack in Oxfordshire, England. Stroke. 1989; 20: 333–339.CrossrefMedlineGoogle Scholar
- 79 Lisabeth LD, Ireland JK, Risser JM, Brown DL, Smith MA, Garcia NM, Morgenstern LB. Stroke risk after transient ischemic attack in a population-based setting. Stroke. 2004; 35: 1842–1846.LinkGoogle Scholar
- 80 Coull AJ, Lovett JK, Rothwell PM, for the Oxford Vascular Study. Population-based study of early risk of stroke after transient ischemic attack or minor stroke: implications for public education and organization of services. BMJ. 2004; 328: 326.CrossrefMedlineGoogle Scholar
- 81 Sherman DG. Reconsideration of TIA diagnostic criteria. Neurology. 2004; 62: S20–S21.CrossrefMedlineGoogle Scholar
- 82 Clark TG, Murphy MF, Rothwell PM. Long term risks of stroke, myocardial infarction, and vascular death in “low-risk” patients with a non-recent transient ischaemic attack. J Neurol Neurosurg Psychiatry. 2003; 74: 577–580.CrossrefMedlineGoogle Scholar
- 83 Eliasziw M, Kennedy J, Hill MD, Buchan AM, Barnett HJ, for the North American Symptomatic Carotid Endarterectomy Trial Group. Early risk of stroke after a transient ischemic attack in patients with internal carotid artery disease. CMAJ. 2004; 170: 1105–1109.CrossrefMedlineGoogle Scholar
- 84 Deleted in proof.Google Scholar
- 85 Deleted in proof.Google Scholar
- 86 Morgenstern LB, Smith MA, Lisabeth LD, Risser JM, Uchino K, Garcia N, Longwell PJ, McFarling DA, Akuwumi O, Al-Wabil A, Al-Senani F, Brown DL, Moye LA. Excess stroke in Mexican Americans compared with non-Hispanic whites: the Brain Attack Surveillance in Corpus Christi Project. Am J Epidemiol. 2004; 160: 376–383.CrossrefMedlineGoogle Scholar
- 87 White H, Boden-Albala B, Wang C, Elkind MS, Rundek T, Wright CB, Sacco RL. Ischemic stroke subtype incidence among whites, blacks, and Hispanics: the Northern Manhattan Study. Circulation. 2005; 111: 1327–1331.LinkGoogle Scholar
- 88 Rosamond WD, Folsom AR, Chambless LE, Wang CH, McGovern PG, Howard G, Copper LS, Shahar E. Stroke incidence and survival among middle-aged adults: 9-year follow-up of the Atherosclerotic Risk in Communities (ARIC) Cohort. Stroke. 1999; 30: 736–743.CrossrefMedlineGoogle Scholar
- 89 Deleted in proof.Google Scholar
- 90 Ayala C, Greenlund KJ, Croft JB, Keenan NL, Donehoo RS, Giles WH, Kittner SJ, Marks JS. Racial/ethnic disparities in mortality by stroke subtype in the United States, 1995–1998. Am J Epidemiol. 2001; 154: 1057–1063.CrossrefMedlineGoogle Scholar
- 91 Johnston SC, Gress DR, Browner WS, Sidney S. Short-term prognosis after emergency department diagnosis of TIA. JAMA. 2000; 284: 2901–2906.CrossrefMedlineGoogle Scholar
- 92 Wolf PA, D’Agostino RB, Kannel WB, Bonita R, Belanger AJ. Cigarette smoking as a risk factor for stroke: the Framingham study. JAMA. 1988; 259: 1025–1029.CrossrefMedlineGoogle Scholar
- 93 Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham study. Stroke. 1991; 22: 983–988.CrossrefMedlineGoogle Scholar
- 94 Seshadri S et al. Lifetime risk of stroke: results from the Framingham study. Stroke. In press.Google Scholar
- 95 Kissela BM, Khoury J, Kleindorfer D, Woo D, Schneider A, Alwell K, Miller R, Ewing I, Moomaw CJ, Szaflarski JP, Gebel J, Shukla R, Broderick JP. Epidemiology of ischemic stroke in patients with diabetes: the greater Cincinnati/Northern Kentucky Stroke Study. Diabetes Care. 2005; 28: 355–359.CrossrefMedlineGoogle Scholar
- 96 Lee IM, Hennekens CH, Berger K, Buring JE, Manson JE. Exercise and risk of stroke in male physicians. Stroke. 1999; 30: 1–6.CrossrefMedlineGoogle Scholar
- 97 Lee IM, Paffenbarger RS Jr. Physical activity and stroke incidence: the Harvard Alumni Health Study. Stroke. 1998; 29: 2049–2054.CrossrefMedlineGoogle Scholar
- 98 Hu FB, Stampfer MJ, Colditz GA, Ascherio A, Rexrode KM, Willett WC, Manson JE. Physical activity and risk of stroke in women. JAMA. 2000; 283: 2961–2967.CrossrefMedlineGoogle Scholar
- 99 Sacco RL, Gan R, Boden-Albala B, Lin IF, Kargman DE, Hauser WA, Shea S, Paik MC. Leisure-time physical activity and ischemic stroke risk: the Northern Manhattan Stroke Study. Stroke. 1998; 29: 380–387.CrossrefMedlineGoogle Scholar
- 100 Evenson KR, Rosamond WD, Cai J, Toole JF, Hutchinson RG, Shahar E, Folsom AR. Physical activity and ischemic stroke risk: the Atherosclerosis Risk in Communities Study. Stroke. 1999; 30: 1333–1339.CrossrefMedlineGoogle Scholar
- 101 Kittner SJ, Stern BJ, Feeser BR, Hebel R, Nagey DA, Buchholz DW, Earley CJ, Johnson CJ, Macko RF, Sloan MA, Wityk RJ, Wozniak MA. Pregnancy and the risk of stroke. N Engl J Med. 1996; 335: 768–774.CrossrefMedlineGoogle Scholar
- 102 Salonen Ros H, Lichtenstein P, Bellocco R, Petersson G, Cnattingius S. Increased risks of circulatory diseases in late pregnancy and puerperium. Epidemiology. 2001; 12: 456–460.CrossrefMedlineGoogle Scholar
- 103 Curb JD, Abbott RD, Rodriguez BL, Masaki KH, Chen R, Popper JS, Petrovitch H, Ross GW, Schatz IJ, Belleau GC, Yano K. High density lipoprotein cholesterol and the risk of stroke in elderly men: the Honolulu Heart Program. Am J Epidemiol. 2004; 160: 150–157.CrossrefMedlineGoogle Scholar
- 104 James AH, Bushnell CD, Jamison MG, Myers ER. Incidence and risk factors for stroke in pregnancy and the puerperium. Obstet Gynecol. 2005; 106: 509–516.CrossrefMedlineGoogle Scholar
- 105 Bousser MG. Stroke in women: the 1997 Paul Dudley White International Lecture. Circulation. 1999; 99: 463–467.CrossrefMedlineGoogle Scholar
- 106 Bonita R. Epidemiology of stroke. Lancet. 1992; 339: 342–344.CrossrefMedlineGoogle Scholar
- 107 Wassertheil-Smoller S, Hendrix SL, Limacher M, Heiss G, Kooperberg C, Baird A, Kotchen T, Curb JD, Black H, Rossouw JE, Aragaki A, Safford M, Stein E, Laowattana S, Mysiw WJ, for the WHI Investigators. Effect of estrogen plus progestin on stroke in postmenopausal women: the Women’s Health Initiative: a randomized trial. JAMA. 2003; 289: 2673–2684.CrossrefMedlineGoogle Scholar
- 108 Anderson GL, Limacher M, Assaf AR, Bassford T, Beresford SA, Black H, Bonds D, Brunner R, Brzyski R, Caan B, Chlebowski R, Curb D, Gass M, Hays J, Heiss G, Hendrix S, Howard BV, Hsia J, Hubbell A, Jackson R, Johnson KC, Judd H, Kotchen JM, Kuller L, LaCroix AZ, Lane D, Langer RD, Lasser N, Lewis CE, Manson J, Margolis K, Ockene J, O’Sullivan MJ, Phillips L, Prentice RL, Ritenbaugh C, Robbins J, Rossouw JE, Sarto G, Stefanick ML, Van Horn L, Wactawski-Wende J, Wallace R, Wassertheil-Smoller S, for the Women’s Health Initiative Steering Committee. Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the Women’s Health Initiative randomized controlled trial. JAMA. 2004; 291: 1701–1712.CrossrefMedlineGoogle Scholar
- 109 Simon JA, Hsia J, Cauley JA, Richards C, Harris F, Fong J, Barrett-Connor E, Hulley SB. Postmenopausal hormone therapy and risk of stroke: the Heart and Estrogen-Progestin Replacement Study (HERS). Circulation. 2001; 103: 638–642.CrossrefMedlineGoogle Scholar
- 110 Viscoli CM, Brass LM, Kernan WN, Sarrel PM, Suissa S, Horwitz RI. A clinical trial of estrogen-replacement therapy after ischemic stroke. N Engl J Med. 2001; 345: 1243–1249.CrossrefMedlineGoogle Scholar
- 111 Rossouw JE, Anderson GL, Prentice RL, LaCroix AZ, Kooperberg C, Stefanick ML, Jackson RD, Beresford SA, Howard BV, Johnson KC, Kotchen JM, Ockene J, for the Writing Group for the Women’s Health Initiative Investigators. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women’s Health Initiative randomized controlled trial. JAMA. 2002; 288: 321–333.CrossrefMedlineGoogle Scholar
- 112 Centers for Disease Control and Prevention (CDC). Prevalence of disabilities and associated health conditions among adults: United States, 1999. MMWR. 2001; 50: 120–125.MedlineGoogle Scholar
- 113 Evenson KR, Rosamond WD, Morris DL. Pre-hospital and in-hospital delays in acute stroke care. Neuroepidemiology. 2001; 20: 65–76.CrossrefMedlineGoogle Scholar
- 114 Kelley-Hayes M, et al. The influence of gender and age on disability following ischemic stroke: the Framingham study. J Stroke Cerebrovasc Dis. 2003; 12: 119–126.CrossrefMedlineGoogle Scholar
- 115 Arora S, Broderick JP, Frankel M, Heinrich JP, Hickenbottom S, Karp H, LaBresh KA, Malarcher A, Moomaw CJ, Reeves MJ, Schwamm L, Weiss P, for the Paul Coverdell Prototype Registries Writing Group. Acute stroke care in the US: results from 4 pilot prototypes of the Paul Coverdell National Acute Stroke Registry. Stroke. 2005; 36: 1232–1240.LinkGoogle Scholar
- 116 California Acute Stroke Pilot Registry (CASPR) Investigators. Prioritizing interventions to improve rates of thrombolysis for ischemic Stroke. Neurology. 2005; 64: 654–659.CrossrefMedlineGoogle Scholar
- 117 California Acute Stroke Pilot Registry Investigators. The impact of standardized stroke orders on adherence to best practices. Neurology. 2005; 65: 360–365.CrossrefMedlineGoogle Scholar
- 118 Fang J, Alderman MH. Trend of stroke hospitalization, United States, 1988–1997. Stroke. 2001; 32: 2221–2226.CrossrefMedlineGoogle Scholar
- 119 Kennedy BS, Kasl SV, Brass LM, Vaccarino V. Trends in hospitalized stroke for blacks and whites in the United States, 1980–1999. Neuroepidemiology. 2002; 21: 131–141.CrossrefMedlineGoogle Scholar
- 120 Kozak LJ. Underreporting of race in the National Hospital Discharge Survey. Advance Data 1995; No. 265.Google Scholar
- 121 Centers for Disease Control and Prevention (CDC). Awareness of stroke warning signs: 17 states and the U.S. Virgin Islands, 2001. MMWR Morbid Mortal Wkly Rep. 2004; 53: 359–362.MedlineGoogle Scholar
- 122 Kothari R, Sauerbeck L, Jauch E, Broderick J, Brott T, Khoury J, Liu T. Patient’s awareness of stroke signs, symptoms, and risk factors. Stroke. 1997; 28: 1871–1875.CrossrefMedlineGoogle Scholar
- 123 Schneider AT, Pancioli AM, Khoury JC, Rademacher E, Tuchfarber A, Miller R, Woo D, Kissela B, Broderick JP. Trends in community knowledge of the warning signs and risk factors for stroke. JAMA. 2003; 289: 343–346.CrossrefMedlineGoogle Scholar
- 124 Silver FL, Rubini F, Black D, Hodgson CS. Advertising strategies to increase public knowledge of the warning signs of stroke. Stroke. 2003; 34: 1965–1968.LinkGoogle Scholar
- 125 Greenlund KJ, Neff LJ, Zheng ZJ, Keenan NL, Giles WH, Ayala CA, Croft JB, Mensah GA. Low public recognition of major stroke symptoms. Am J Prev Med. 2003; 25: 315–319.CrossrefMedlineGoogle Scholar
- 126 Pancioli AM, Broderick J, Kothari R, Brott T, Tuchfarber A, Miller R, Khoury J, Jauch E. Public perception of stroke warning signs and knowledge of potential risk factors. JAMA. 1998; 279: 1288–1292.CrossrefMedlineGoogle Scholar
- 127 Samsa GP, Cohen SJ, Goldstein LB, Bonito AJ, Duncan PW, Enarson C, DeFriese GH, Horner RD, Matchar DB. Knowledge of risk among patients at increased risk for Stroke. Stroke. 1997; 28: 916–921.CrossrefMedlineGoogle Scholar
- 128 Ferris A, Robertson RM, Fabunmi R, Mosca L, for the American Heart Association and American Stroke Association. American Heart Association and American Stroke Association national survey of stroke risk awareness among women. Circulation. 2005; 111: 1321–1326.LinkGoogle Scholar
- 129 Robinson KA, Merrill RM. Relation among stroke knowledge, lifestyle, and stroke-related screening results. Geriatr Nurs. 2003; 24: 300–305.CrossrefMedlineGoogle Scholar
- 130 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.CrossrefMedlineGoogle Scholar
- 131 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.MedlineGoogle Scholar
- 132 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.CrossrefMedlineGoogle Scholar
- 133 Metz R. Cost-effective, risk-free, evidence-based medicine. Arch Intern Med. 2003; 163: 2795.CrossrefMedlineGoogle Scholar
- 134 Lynch JK, Hirtz DG, DeVeber G, Nelson KB. Report of the National Institute of Neurological Disorders and Stroke workshop on perinatal and childhood stroke. Pediatrics. 2002; 109: 116–123.CrossrefMedlineGoogle Scholar
- 135 Lee J, Croen LA, Backstrand KH, Yoshida CK, Henning LH, Lindan C, Ferriero DM, Fullerton HJ, Barkovich AJ, Wu YW. Maternal and infant characteristics associated with perinatal arterial stroke in the infant. JAMA. 2005; 293: 723–729.CrossrefMedlineGoogle Scholar
- 136 Broderick J, Talbot GT, Prenger E, Leach A, Brott T. Stroke in children within a major metropolitan area: the surprising importance of intracerebral hemorrhage. J Child Neurol. 1993; 8: 250–255.CrossrefMedlineGoogle Scholar
- 137 Earley CJ, Kittner SJ, Feeser BR, Gardner J, Epstein A, Wozniak MA, Wityk R, Stern BJ, Price TR, Macko RF, Johnson C, Sloan MA, Buchholz D. Stroke in children and sickle-cell disease: Baltimore-Washington Cooperative Young Stroke Study. Neurology. 1998; 51: 169–176.CrossrefMedlineGoogle Scholar
- 138 deVeber GA, MacGregor D, Curtis R, Mayank S. Neurologic outcome in survivors of childhood arterial ischemic stroke and sinovenous thrombosis. J Child Neurol. 2000; 15: 316–324.CrossrefMedlineGoogle Scholar
- 139 Fullerton HJ, Wu YW, Zhao S, Johnston SC. Risk of stroke in children: ethnic and gender disparities. Neurology. 2003; 61: 189–194.CrossrefMedlineGoogle Scholar
- 140 Strater R, Becker S, von Eckardstein A, Heinecke A, Gutsche S, Junker R, Kurnik K, Schobess R, Nowak-Gottl U. Prospective assessment of risk factors for recurrent stroke during childhood: a 5-year follow-up study. Lancet. 2002; 360: 1540–1545.CrossrefMedlineGoogle Scholar
- 141 Fullerton HJ, Chetkovich DM, Wu YW, Smith WS, Johnston SC. Deaths from stroke in U.S. children, 1979 to 1998. Neurology. 2002; 59: 34–39.CrossrefMedlineGoogle Scholar
- 142 Fullerton HJ, Adams RJ, Zhao S, Johnston SC. Declining stroke rates in Californian children with sickle cell disease. Blood. 2004; 104: 336–339.CrossrefMedlineGoogle Scholar
- 143 Kissela B, Schneider A, Kleindorfer D, Khoury J, Miller R, Alwell K, Woo D, Szaflarski J, Gebel J, Moomaw C, Pancioli A, Jauch E, Shukla R, Broderick J. Stroke in a biracial population: the excess burden of stroke among blacks. Stroke. 2004; 35: 426–431.LinkGoogle Scholar
- 144 Wolf PA, D’Agostino RB, Belanger AJ, Kannel WB. Probability of stroke: a risk profile from the Framingham Study. Stroke. 1991; 22: 312–318.CrossrefMedlineGoogle Scholar
- 145 Fields LE, Burt VL, Cutler JA, Hughes J, Roccella EJ, Sorlie P. The burden of adult hypertension in the United States, 1999–2000: a rising tide. Hypertension. 2004; 44: 398–404.LinkGoogle Scholar
- 146 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.CrossrefMedlineGoogle Scholar
- 147 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.CrossrefMedlineGoogle Scholar
- 148 Brett KM, et al. Utilization of ambulatory medical care by women: United States, 1997–98. Vital Health Stat 13. 2001; 149: 1–46.Google Scholar
- 149 Muntner P, He J, Cutler JA, Wildman RP, Whelton PK. Trends in blood pressure among children and adolescents. JAMA. 2004; 291: 2107–2113.CrossrefMedlineGoogle Scholar
- 150 Vital and Health Statistics. No. 356, April 27, 2005.Google Scholar
- 151 Hajjar I, Kotchen TA. Trends in prevalence, awareness, treatment and control of hypertension in the Unites States, 1988–2000. JAMA. 2003; 290: 199–206.CrossrefMedlineGoogle Scholar
- 152 Psaty BM, Manolio TA, Smith NL, Heckbert SR, Gottdiener JS, Burke GL, Weissfeld J, Enright P, Lumley T, Powe N, Furberg CD, for the Cardiovascular Health Study. 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.CrossrefMedlineGoogle Scholar
- 153 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.CrossrefMedlineGoogle Scholar
- 154 MacMahon S, et al. The epidemiological association between blood pressure and stroke: implications for primary and secondary prevention. Hypertens Res. 1994; 17 (suppl 1): S23–S32CrossrefGoogle Scholar
- 155 Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA. 1996; 275: 1557–1562.CrossrefMedlineGoogle Scholar
- 156 Deleted in proof.Google Scholar
- 157 CDC/NCHS.Health, United States, 2004. Data based on 3 measures of blood pressure.Google Scholar
- 158 Centers for Disease Control and Prevention (CDC). Racial/ethnic disparities in prevalence, treatment, and control of hypertension—United States, 1999–2002. MMWR Morb Mortal Wkly Rep. 2005; 54 (1): 7–9.MedlineGoogle Scholar
- 159 Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalizations. N Engl J Med. 2004; 351: 1296–1305.CrossrefMedlineGoogle Scholar
- 160 Coresh J, Astor BC, Greene T, Eknoyan G, Levey AS. Prevalence of chronic kidney disease and decreased kidney function in the adult United States population: Third National Health and Nutrition Examination Survey. Am J Kidney Dis. 2003; 41: 1–12.CrossrefMedlineGoogle Scholar
- 161 Collins AJ, Li S, Gilbertson DT, Liu J, Chen SC, Herzog CA. Chronic kidney disease and cardiovascular disease in the Medicare population. Kidney Int Suppl. 2003; 87: S24–S31.CrossrefGoogle Scholar
- 162 Perspectives in Pediatric Cardiology, Volume 6. Armonk, NY: Futura Publishing Co; 1998Google Scholar
- 163 Botto LD, Correa A, Erickson JD. Racial and temporal variations in the prevalence of heart defects. Pediatrics. 2001; 107: E32.CrossrefMedlineGoogle Scholar
- 164 Prevalence and incidence of cardiac malformations. In: Moller JH, ed. Surgery of Congenital Heart Disease: Pediatric Cardiac Care Consortium 1984–1995. Armonk, NY: Futura Publishing Co; 1998: 20.Google Scholar
- 165 Hoffman JI, Kaplan S. The incidence of congenital heart disease. J Am Coll Cardiol. 2002; 39: 1890–1900.CrossrefMedlineGoogle Scholar
- 166 Larson EW, Edwards WD. Risk factors for aortic dissection: a necropsy study of 161 cases. Am J Cardiol. 1984; 53: 849–855.CrossrefMedlineGoogle Scholar
- 167 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.CrossrefMedlineGoogle Scholar
- 168 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–F63CrossrefMedlineGoogle Scholar
- 169 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.CrossrefMedlineGoogle Scholar
- 170 Redfield MM, Jacobsen SJ, Burnett JC Jr, 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.CrossrefMedlineGoogle Scholar
- 171 Lloyd-Jones DM, Larson MG, Leip EP, Beiser A, D’Agostino RB, Kannel WB, Murabito JM, Vasan RS, Benjamin EJ, Levy D, for the Framingham Heart Study. Lifetime risk for developing congestive heart failure: the Framingham Heart Study. Circulation. 2002; 106: 3068–3072.LinkGoogle Scholar
- 172 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.CrossrefMedlineGoogle Scholar
- 173 Bibbins-Domingo K, Lin F, Vittinghoff E, Barrett-Connor E, Hulley SB, Grady D, Shlipak MG. Predictors of heart failure among women with coronary disease. Circulation. 2004; 110: 1424–1430.LinkGoogle Scholar
- 174 Go AS. The epidemiology of atrial fibrillation in elderly persons: the tip of the iceberg. Am J Geriatr Cardiol. 2005; 14: 56–61.CrossrefMedlineGoogle Scholar
- 175 Lloyd-Jones DM, Wang TJ, Leip EP, Larson MG, Levy D, Vasan RS, D’Agostino RB, Massaro JM, Beiser A, Wolf PA, Benjamin EJ. Lifetime risk for development of atrial fibrillation: the Framingham Heart Study. Circulation. 2004; 110: 1042–1046.LinkGoogle Scholar
- 176 Khairallah F, Ezzedine R, Ganz LI, London B, Saba S. Epidemiology and determinants of outcome of admissions for atrial fibrillation in the United States from 1996 to 2001. Am J Cardiol. 2004; 94: 500–504.CrossrefMedlineGoogle Scholar
- 177 Centers for Disease Control and Prevention. Atrial fibrillation as a contributing cause of death and Medicare hospitalization: United States, 1999. MMWR. 2003; 52: 128, 130–131.Google Scholar
- 178 Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, Selby JV, Singer DE. Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: The Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. JAMA. 2001; 285: 2370–2375.CrossrefMedlineGoogle Scholar
- 179 Penado S, Cano M, Acha O, Hernandez JL, Riancho JA. Atrial fibrillation as a risk factor for stroke recurrence. Am J Med. 2003; 114: 206–210.CrossrefMedlineGoogle Scholar
- 180 Dulli DA, Stanko H, Levine RL. Atrial fibrillation is associated with severe acute ischemic stroke. Neuroepidemiology. 2003; 22: 118–123.CrossrefMedlineGoogle Scholar
- 181 Eaker ED, Sullivan LM, Kelly-Hayes M, D’Agostino RB Sr, Benjamin EJ. Does job strain increase the risk for coronary heart disease or death in men and women? The Framingham Offspring Study. Am J Epidemiol. 2004; 159: 950–958.CrossrefMedlineGoogle Scholar
- 182 Newburger JW, Takahashi M, Gerber MA, Gewitz MH, Tani LY, Burns JC, Shulman ST, Bolger AF, Ferrieri P, Baltimore RS, Wilson WR, Baddour LM, Levison ME, Pallasch TJ, Falace DA, Taubert KA, for the Committee on Rheumatic Fever, Endocarditis and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association and American Academy of Pediatrics. Diagnosis, treatment, and long-term management of Kawasaki disease: a statement for health professionals from the Committee on Rheumatic Fever, Endocarditis and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. Circulation. 2004; 110: 2747–2771.LinkGoogle Scholar
- 183 Taubert KA, Rowley AH, Shulman ST. Seven-year national survey of Kawasaki disease and acute rheumatic fever. Pediatr Infect Dis J. 1994; 13: 704–708.CrossrefMedlineGoogle Scholar
- 184 Holman RC, Curns AT, Belay ED, Steiner CA, Schonberger LB. Kawasaki syndrome hospitalizations in the United States, 1997 and 2000. Pediatrics. 2003; 112: 495–501.CrossrefMedlineGoogle Scholar
- 185 Hirsch AT, Criqui MH, Treat-Jacobson D, Regensteiner JG, Creager MA, Olin JW, Krook SH, Hunninghake DB, Comerota AJ, Walsh ME, McDermott MM, Hiatt WR. Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA. 2001; 286: 1317–1324.CrossrefMedlineGoogle Scholar
- 186 Criqui MH, Langer RD, Fronek A, Feigelson HS, Klauber MR, McCann TJ, Browner D. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med. 1992; 326: 381–386.CrossrefMedlineGoogle Scholar
- 187 Selvin E, Erlinger TP. Prevalence of and risk factors for peripheral arterial disease in the United States: National Health and Nutrition Examination Survey, 1999-2000. Circulation. 2004; 110: 738–743.LinkGoogle Scholar
- 188 Becker GJ, McClenny TE, Kovacs ME, Raabe RD, Katzen BT. The importance of increasing public and physician awareness of peripheral arterial disease. J Vasc Interv Radiol. 2002; 13: 7–11.CrossrefMedlineGoogle Scholar
- 189 Criqui MH, Fronek A, Klauber MR, Barrett-Connor E, Gabriel S. The sensitivity, specificity, and predictive value of traditional clinical evaluation of peripheral arterial disease: results from noninvasive testing in a defined population. Circulation. 1985; 71: 516–522.CrossrefMedlineGoogle Scholar
- 190 McDermott MM, Fried L, Simonsick E, Ling S, Guralnik JM. Asymptomatic peripheral arterial disease is independently associated with impaired lower extremity functioning: the women’s health and aging study. Circulation. 2000; 101: 1007–1012.CrossrefMedlineGoogle Scholar
- 191 Criqui MH, et al. Peripheral arterial disease in large vessels is epidemiologically distinct from small vessel disease: an analysis of risk factors. Am J Epidemiol. 1989; 129: 1110–1119.CrossrefMedlineGoogle Scholar
- 192 McDermott MM, Greenland P, Liu K, Guralnik JM, Celic L, Criqui MH, Chan C, Martin GJ, Schneider J, Pearce WH, Taylor LM, Clark E. The ankle brachial index is associated with leg function and physical activity: the Walking and Leg Circulation Study. Ann Intern Med. 2002; 136: 873–883.CrossrefMedlineGoogle Scholar
- 193 McDermott MM, Liu K, Greenland P, Guralnik JM, Criqui MH, Chan C, Pearce WH, Schneider JR, Ferrucci L, Celic L, Taylor LM, Vonesh E, Martin GJ, Clark E. Functional decline in peripheral arterial disease: associations with the ankle brachial index and leg symptoms. JAMA. 2004; 292: 453–461.CrossrefMedlineGoogle Scholar
- 194 Newman AB, Sutton-Tyrrell K, Vogt MT, Kuller LH. Morbidity and mortality in hypertensive adults with a low ankle/arm blood pressure index. JAMA. 1993; 270: 487–489.CrossrefMedlineGoogle Scholar
- 195 Levy PJ. Epidemiology and pathology of peripheral arterial disease. Clin Cornerstone. 2002; 4: 1–15.Google Scholar
- 196 Murabito JM, Evans JC, D’Agostino RB Sr, Wilson PW, Kannel WB. Temporal trends in the incidence of intermittent claudication from 1950 to 1999. Am J Epidemiol. 2005; 162: 430–437.CrossrefMedlineGoogle Scholar
- 197 Criqui MH, Vargas V, Denenberg JO, Ho E, Allison M, Langer RD, Gamst A, Bundens WP, Fronek A. Ethnicity and peripheral arterial disease: the San Diego Population Study. Circulation. 2005; 112: 2703–2707.LinkGoogle Scholar
- 198 Navas-Acien A, Selvin E, Sharrett AR, Calderon-Aranda E, Silbergeld E, Guallar E. Lead, cadmium, smoking, and increased risk of peripheral arterial disease. Circulation. 2004; 109: 3196–3201.LinkGoogle Scholar
- 199 O’Hare AM, Glidden DV, Fox CS, Hsu CY. High prevalence of peripheral arterial disease in persons with renal insufficiency: results from the National Health and Nutrition Examination Survey 1999–2000. Circulation. 2004; 109: 320–323.LinkGoogle Scholar
- 200 Nerheim P, Birger-Botkin S, Piracha L, Olshansky B. Heart failure and sudden death in patients tachycardia-induced cardiomyopathy and recurrent tachycardia. Circulation. 2004; 110: 247–252.LinkGoogle Scholar
- 201 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.CrossrefMedlineGoogle Scholar
- 202 Maron BJ, Shirani J, Poliac LC, Mathenge R, Roberts WC, Mueller FO. Sudden death in young competitive athletes: clinical, demographic, and pathological profiles. JAMA. 1996; 276: 199–204.CrossrefMedlineGoogle Scholar
- 203 White RH. The epidemiology of venous thromboembolism. Circulation. 2003; 107 (suppl): I-4–I-8.LinkGoogle Scholar
- 204 Goldhaber SZ. Pulmonary embolism. N Engl J Med. 1998; 339: 93–104.CrossrefMedlineGoogle Scholar
- 205 Tsai AW, Cushman M, Rosamond WD, Heckbert SR, Tracy RP, Aleksic N, Folsom AR. Coagulation factors, inflammation markers, and venous thromboembolism: the Longitudinal Investigation of Thromboembolism Etiology (LITE). Am J Med. 2002; 113: 636–642.CrossrefMedlineGoogle Scholar
- 206 Semin Thromb Hemost. 2002; 28: suppl 2.Google Scholar
- 207 Cushman M, Tsai AW, White RH, Heckbert SR, Rosamond WD, Enright P, Folsom AR. Deep vein thrombosis and pulmonary embolism in two cohorts: the Longitudinal Investigation of Thromboembolism Etiology. Am J Med. 2004; 117: 19–25.CrossrefMedlineGoogle Scholar
- 208 Fowkes FJ, Price JF, Fowkes FG. Incidence of diagnosed deep vein thrombosis in the general population: systematic review. Eur J Vasc Endovasc Surg. 2003; 25: 1–5.CrossrefMedlineGoogle Scholar
- 209 Horlander KT, Mannino DM, Leeper KV. Pulmonary embolism mortality in the United States, 1979–1998: an analysis using multiple-cause mortality data. Arch Intern Med. 2003; 163: 1711–1717.CrossrefMedlineGoogle Scholar
- 210 Centers for Disease Control and Prevention (CDC). Centers for Disease Control and Prevention (CDC). Cigarette smoking among adults–United States, 2003. MMWR. 2004; 54: 1121–1124.Google Scholar
- 211 Centers for Disease Control and Prevention (CDC). Annual smoking-attributable mortality, years of potential life lost, and productivity losses: United States, 1997-2001. MMWR. 2005; 54: 625–628.MedlineGoogle Scholar
- 212 Centers for Disease Control and Prevention. National survey on drug use and health, U.S., 1999–2001. MMWR Mortal Morbid Wkly Rep. 2004; 53.Google Scholar
- 213 Grunbaum JA, Kann L, Kinchen S, Ross J, Hawkins J, Lowry R, Harris WA, McManus T, Chyen D, Collins J. Youth risk behavior surveillance: United States, 2003, MMWR Surveill Summ. 2004; 53: 1–96.MedlineGoogle Scholar
- 214 Winkleby MA, Robinson TN, Sundquist J, Kraemer HC. Ethnic variation in cardiovascular disease risk factors among children and young adults: findings from the Third National Health and Nutrition Examination Survey, 1988–1994. JAMA. 1999; 281: 1006–1013.CrossrefMedlineGoogle Scholar
- 215 Federal Interagency Forum on Child and Family Statistics. America’s Children: Key National Indicators of Well-Being, 2005. Washington, DC: US Government Printing Office; 2005.Google Scholar
- 216 Third National Report on Human Exposure to Environmental Chemicals. http://www.cdc.gov/exposurereport/.Google Scholar
- 217 Deleted in proof.Google Scholar
- 218 Deleted in proof.Google Scholar
- 219 Deleted in proof.Google Scholar
- 220 Centers for Disease Control and Prevention (CDC). Cigarette smoking among high school students: 11 states, 1991-1997. MMWR. 1999; 48: 686–692.MedlineGoogle Scholar
- 221 Centers for Disease Control and Prevention (CDC). Annual smoking-attributable mortality, years of potential life lost, and productivity losses–United States, 1997-2001. MMWR. 2005; 54: 625–628.MedlineGoogle Scholar
- 222 Surgeon General’s Health Consequences of Smoking 2004Google Scholar
- 223 MMWR. 2005;54, No. 25.Google Scholar
- 224 Goldenberg I, Jonas M, Tenenbaum A, Boyko V, Matetzky S, Shotan A, Behar S, Reicher-Reiss H, for the Bezafibrate Infarction Prevention Study Group. Current smoking, smoking cessation, and the risk of sudden cardiac death in patients with coronary artery disease. Arch Intern Med. 2003; 163: 2301–2305.CrossrefMedlineGoogle Scholar
- 225 Tobacco-Related Mortality, Fact Sheet. Available at: CDC.gov/tobacco. Accessed February 2004.Google Scholar
- 226 Anthonisen NR, Skeans MA, Wise RA, Manfreda J, Kanner RE, Connett JE, for the Lung Health Study Research Group. The effects of a smoking cessation intervention on 14.5-year mortality: a randomized clinical trial. Ann Intern Med. 2005; 142: 233–239.CrossrefMedlineGoogle Scholar
- 227 Smoking Among Adults: Coronary Heart Disease and Stroke. Available at: www.cdc.gov/tobacco/sgr/sgr_2004/Factsheets/3.htm.Google Scholar
- 228 Centers for Disease Control and Prevention (CDC). Cigarette use among high school students: United States, 1991–2003. MMWR. 2004; 53; 499–502.MedlineGoogle Scholar
- 229 Deleted in proof.