Circulation. 2004;110:e7-e12
doi: 10.1161/01.CIR.0000135583.40730.21
(Circulation. 2004;110:e7-e12.)
© 2004 American Heart Association, Inc.
Perspective on Selected Issues in Cardiovascular Disease Research With a Focus on Black Americans
Michelle A. Albert, MD, MPH;
Jose Torres;
Robert J. Glynn, PhD;
Paul M Ridker, MD, MPH
From the Center for Cardiovascular Disease Prevention and the Leducq Center for Cardiovascular Research, Divisions of Cardiovascular Diseases and of Preventive Medicine, Brigham and Womens Hospital, Harvard Medical School, Boston, Mass.
Correspondence to Dr Michelle A. Albert, Cardiovascular Division, Brigham and Womens Hospital, 75 Francis St, Boston MA 02115. E-mail maalbert{at}partners.org
 |
Introduction
|
|---|
Case Presentation: Mr A is a healthy 38-year-old black male
who comes to the clinic as a self-referral after a blood pressure
check during "Health Day" at his job. Mr A is concerned because
"high blood pressure" runs in his family. He reveals that his
58-year-old mother recently suffered a mild stroke and also
takes water pills to reduce swelling in her legs. He denies
any other health problems, is a non-smoker, and takes no medications.
On physical examination, his supine blood pressure is 165/85,
his heart rate is 74 bpm, and his weight is 72 kg. An ECG shows
normal sinus rhythm at 76 bpm and evidence of left ventricular
hypertrophy. A fasting lipid profile shows a total cholesterol
level of 196 mg/dL, a low-density lipoprotein cholesterol (LDL-C)
level of 120 mg/dL, a high-density lipoprotein cholesterol (HDL-C)
level of 50 mg/dL, a triglyceride level of 130 mg/dL, and C-reactive
protein level of 3.5 mg/L. What clinical strategy would be most
appropriate for Mr A? What is the available scientific evidence
to support your choice(s)?
Despite advances in the diagnosis and treatment of cardiovascular disease (CVD), morbidity and mortality from CVD is higher among black Americans than among white, Hispanic, and Asian Americans.1 Although black Americans are often considered to have less obstructive coronary heart disease than age-matched whites,2,3 the prevalence of traditional risk factors for CVD such as hypertension, diabetes mellitus, smoking, and obesity disproportionately affects black Americans. However, the relative importance of these risk factors and others, such as left ventricular hypertrophy, dyslipidemia, and novel risk determinants such as C-reactive protein and lipoprotein (a), on morbidity and mortality is unclear. At the population level, research efforts have focused primarily on the components of the Framingham Cardiovascular Risk Equation that were developed in a predominantly white cohort. Other important cardiovascular risk determinants that likely contribute to the disparity in CVD noted between ethnic groups include socioeconomic status, cultural issues, access to health care, and care provided by health professionals according to race/ethnicity.
 |
Selected Traditional Risk Factors
|
|---|
Hypertension
Epidemiological studies have documented a strong relationship
between hypertension and CVD among blacks. Data from the National
Health and Nutrition Examination Survey (NHANES) indicate that
at least 33.5% of blacks and 28.9% of whites have hypertension
and that black race was an independent predictor of hypertension.
4 The development of hypertension and its relationship to CVD
is multifactorial and likely includes both environmental and
physiological/genetic components, including endothelial dysfunction,
subendocardial fibrosis, and left ventricular hypertrophy (LVH).
5,6 The relationship of LVH to cardiac death
6,7 is of particular
importance in blacks because of the higher prevalence of hypertension
associated LVH in this ethnic group. Echocardiographic data
from the Coronary Artery Risk Development in Young Adults study
showed that LV mass was higher in blacks than in whites and
correlated with systolic blood pressure.
8 LVH in the presence
of hypertension is associated with an increased risk of sudden
cardiac death, probably due in part to complex ventricular arrhythmias,
factors related to myocardial oxygen supply/demand, and subendocardial
fibrosis.
7,9 In one study that included only black males, among
those men with hypertensive LVH, asymptomatic non-sustained
ventricular tachycardia independently predicted subsequent cardiovascular
events.
10 These findings warrant further investigation, particularly
because black Americans have a higher prevalence of out of hospital
sudden cardiac death than other race/ethnic groups, an outcome
that likely reflects both physiological and access-to-care issues.
Other work demonstrated that normotensive black and white youths with a family history of hypertension who had LVH at baseline were more likely to have greater blood pressure reactivity to stress at follow-up.11 This finding suggests possible important interactions between environmental stress and physiology that could result in deleterious cardiovascular consequences over the long-term. Further research evaluating the prevalence of LVH in normotensive and hypertensive blacks and the direct relationship to CVD mortality could be critical to improving our understanding and attenuating observed race related differences in hypertensive heart disease.
Dyslipidemia
Longitudinal population data that examine the distribution of lipid levels or the predictive power of these lipid values for coronary artery disease among various ethnic groups are limited. One such studyNHANES IIIshowed that blacks have lower nonHDL-C levels than whites or Mexican-Americans.12 Additionally, studies have indicated that blacks tend to have lower total cholesterol and triglyceride levels but higher HDL-C levels than whites.13,14 Meanwhile, a large multi-ethnic study suggested that HDL-C was more protective in white persons for coronary artery disease (CAD), but that there were no significant differences in the predictive capacity of LDL-C across ethnic groups.15 International data that evaluate the lipid profile of people of African descent are also consistent with the United States data regarding lower triglyceride and higher HDL-C levels.16 These findings are important and require further investigation, as a major target of CAD risk reduction involves education and lipid-lowering therapy. It may be that target lipid goals are different among blacks, or alternatively, that cardiovascular mortality benefit from triglyceride lowering or HDL-C increases would be substantial in high-risk individuals even if their triglyceride and HDL-C levels are within recommended target range. Evidence that supports the latter assertion is noted in the Heart Protection Study, where participants benefited significantly from simvastatin therapy regardless of whether they had triglyceride levels above or below 178 mg/dL or HDL-C levels above or below 42.9 mg/dL.17 Although some authors have recognized that these differences in lipid levels may contribute to the lower observed rates of coronary heart disease in persons of African heritage, it is interesting to note that whereas blacks in the United States also traditionally experience lower rates of CAD, they still have higher morbidity and mortality from CVD than other ethnic groups, a circumstance in which lipoprotein distribution potentially plays a role.
Until the publication of Antihypertensive and Lipid-Lowering treatment to prevent Heart Attack Trial-Lipid Lowering Trial (ALLHAT-LLT), black American representation in major lipid lowering trials was generally less than 8%; therefore, limited data exist on any blackwhite differences in cholesterol lowering.1820 Among blacks, ALLHAT-LLT demonstrated a 27% reduction in coronary events with pravastatin therapy compared with usual care, a finding that showed a greater benefit in this subgroup compared with the non-black population.21
Despite differences in lipid parameters according to race/ethnicity, the clustering of certain CVD risk factors can result in a risk profile that arguably abolishes the effect of any lipid differences noted between blacks and whites. For example, a non-interventional outpatient study noted that among patients with type II diabetes, almost 50% of black patients compared with 42% of white patients had LDL-C levels above and HDL-C below the recommended goals, but blacks were still more likely than whites to have HDL-C or triglyceride levels within the recommended target range.22 In other data from the Bogalusa Heart Study, triglyceride levels were lower among black than white females despite their increased body mass index. Overall, although high triglyceride levels were positively associated with increased visceral fatness and insulin resistance, particularly at levels above 150 mg/dL, the combination of high triglyceride and low HDL-C levels tended to increase the likelihood of diabetes and hypertension and was present in 9% of white males, 3% of white females, 4% of black males, and 0% of black females.23 These data highlight several issues: (1) cardiovascular risk factors cluster to influence disease; (2) the contribution of triglycerides to CAD risk may vary by race/ethnicity; and (3) although improvement of LDL-C and HDL-C are important antiatherogenic targets, further research is needed to understand the observed differences in lipid levels and CAD outcomes by race/ethnicity. Specifically, data on the mechanisms of these differences, as well as the relationship/impact of these differences to other risk factors for CVD such as obesity, are necessary.
Metabolic Syndrome
The metabolic syndrome is present in almost 25% of Americans and the prevalence varies by ethnicity.24 Moreover, although the distribution of components of the metabolic syndrome might be similar across the 4 major race/ethnic groups in the United States, the relative contribution of the various components of the metabolic syndrome to CVD also varies by ethnicity.25 Among black women, blood pressure and dyslipidemia appeared to have the strongest associations with CVD, whereas obesity was more tightly linked with CVD for Hispanic and white women. These findings require further investigation, as it is likely that these factors also cluster with other factors such as fibrinolytic and inflammatory parameters to influence cardiovascular risk.
Additionally, the relationship between obesity and its associated correlates with cardiovascular end points such as congestive heart failure and sudden death among blacks is unknown. Both are conditions that occur in higher frequency and account for a significant proportion of CVD burden among blacks. Individual analyses of these potential relationships might provide insight into the impact of the metabolic syndrome on CVD risk as well as the pathobiology of CVD in various ethnic groups. For example, it is possible that there exists a pathophysiological link between increased body mass index and sudden death via arrhythmias in addition to de novo CAD that varies by ethnicity. Such a hypothesis arises from data that demonstrate an association between increased LVH and characteristics of the insulin resistance syndrome, including insulin levels, systolic blood pressure, and waist girth. This hypothesis is also supported by autopsy data that indicate an excess of sudden cardiac death among older blacks compared with whites due to stable plaques, where the presence of stable plaque was associated with LVH and hypertension.26,27
 |
Novel Cardiovascular Risk Factors
|
|---|
Little comparative information across race/ethnic groups in
the United States is known about any relationship between novel
risk factors of thrombosis and inflammation and CVD. For example,
although multiple prospective studies show that C-reactive protein
(CRP) is an independent predictor of vascular risk, rigorous
prospective data in minority groups are virtually nonexistent.
Most of the data regarding ethnicity and CRP relate to ethnic
groups in Europe, where CRP levels were higher among the South
Asian population compared with Europeans and lower in African-Caribbeans
than Europeans in the United Kingdom.
2830 In the United
States, data from NHANES, as well as from a study of black women
<30 years old, suggest that CRP levels are higher in blacks
than in their white counterparts.
31,32 Although these data likely
reflect both environmental and genetic factors, they are nonetheless
disturbing, as both groups studied lacked clinical cardiovascular
disease. Data on other inflammatory markers of atherosclerosis,
such as adhesion molecules and interleukins, are also sparse.
Similarly, although elevated lipoprotein (a) (Lp[a]) levels are associated with incident CAD in whites, among black individuals, Lp(a) levels are higher and the data are conflicting regarding the strength of association for CAD.3335 This discrepancy in risk is in part attributed to the epidemiological observation of lower LDL and higher HDL levels in black subjects as compared with white subjects. Additionally, some groups have argued that apolipoprotein (a) size is an important co-contributor to cardiovascular risk in black subjects.
Other data have suggested enhanced fibrinolytic potential in black individuals compared with white individuals. One study demonstrated that tPA antigen levels were higher in blacks, and subsequently higher coronary artery patency rates are noted after fibrinolysis.36 Additional data also show that PAI-1 levels were lower among blacks than among whites and Hispanics and that there was an association between the PAI-1 4G/5G polymorphism and serum levels of PAI-1, as well as with ethnicity.37 These data further emphasize the need for large-scale prospective data that investigate the interrelations between novel markers of thrombosis and inflammation and cardiovascular disease across ethnic groups.
Socioeconomic Status
The most frequently used measures of socioeconomic status (SES) in medical research are income, education level, and employment type. Among all ethnic groups, multiple studies demonstrate that lower SES is associated with worse cardiovascular status.38,39 Although over the last decade a solid black middle class has emerged, socio-demographic data indicate that overall blacks are among the poorest Americans, a factor that undeniably affects their health. Further, some data suggest that increasing income and education among some blacks correlates with improved health, whereas other data indicate that the health of income/education advantaged blacks still overall remains poor.40 For example, national data demonstrate that the infant mortality rate of educated black women, a sensitive measure of all cause morbidity and mortality, is 2 times higher than the rate for white women and is also higher than that of women from other race/ethnic groups.41 Likewise, cardiovascular mortality statistics in population cohorts that are comprised of persons of similar employment or insurance status indicate that black participants in those cohorts have higher cardiovascular mortality rates than white participants.42 These data suggest that in addition to the traditional cardiovascular risk factors, other variables such as racism, neighborhood factors, and stress likely also impact SES and as such must be studied in conjunction with the former risk characteristics to understand outcomes.
Of the large epidemiological cohort studies that examine cardiovascular risk determinants, few collect information about stress or neighborhood factors. One interesting study reported that among black men living in disadvantaged neighborhoods, increased income and education were positively related to the insulin resistance syndrome, whereas among whites and black women, there was an inverse association between advantaged neighborhood status and the insulin resistance syndrome.43 Other data indicate that among black children, both lower family and neighborhood SES were associated with hostility and greater cardiovascular reactivity to stressors, but among white children, only lower family SES was associated with increased cardiovascular reactivity, a factor related to increased left ventricular mass.44 Because SES is such a complex and difficult measure to capture, particularly in minority communities, one potential strategy might be to use an SES score that is composed of multiple variables, including and among others income, education, occupation status, community status/involvement, and violence. Although the latter strategy has been used in the social science community and in health population studies in Europe, comparative epidemiological or clinical trial data in the United States that utilize a combined measure of SES beyond education and income are sparse.
 |
Case Presentation Continued: Treatment
|
|---|
Application of current Adult Treatment Panel III guidelines
to Mr As case presentation would result in treatment
of his hypertension most likely with diuretic and/or ß-blocker
therapy, as well as a recommendation for increased physical
activity. According to the guidelines, Mr A has 2 major risk
factors for coronary heart disease: Hypertension and a family
history of premature CHD. Despite the latter, his calculated
Framingham 10-year estimate of cardiovascular risk is 1%. Although
Mr As CRP level would be considered elevated, there are
currently no firm guidelines that recommend treatment of the
latter; however, there are available data that suggest that
CRP adds predictive data to the Framingham risk calculation.
45,46
 |
Conclusion
|
|---|
Elimination of race/ethnic disparities in cardiovascular health
is a solvable problem that will require a multifaceted approach.
Although this article focused on CVD risk factor investigation,
currently the most immediate strategy toward eliminating disparities
and improving health of blacks in the United States involves
provision of equal and affordable care to all race/ethnic groups,
adherence to national cardiovascular guidelines, and the nurturing,
recruitment, and retention of minority clinicians and researchers.
In addition to these issues, aggressive effort must be put forth
by researchers to recruit participants from minority groups
into clinical trials and cohorts. This has proven difficult
for many reasons, including lack of participant trust, lack
of faith in the medical system, carryover from the Tuskegee
experiment, and circumstances surrounding the continued racial
divide in this country.
47 The
Table demonstrates the representation
of blacks in some of the major randomized clinical trials.
48
Furthermore, as many of the precursors of cardiovascular disease are present in children and young adults, particularly in minority groups, public health strategies such as smoking cessation and increased physical activity should also target these groups.49 From a risk factor research perspective, not only must available data be used more effectively, but also novel questions for investigation and approaches to research operation may be required. For example, the composition and structure of research teams may need reconfiguration to include a multidisciplinary network of nurses, social workers, community advocates, and academic researchers instead of the traditional academic center-focused model. From a clinical perspective, individual physicians must strive to ensure that all of their patients achieve target levels of modifiable risk indicators regardless of race/ethnicity and that culturally sensitive educational tools are available for patient treatment.
 |
References
|
|---|
- Trends in ischemic heart disease rates for blacks and whites: United States, 19811995. MMWR Morbid Mortal Wkly Rep. 1998; 47: 945949.[Medline]
[Order article via Infotrieve]
- Clark LT, Ferdinand KC, Flack JM, et al. Coronary heart disease in African Americans. Heart Dis. 2001; 3: 97108.[CrossRef][Medline]
[Order article via Infotrieve]
- Keil JE, Sutherland SE, Knapp RG, et al. Mortality rates and risk factors for coronary disease in black as compared with white men and women. N Engl J Med. 1993; 329: 7378.[Abstract/Free Full Text]
- Hajjar I, Kotchen TA. Trends in prevalence, awareness, treatment, and control of hypertension in the United States, 19882000. JAMA. 2003; 290: 199206.[Abstract/Free Full Text]
- Frohlich ED. State of the art lecture: risk mechanisms in hypertensive heart disease. Hypertension. 1999; 34: 782789.[Abstract/Free Full Text]
- Tin LL, Beevers DG, Lip GY. Hypertension, left ventricular hypertrophy, and sudden death. Curr Cardiol Rep. 2002; 4: 449457.[Medline]
[Order article via Infotrieve]
- Saadeh AM, Jones JV. Predictors of sudden cardiac death in never previously treated patients with essential hypertension: long-term follow-up. J Hum Hypertens. 2001; 15: 677680.[CrossRef][Medline]
[Order article via Infotrieve]
- Gardin JM, Wagenknecht LE, Anton-Culver H, et al. Relationship of cardiovascular risk factors to echocardiographic left ventricular mass in healthy young black and white adult men and women: the CARDIA study. Coronary Artery Risk Development in Young Adults. Circulation. 1995; 92: 380387.[Abstract/Free Full Text]
- Hennersdorf MG, Niebch V, Perings C, et al. T wave alternans and ventricular arrhythmias in arterial hypertension. Hypertension. 2001; 37: 199203.[Abstract/Free Full Text]
- Greenberg MD, Papademetriou V, Narayan P, et al. Nonsustained ventricular tachycardia as a predictor of cardiovascular events in black men with hypertensive left ventricular hypertrophy. J Clin Hypertens (Greenwich). 2000; 2: 1419.[Medline]
[Order article via Infotrieve]
- Murdison KA, Treiber FA, Mensah G, et al. Prediction of left ventricular mass in youth with family histories of essential hypertension. Am J Med Sci. 1998; 315: 118123.[CrossRef][Medline]
[Order article via Infotrieve]
- Gardner CD, Winkleby MA, Fortmann SP. Population frequency distribution of non-high-density lipoprotein cholesterol: Third National Health and Nutrition Examination Survey [NHANES III], 19881994. Am J Cardiol. 2000; 86: 299304.[CrossRef][Medline]
[Order article via Infotrieve]
- Watkins LO, Neaton JD, Kuller LH. Racial differences in high-density lipoprotein cholesterol and coronary heart disease incidence in the usual-care group of the Multiple Risk Factor Intervention Trial. Am J Cardiol. 1986; 57: 538545.[CrossRef][Medline]
[Order article via Infotrieve]
- Hutchinson RG, Watson RL, Davis CE, et al. Racial differences in risk factors for atherosclerosis: the ARIC Study. Angiology. 1997; 48: 279290.[Medline]
[Order article via Infotrieve]
- Jones DW, Chambless LE, Folsom AR, et al. Risk factors for coronary heart disease in African Americans: the atherosclerosis risk in communities study, 19871997. Arch Intern Med. 2002; 162: 25652571.[Abstract/Free Full Text]
- Zoratti R. A review on ethnic differences in plasma triglycerides and high-density-lipoprotein cholesterol: is the lipid pattern the key factor for the low coronary heart disease rate in people of African origin? Eur J Epidemiol. 1998; 14: 921.[CrossRef][Medline]
[Order article via Infotrieve]
- MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002; 360: 722.[CrossRef][Medline]
[Order article via Infotrieve]
- Sacks FM, Pfeffer MA, Moye LA, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators. N Engl J Med. 1996; 335: 10019.[Abstract/Free Full Text]
- Prisant LM, Downton M, Watkins LO, et al. Efficacy and tolerability of lovastatin in 459 African-Americans with hypercholesterolemia. Am J Cardiol. 1996; 78: 420424.[CrossRef][Medline]
[Order article via Infotrieve]
- Major outcomes in moderately hypercholesterolemic, hypertensive patients randomized to pravastatin vs usual care: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT-LLT). JAMA. 2002; 288: 29983007.[Abstract/Free Full Text]
- Curry C, Clark L, Watkins, L et al. Clinical implications of ALLHAT for African-Americans. Urban Cardiol. 2003; 10: 916.
- Cook CB, Erdman DM, Ryan GJ, et al. The pattern of dyslipidemia among urban African-Americans with type 2 diabetes. Diabet Care. 2000; 23: 319324.[Abstract]
- Frontini MG, Srinivasan SR, Elkasabany A, et al. Distribution and cardiovascular risk correlates of serum triglycerides in young adults from a biracial community: the Bogalusa Heart Study. Atherosclerosis. 2001; 155: 201209.[CrossRef][Medline]
[Order article via Infotrieve]
- Park YW, Zhu S, Palaniappan L, et al. The metabolic syndrome: prevalence and associated risk factor findings in the US population from the Third National Health and Nutrition Examination Survey, 19881994. Arch Intern Med. 2003; 163: 427436.[Abstract/Free Full Text]
- Howard BV, Criqui MH, Curb JD, et al. Risk factor clustering in the insulin resistance syndrome and its relationship to cardiovascular disease in postmenopausal white, black, Hispanic, and Asian/Pacific Islander women. Metabolism. 2003; 52: 362371.[CrossRef][Medline]
[Order article via Infotrieve]
- Davis CL, Kapuku G, Snieder H, et al. Insulin resistance syndrome and left ventricular mass in healthy young people. Am J Med Sci. 2002; 324: 7275.[Medline]
[Order article via Infotrieve]
- Burke AP, Farb A, Pestaner J, et al. Traditional risk factors and the incidence of sudden coronary death with and without coronary thrombosis in blacks. Circulation. 2002; 105: 419424.[Abstract/Free Full Text]
- Chatha K, Anderson NR, Gama R. Ethnic variation in C-reactive protein: UK resident Indo-Asians compared with Caucasians. J Cardiovasc Risk. 2002; 9: 139141.[CrossRef][Medline]
[Order article via Infotrieve]
- Forouhi NG, Sattar N, McKeigue PM. Relation of C-reactive protein to body fat distribution and features of the metabolic syndrome in Europeans and South Asians. Int J Obes Relat Metab Disord. 2001; 25: 13271331.[CrossRef][Medline]
[Order article via Infotrieve]
- Heald AH, Anderson SG, Ivison F, et al. C-reactive protein and the insulin-like growth factor (IGF)-system in relation to risk of cardiovascular disease in different ethnic groups. Atherosclerosis. 2003; 170: 7986.[CrossRef][Medline]
[Order article via Infotrieve]
- Palaniappan L, Anthony MN, Mahesh C, et al. Cardiovascular risk factors in ethnic minority women aged < or =30 years. Am J Cardiol. 2002; 89: 524549.[CrossRef][Medline]
[Order article via Infotrieve]
- Wener MH, Daum PR, McQuillan GM. The influence of age, sex, and race on the upper reference limit of serum C-reactive protein concentration. J Rheumatol. 2000; 27: 23512359.[Medline]
[Order article via Infotrieve]
- Sorrentino MJ, Vielhauer C, Eisenbart JD, et al. Plasma lipoprotein (a) protein concentration and coronary artery disease in black patients compared with white patients. Am J Med. 1992; 93: 658662.[CrossRef][Medline]
[Order article via Infotrieve]
- Guyton JR, Dahlen GH, Patsch W, et al. Relationship of plasma lipoprotein Lp(a) levels to race and to apolipoprotein B. Arteriosclerosis. 1985; 5: 265272.[Abstract/Free Full Text]
- Moliterno DJ, Jokinen EV, Miserez AR, et al. No association between plasma lipoprotein(a) concentrations and the presence or absence of coronary atherosclerosis in African-Americans. Arterioscler Thromb Vasc Biol. 1995; 15: 8505.[Abstract/Free Full Text]
- Sane DC, Stump DC, Topol EJ, et al. Racial differences in responses to thrombolytic therapy with recombinant tissue-type plasminogen activator: increased fibrin(ogen)olysis in blacks. The Thrombolysis and Angioplasty in Myocardial Infarction Study Group. Circulation. 1991; 83: 170175.[Abstract/Free Full Text]
- Festa A, DAgostino R Jr, Rich SS, et al. Promoter (4G/5G) plasminogen activator inhibitor-1 genotype and plasminogen activator inhibitor-1 levels in blacks, Hispanics, and non-Hispanic whites: the Insulin Resistance Atherosclerosis Study. Circulation. 2003; 107: 24222427.[Abstract/Free Full Text]
- Marmot MG. Understanding social inequalities in health. Perspect Biol Med. 2003; 46: S9S23.[Medline]
[Order article via Infotrieve]
- Kaplan GA, Keil JE. Socioeconomic factors and cardiovascular disease: a review of the literature. Circulation. 1993; 88: 19731998.[Abstract/Free Full Text]
- Winkleby MA, Kraemer HC, Ahn DK, et al. Ethnic and socioeconomic differences in cardiovascular disease risk factors: findings for women from the Third National Health and Nutrition Examination Survey, 19881994. JAMA. 1998; 280: 356362.[Abstract/Free Full Text]
- Lu MC, Halfon N. Racial and ethnic disparities in birth outcomes: a life-course perspective. Matern Child Health J. 2003; 7: 1330.[CrossRef][Medline]
[Order article via Infotrieve]
- Kaiser Family Foundation. Racial/Ethnic Differences in Cardiac Care: The Weight of the Evidence. Available at: http://www.kff.org/uninsured/20021009c-index.cfm. Accessed June 25, 2004.
- Diez Roux AV, Jacobs DR, Kiefe CI. Neighborhood characteristics and components of the insulin resistance syndrome in young adults: the coronary artery risk development in young adults (CARDIA) study. Diabet Care. 2002; 25: 19761982.[Abstract/Free Full Text]
- Gump BB, Matthews KA. Vigilance and cardiovascular reactivity to subsequent stressors in men: a preliminary study. Health Psychol. 1998; 17: 9396.[CrossRef][Medline]
[Order article via Infotrieve]
- Ridker PM, Rifai N, Rose L, et al. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med. 2002; 347: 15571565.[Abstract/Free Full Text]
- Albert MA, Glynn RJ, Ridker PM. Plasma concentration of C-reactive protein and the calculated Framingham coronary heart disease risk score. Circulation. 2003; 108: 161165.[Abstract/Free Full Text]
- Corbie-Smith G. The continuing legacy of the Tuskegee Syphilis Study: considerations for clinical investigation. Am J Med Sci. 1999; 317: 58.[CrossRef][Medline]
[Order article via Infotrieve]
- Hall WD. Representation of blacks, women, and the very elderly (aged > or = 80) in 28 major randomized clinical trials. Ethn Dis. 1999; 9: 333340.[Medline]
[Order article via Infotrieve]
- Winkleby MA, Robinson TN, Sundquist J, et al. Ethnic variation in cardiovascular disease risk factors among children and young adults: findings from the Third National Health and Nutrition Examination Survey, 19881994. JAMA. 1999; 281: 10061013.[Abstract/Free Full Text]
This article has been cited by other articles:

|
 |

|
 |
 
G. M. Campos, C. Rabl, K. Mulligan, A. Posselt, S. J. Rogers, A. C. Westphalen, F. Lin, and E. Vittinghoff
Factors Associated With Weight Loss After Gastric Bypass
Arch Surg,
September 1, 2008;
143(9):
877 - 884.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
S. B. Wyatt, E. L. Akylbekova, M. R. Wofford, S. A. Coady, E. R. Walker, M. E. Andrew, W. J. Keahey, H. A. Taylor, and D. W. Jones
Prevalence, Awareness, Treatment, and Control of Hypertension in the Jackson Heart Study
Hypertension,
March 1, 2008;
51(3):
650 - 656.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
R. S. Stafford, V. Monti, C. D. Furberg, and J. Ma
Long-Term and Short-Term Changes in Antihypertensive Prescribing by Office-Based Physicians in the United States
Hypertension,
August 1, 2006;
48(2):
213 - 218.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
R. P. Hertz, A. N. Unger, J. A. Cornell, and E. Saunders
Racial Disparities in Hypertension Prevalence, Awareness, and Management
Arch Intern Med,
October 10, 2005;
165(18):
2098 - 2104.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
A. Khera, D. K. McGuire, S. A. Murphy, H. G. Stanek, S. R. Das, W. Vongpatanasin, F. H. Wians Jr, S. M. Grundy, and J. A. de Lemos
Race and Gender Differences in C-Reactive Protein Levels
J. Am. Coll. Cardiol.,
August 2, 2005;
46(3):
464 - 469.
[Abstract]
[Full Text]
[PDF]
|
 |
|