Skip main navigation

Does Body Mass Index Impact on the Relationship Between Systolic Blood Pressure and Cardiovascular Disease?

Meta-Analysis of 419 488 Individuals From the Asia Pacific Cohort Studies Collaboration
and on behalf of the Asia Pacific Cohort Studies Collaboration
Originally published 2012;43:1478–1483


Background and Purpose—

Elevated blood pressure and excess body mass index (BMI) are established risk factors for cardiovascular disease (CVD) but controversy exists as to whether, and how, they interact.


The interactions between systolic blood pressure and BMI on coronary heart disease, ischemic and hemorrhagic stroke and CVD were examined using data from 419 448 participants (≥30 years) in the Asia-Pacific region. BMI was categorized into 5 groups, using standard criteria, and systolic blood pressure was analyzed both as a categorical and continuous variable. Cox proportional hazard models, stratified by sex and study, were used to estimate hazard ratios, adjusting for age and smoking and the interaction was assessed by likelihood ratio tests.


During 2.6 million person-years of follow-up, there were 10 877 CVD events. Risks of CVD and subtypes increased monotonically with increasing systolic blood pressure in all BMI subgroups. There was some evidence of a decreasing hazard ratio, per additional 10 mm Hg systolic blood pressure, with increasing BMI, but the differences, although significant, are unlikely to be of clinical relevance. The hazard ratio for CVD was 1.34 (95% CI, 1.32–1.36) overall with individual hazard ratios ranging between 1.28 and 1.36 across all BMI groups. For coronary heart disease, ischemic stroke, and hemorrhagic stroke, the overall hazard ratios per 10 mm Hg systolic blood pressure were 1.24, 1.46, and 1.65, respectively.


Increased blood pressure is an important determinant of CVD risk irrespective of BMI. Although its effect tends to be weaker in people with relatively high BMI, the difference is not sufficiently great to warrant alterations to existing guidelines.


Elevated blood pressure1,2 and excess weight35 are established major risk factors for cardiovascular disease (CVD). The global prevalence of hypertension is estimated at >1 billion6 and the number categorized as overweight (body mass index [BMI] in excess of 25 kg/m2) is 1.1 billion.4 According to the Global Burden of Disease Study, blood pressure (BP) and BMI combined account for >60% of the global burden of CVD.7 These 2 risk factors frequently coexist due, in part, to a causal positive relationship between BMI and BP.

However, current estimates of effects of BP and BMI on risk of coronary heart disease (CHD) and stroke are based on the assumption that there is no interaction between them despite evidence to the contrary. Previous findings from some early cohort studies suggested that BMI modifies the relationship between BP and subsequent risk of CHD in an antagonistic fashion, that is, that the relationship between BP and vascular risk is diminished with increasing BMI.813 From this, it was hypothesized that lean hypertensive men are especially vulnerable to mortality from CHD.811 Subsequent cohorts have produced inconsistent reports with some studies,14,15 most notably the large Swedish study of young male conscripts, reporting a synergistic effect of BMI on the relationship between BP and CVD risk,14 whereas other studies have reported no evidence of an interaction, antagonistic or otherwise.1618

Discrepancies in earlier observations regarding an interaction between BMI and BP on subsequent risk of CVD may have partly arisen from differences in participant characteristics (such as age) as well as methodological challenges, including limited statistical power to reliably detect an interaction and differences in the statistical methods used to explore this issue.16,19 Moreover, the relationships between both BP and BMI with CHD and stroke subtype differ, but no study has yet had adequate power to examine the possible interaction between these 2 risk factors separately for the major subtypes of stroke (ischemic and hemorrhagic).

In the current study, we attempted to overcome these limitations by investigating the joint relationship between systolic BP (SBP) and BMI on CVD and then separately for CHD, ischemic, and hemorrhagic stroke using individual participant data from the Asia Pacific Cohort Studies Collaboration (APCSC). This Collaboration contains a large number of CHD and stroke events with an unusually high number of hemorrhagic strokes and a wide range of BP and BMI levels.


Identification of Studies and Collection of Data

APCSC is an overview, using individual participant data, of prospective cohort studies from the Asia-Pacific region. The design and methods of the APCSC have been previously described in detail.2,3,20 All studies in APCSC had follow-up for at least 5000 person-years and recorded date of birth (or age), sex, and BP at baseline and date of death (or the age at death) during follow-up. Studies were excluded from APCSC if enrollment was dependent on having a particular condition or a risk factor. For this report, only participants aged >30 years with information on both SBP and BMI at study entry were included in the analysis. BP was generally measured at rest in the seated position using a standard mercury sphygmomanometer. Because the association between SBP and CVD is stronger than that for other BP indices,2,21,22 SBP was used as the BP index in this report. Height and weight were measured by standard methods and BMI was calculated as weight (kg) divided by squared height (m2). Participants at extreme ends of the BMI spectrum (<12 or >60 kg/m2) were excluded from the analysis.23 Smoking status was dichotomized into current/not current smoker.


All studies reported deaths by underlying cause; a subset of studies also reported nonfatal CVD events. Most studies used database linkages to identify deaths, whereas others also included scheduled follow-up visits or examined hospital records, particularly to identify nonfatal events, defined as those that did not result in death within 28 days.24 Outcomes were classified according to the Ninth Revision of International Classification of Disease. The outcomes considered in this analysis were: CHD (Ninth Revision of International Classification of Disease: 410–414), hemorrhagic stroke (431.0–432.9), ischemic stroke (433.0–434.9), and CVD (390–459). Because most studies identified events using record linkage, verification of stroke was not routinely reported. All data provided were checked for completeness and consistency and recoded, when necessary, to maximize comparability across cohorts. Summary reports were referred back to the principal investigators of each collaborating study for review and confirmation.

Statistical Methods

Stratified Cox proportional hazard models were used to examine the joint effects of SBP and BMI on CVD. Baseline hazards were allowed to be different by sex and cohort by using these variables as strata in the Cox models. Age and smoking status were included as confounders in the models. For the primary analysis, BMI was categorized according to 5 groups that are used clinically to determine an individual's weight status following the World Health Organization criteria for Asia-Pacific populations25: 12.0≤ BMI <18.5, underweight; 18.5≤ BMI <23.0, normal; 23.0≤ BMI <25.0, high-normal; 25.0≤ BMI <30.0, overweight; and 30.0≤ BMI ≤60.0 kg/m2, obese. In a secondary analysis, BMI was classified according to 5 equal-sized groups to facilitate a more equal distribution of events in the population.

Repeat measurements of SBP taken after a median of 4 years were available for 67 210 participants. These repeated measures were used to estimate the regression dilution attenuation coefficients for SBP using a linear mixed regression model that accounted for the heterogeneity of variance between studies and within-subject correlation.26,27 Hazard ratios (HR; 95% CIs) for all outcomes were estimated by analyzing SBP as both a continuous (per 10-mm Hg increase) and categorical variable (SBP <120; 120≤ SBP <140, 140≤ SBP <160, and SBP ≥160 mm Hg) within each category of BMI. We also examined the joint relationships between SBP and BMI by comparing the HRs of cardiovascular events across the 20 groups defined by the 4 SBP and 5 BMI categories relative to the reference group set at the lowest SBP and normal weight values (SBP <120 mm Hg and 18.5≤ BMI <23.0 kg/m2). The interaction between SBP and BMI on cardiovascular outcomes was assessed using likelihood ratio tests.27 The analyses were rerun after left-censoring by 2 years to protect against reverse causality. All statistical analyses were performed using SAS Release 9.20 (SAS Institute Inc, Cary, NC).


Baseline Data

Overall, 39 cohorts with individual data from 419 488 (78% Asian; 41% female) individuals contributed to this analysis (online-only Supplemental Table I). Mean SBP at baseline varied, between studies, from 120.3 to 157.1 mm Hg and mean BMI varied from 21.5 to 26.9 kg/m2. Both risk factors tended to be higher in those cohorts sourced from Australia or New Zealand compared with those from Asia.


Overall, there were 2 619 241 person-years of follow-up (mean follow-up, 6.2 years). The mean follow-up was 5.5 years and 8.9 years in cohorts from Asia and Australia–New Zealand, respectively. During follow-up, there were 10 877 CVD events (59% in Asia, 34% women, 71% fatal). Of these, there were 7010 strokes (1993 ischemic, 1508 hemorrhagic, and 3509 unclassified strokes) and 3867 CHD events.

The Impact of BMI on the SBP–CVD Association

The age and smoking-adjusted HR for CVD increased continuously with increasing SBP irrespective of BMI category (Figure 1); overall, for every 10-mm Hg increase in SBP, there was a 34% (95% CI, 32%–36%) increase in the risk of CVD (Figure 2). Irrespective of how BMI was classified (either according to the World Health Organization criteria or by fifths of the population), there was evidence to suggest that the association was slightly, but significantly, attenuated with increasing BMI such that the most obese individuals had the lowest risk of CVD per unit increase in SBP (Figure 2; online-only Supplemental Figure I). Left-censoring had no material impact of the results (online-only Supplemental Figure II). Compared with individuals with a normal weight and SBP <120 mm Hg, the risk of CVD was >4 times as high in obese individuals with SBP ≥160 mm Hg (HR, 4.4; 95% CI, 3.9–5.1; Figure 3).

Figure 1.

Figure 1. Hazard ratios, stratified by study and sex and adjusted for age and smoking status, for cardiovascular outcomes by usual systolic blood pressure (SBP) groups within body mass index (BMI; kg/m2) categories. In each BMI category, SBP <120 mm Hg was set as the reference group for CHD, ischemic stroke, and CVD, but, because there were no hemorrhagic stroke events within this group in the highest BMI category, SBP <140 mm Hg was set as the reference group for hemorrhagic stroke. Bars show 95% CIs intervals. “Usual” SBP denotes correction for regression dilution bias. A, coronary heart disease; B, ischemic stroke; C, hemorrhagic stroke; D, cardiovascular disease. CHD indicates coronary heart disease; CVD, cardiovascular disease.

Figure 2.

Figure 2. Hazard ratios, stratified by study and sex and adjusted for age and smoking status, for cardiovascular outcomes associated with a 10-mm Hg increase in usual systolic blood pressure among body mass index (BMI) categories. Bars show 95% CIs. The diamonds show overall results across all BMI categories. The vertical diagonal of the diamond indicates the estimate and the horizontal diagonal indicates the 95% CIs.

Figure 3.

Figure 3. Hazard ratios, stratified by study and sex and adjusted for age and smoking status, for cardiovascular outcomes by systolic blood pressure (SBP) and body mass index (BMI) categories. The reference group has the lowest SBP and normal weight (SBP <120 mm Hg and BMI 18.5–25.0 kg/m2). A, coronary heart disease; B, ischemic stroke; C, hemorrhagic stroke; D, cardiovascular disease.

The Impact of BMI on the SBP–CHD Association

Across all categories of BMI, the age and smoking-adjusted HRs for CHD rose with increasing levels of SBP (Figure 1); overall, for every 10-mm Hg increase in SBP, there was a 24% (95% CI, 21%–27%) increase in the risk of CHD (Figure 2). Like with total CVD, the association was not consistent across BMI with evidence to indicate a diminution in the relationship between SBP and risk of CHD as BMI increased throughout the normal to overweight range (probability value for interaction=0.01). In obese individuals, although the HR was elevated, the 95% CIs were wide due to a relatively small number of events. When BMI was classified by fifths (as opposed to the World Health Organization criteria), a more linear attenuation in the relationship between SBP and CHD risk became apparent (P for interaction=0.01; online-only Supplemental Figure I). The relationship remained largely unchanged after left-censoring (online-only Supplemental Figure II). Compared with individuals with normal weight and SBP <120 mm Hg, the risk of CHD was 4 times as high in obese individuals with SBP >160 mm Hg (HR, 4.1; 95% CI, 3.3–5.1; Figure 3).

The Impact of BMI on the SBP–Ischemic Stroke Association

The age and smoking-adjusted HRs for ischemic stroke increased continuously with increasing SBP irrespective of BMI category (Figure 1); overall, for every 10-mm Hg increase in SBP, there was a 46% (95% CI, 41%–51%) increase in the risk of ischemic stroke (Figure 2). The relationship between SBP and ischemic stroke was constant across a wide range of BMI values (Figure 2). It was significantly weaker among those classified as obese, although this was most likely a chance finding due to the small number of events because there was no indication of an interaction with BMI when examined by population fifths (P for interaction=0.24; online-only Supplemental Figure I) or after left-censoring (online-only Supplemental Figure II). Compared with individuals with a normal weight and SBP <120 mm Hg, the risk of ischemic stroke was nearly 6 times as high in obese individuals with SBP ≥160 mm Hg (HR, 5.9; 95% CI, 4.2–8.3; Figure 3).

The Impact of BMI on the SBP–Hemorrhagic Stroke Association

Irrespective of BMI category, the age and smoking-adjusted HRs for hemorrhagic stroke rose steeply, and continuously, as SBP increased (Figure 1). The HR for hemorrhagic stroke risk associated with a 10-mm Hg increase in SBP level was consistent across the BMI categories with no evidence of interaction (HR, 1.65; 95% CI, 1.59–1.71; P for interaction=0.18; Figure 2). These findings remained unchanged in analyses in which BMI was classified by population fifths (online-only Supplemental Figure I) or after left-censoring (online-only Supplemental Figure II). Compared with individuals with a normal weight and SBP <120 mm Hg, the risk of hemorrhagic stroke was >7 times as high in obese individuals with SBP >160 mm Hg (HR, 7.5; 95% CI, 5.0–11.2; Figure 3). However, at SBP >160 mm Hg, the risk of hemorrhagic stroke was greater in each of the other BMI categories than in the obese group, although given the small numbers of events on which this subgroup analysis is based (n=37 hemorrhagic stroke events in those <18.5 kg/m2 and n=38 in 18.5< BMI <22.9 kg/m2), caution in interpreting this result is warranted.


These analyses, based on prospective data from >400 000 individuals, demonstrate the strong role of BP in determining future risk of CHD and stroke across all levels of BMI. Irrespective of an individual's BMI, increases in SBP above levels of 120 mm Hg are associated, in a dose–response pattern, with a concomitant increase in the risk of CVD, CHD, and both ischemic and hemorrhagic stroke.

Findings from this study suggest that for incident CVD and CHD, but not stroke, the magnitude of the excess risk associated with changes in SBP diminished with increasing BMI such that the relationship between SBP and CHD risk was actually weaker among overweight individuals compared with the leanest individuals. Although the antagonistic interactions were statistically significant, the actual differences in BP-related CHD and CVD risk by BMI category were small and are unlikely to translate into meaningful clinical differences. These findings are consistent with some earlier reports that reported an antagonistic effect of BMI on the BP-related risk of CHD or CVD. For example, the Tecumseh Community Health Study,9 Israeli Ischemic Heart Study10 and Whitehall Study13 all reported a greater excess risk from higher SBP among lean individuals compared with those of ideal weight. In contrast, the Honolulu Heart Program,16 the British Regional Heart Study,17 and the Swedish Young Male Cohort Study14 did not report any effect modification on the risk of CHD.

Limited sample size and short study duration of study follow-up resulting in a small number of events are likely to have generated random noise within any 1 study. Given that the magnitude of any interaction between BMI and SBP on subsequent risk of CVD is likely to be rather modest, a large number of cardiovascular events across the BMI spectrum is required to reliably detect it. Thus, an insufficient number of events within the extreme World Health Organization categories of BMI may explain some of the less robust associations from the current study.

The precise biological mechanisms that may mediate the antagonistic effect of BMI on SBP and CHD and stroke subtypes risk remain unknown, although several explanations have been proffered. It has been suggested that hypertension among lean individuals occurs as a result of different and more hazardous biological mechanisms compared with hypertension in the obese, in whom weight gain is likely to be a key determinant of BP level.28

The explanation of their opposing findings of a synergistic effect of BMI on SBP-related CVD risk in the Swedish conscripts study is that of competing risks, obese hypertensives may be more likely to succumb to mortality from non-BP-related causes such as cancer than lean hypertensives, thereby creating a spurious “protective” effect of obesity on SBP-related risk of CVD. However, because greater risk among lean hypertensive persons compared with obese hypertensives has also been reported for total mortality, this is unlikely to account fully for the effect that we observed in the current study.19,29

The antagonistic effect that BMI may have on SBP and CVD risk may also potentially be due to confounding by cigarette smoking. Individuals who currently smoke or have quit smoking tend to have lower BMIs and an increased risk of death compared with never-smokers,12 which could therefore distort the relationship between BMI and mortality. However, like in the present study, the excess risk for CHD among lean hypertensives remains. A second possible explanation for the antagonistic effect is the existence of preclinical illness at baseline resulting in “reverse causality.” Compared with other subgroups, lean hypertensives could be disproportionately more affected by underlying disease.12 In the present study, to try to minimize the possibility of “reverse causation,” the data were left-censored by 2 years. Overall, this made little material difference to the study findings, although the possibility remains that 2 years was not a sufficiently long enough period of time to completely eliminate those individuals with pre-existing illness.

The current analysis has both strengths and limitations. The large sample size allowed a more reliable examination of the impact of BMI on SBP-related cardiovascular risk than had previously been possible. It also enabled the use of a stratified Cox model, which included 4 SBP categories and 5 BMI categories and their interaction terms and confounders. Unlike previous studies that used a separate Cox model for each category of BMI,14,15 our combined model is more statistically appropriate for the investigation of interactions between risk factors and disease outcomes. We were also able to adjust for the possible confounding effect of cigarette smoking and for error in the measurement of SBP by correcting for regression dilution error. Moreover, this is the first comprehensive study showing the interaction between SBP and BMI on CHD and stroke subtypes. The major weaknesses of the study include the lack of standard methods of data collection across the cohorts and a possible misclassification of events, particularly with respect to stroke subtype, which requires verification, by imaging or through autopsy data, which was not always possible.

The rationale for undertaking this study was largely because current hypertension and stroke guidelines emphasize the separate roles of SBP and BMI in determining vascular risk without considering the existence of an interaction. Because the main CVD risk algorithms30,31 do not include a term for the SBP by BMI interaction, this could result in a slight overestimation of CVD risk among overweight subjects. However, we find that the magnitude of the interaction is modest and hence such an omission is unlikely to have major implications for current risk scores. Moreover, given that trial data indicate that the reduction in major cardiovascular risks with BP-lowering therapy is consistent across categories of BMI,32 we conclude that current hypertension and stroke guidelines do not require modification to allow for an individual's current body size.

Source of Funding

Supported by the National Health and Medical Research Council of Australia program grant 571281.


Dr Murakami was supported by the Banyu Fellowship Program sponsored by Banyu Life Science Foundation International.


For a list of collaborators in the Asia Pacific Cohort Studies Collaboration see the online-only Appendix.

The online-only Data Supplement is available with this article at

Correspondence to Mark Woodward, PhD,
Professorial Unit, The George Institute for Global Health, University of Sydney, PO Box M201, Missenden Road, NSW 2050, Australia
. E-mail


  • 1. Lewington S, Clarke R, Qizilbash N, Peto R, Collins R. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet. 2002; 360:1903–1913.CrossrefMedlineGoogle Scholar
  • 2. Asia Pacific Cohort Studies Collaboration.Blood pressure and cardiovascular diseases in the Asia-Pacific region. J Hypertens.2003; 21:707–716.CrossrefMedlineGoogle Scholar
  • 3. Asia Pacific Cohort Studies Collaboration.Body mass index and cardiovascular disease in the Asia-Pacific region: an overview of 33 cohorts involving 310 000 participants. Int J Epidemiol.2004; 33:751–758.CrossrefMedlineGoogle Scholar
  • 4. Haslam DW, James WPT. Obesity. Lancet. 2005; 366:1197–1209.CrossrefMedlineGoogle Scholar
  • 5. Whitlock G, Lewington S, Sherliker P, Clarke R, Emberson J, Halsey J , et al. Prospective Studies Collaboration. Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies. Lancet. 2009; 373:1083–1096.CrossrefMedlineGoogle Scholar
  • 6. Kearney PM, Whelton M, Reynolds K, Muntner P, Whelton PK, He J. Global burden of hypertension: analysis of worldwide data. Lancet. 2005; 365:217–223.CrossrefMedlineGoogle Scholar
  • 7. Ezzati M, Vander Hoorn S, Lopez AD, Danaei G, Rodgers A, Mathers CD , et al. Comparative quantification of mortality and burden of disease attributable to selected risk factors. In: , Lopez AD, Mathers CD, Ezzati M, Jamison DT, Murray CJL eds. Global Burden of Disease and Risk Factors.Washington, DC: World Bank; 2006: 241– 268.Google Scholar
  • 8. Barrett-Connor E, Khaw KT. Is hypertension more benign when associated with obesity?Circulation. 1985; 72:53–60.LinkGoogle Scholar
  • 9. Carman WJ, Barrett-Connor E, Sowers M, Khaw KT. Higher risk of cardiovascular mortality among lean hypertensive individuals in Tecumseh, Michigan. Circulation. 1994; 89:703–711.LinkGoogle Scholar
  • 10. Goldbourt U, Holtzman E, Cohen-Mandelzweig L, Neufeld HN. Enhanced risk of coronary heart disease mortality in lean hypertensive men. Hypertension. 1987; 10:22–28.LinkGoogle Scholar
  • 11. Cambien F, Chretien JM, Ducimetiere P, Guize L, Richard JL. Is the relationship between blood pressure and cardiovascular risk dependent on body mass index?Am J Epidemiol. 1985; 122:434–442.CrossrefMedlineGoogle Scholar
  • 12. Stamler R, Ford CE, Stamler J. Why do lean hypertensives have higher mortality rates than other hypertensives? Findings of the Hypertension Detection and Follow-Up Program.Hypertension. 1991; 17:553–564.LinkGoogle Scholar
  • 13. Elliott P, Shipley MJ, Jarrett RJ. Obesity and hypertension. Lancet. 1988; 1:995CrossrefMedlineGoogle Scholar
  • 14. Silventoinen K, Magnusson PK, Neovius M, Sundstrom J, Batty GD, Tynelius P , et al. Does obesity modify the effect of blood pressure on the risk of cardiovascular disease? A population-based cohort study of more than one million Swedish men.Circulation. 2008; 118:1637–1642.LinkGoogle Scholar
  • 15. Wang H, Cao J, Li J, Chen J, Wu X, Duan X , et al. Blood pressure, body mass index and risk of cardiovascular disease in Chinese men and women. BMC Public Health. 2010; 10:189CrossrefMedlineGoogle Scholar
  • 16. Bloom E, Reed D, Yano K, MacLean C. Does obesity protect hypertensives against cardiovascular diseases?JAMA. 1986; 256:2972–2975.CrossrefMedlineGoogle Scholar
  • 17. Phillips A, Shaper AG. Relative weight and major ischaemic heart disease events in hypertensive men. Lancet. 1989; 1:1005–1008.CrossrefMedlineGoogle Scholar
  • 18. Kannel WB, Zhang T, Garrison RJ. Is obesity-related hypertension less of a cardiovascular risk? The Framingham Study.Am Heart J. 1990; 120:1195–1201.CrossrefMedlineGoogle Scholar
  • 19. Bender R, Jockel KH, Richter B, Spraul M, Berger M. Body weight, blood pressure, and mortality in a cohort of obese patients. Am J Epidemiol. 2002; 156:239–245.CrossrefMedlineGoogle Scholar
  • 20. Woodward M, Barzi F, Martiniuk A, Fang X, Gu DF, Imai Y , et al. Cohort profile: the Asia Pacific Cohort Studies Collaboration. Int J Epidemiol. 2006; 35:1412–1416.CrossrefMedlineGoogle Scholar
  • 21. Miura K, Dyer AR, Greenland P, Daviglus ML, Hill M, Liu K , et al. Chicago Heart Association.Pulse pressure compared with other blood pressure indexes in the prediction of 25-year cardiovascular and all-cause mortality rates: the Chicago Heart Association Detection Project in Industry Study. Hypertension. 2001; 38:232–237.LinkGoogle Scholar
  • 22. Asia Pacific Cohort Studies Collaboration.Blood pressure indices and cardiovascular disease in the Asia Pacific region: a pooled analysis. Hypertension.2003; 42:69–75.LinkGoogle Scholar
  • 23. Parr CL, Batty GD, Lam TH, Barzi F, Fang X, Ho SC , et al. Asia-Pacific Cohort Studies Collaboration.Body-mass index and cancer mortality in the Asia-Pacific Cohort Studies Collaboration: pooled analyses of 424 519 participants. Lancet Oncol. 2010; 11:741–752.CrossrefMedlineGoogle Scholar
  • 24. Asia Pacific Cohort Studies Collaboration.Joint effects of systolic blood pressure and serum cholesterol on cardiovascular disease in the Asia Pacific region. Circulation.2005; 112:3384–3390.LinkGoogle Scholar
  • 25. WHO/IASO/IOTF.The Asia-Pacific Perspective: Redefining Obesity and Its Treatment.Melbourne, Australia: Health Communications Australia; 2000.Google Scholar
  • 26. MacMahon S, Peto R, Cutler J, Collins R, Sorlie P, Neaton J , et al. Blood pressure, stroke, and coronary heart disease. Part 1, prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias. Lancet. 1990; 335:765–774.CrossrefMedlineGoogle Scholar
  • 27. Woodward M. Epidemiology: Study Design and Data Analysis,II ed.Boca Raton, FL: Chapman & Hall/CRC Press; 2005: 450– 452.Google Scholar
  • 28. Dustan HP. Mechanisms of hypertension associated with obesity. Ann Intern Med. 1983; 98:860–864.CrossrefMedlineGoogle Scholar
  • 29. Menotti A, Giampaoli S, Pasquali M, Seccareccia F, Stuart K. Prognosis of lean and fat hypertensives. Cardiology. 1988; 75:448–457.CrossrefMedlineGoogle Scholar
  • 30. Ridker PM, Buring JE, Rifai N, Cook RN. Development and validation of improved algorithms for the assessment of global cardiovascular risk in women: the Reynolds risk score. JAMA. 2007; 297:611–619.CrossrefMedlineGoogle Scholar
  • 31. D'Agostino RB, Vasan RS, Pencina MJ, Wolf PA, Cobain MR, Massaro JM , et al. General cardiovascular risk profile for use in primary care. Circulation. 2008; 117:743–753.LinkGoogle Scholar
  • 32. Czernichow S, Ninomiya T, Huxley R, Kengne AP, Batty GD, Grobbee DE , et al. Impact of blood pressure lowering on cardiovascular outcomes in normal weight, overweight, and obese individuals: the Perindopril Protection Against Recurrent Stroke Study trial. Hypertension. 2010; 55:1193–1198.LinkGoogle Scholar


eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.

Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.