Cardiovascular disease (CVD) in African Americans remains a clinical problem that requires investigation. This supplement to The Journal of Clinical Hypertension presents a comprehensive summary of the hypotheses, dilemmas, data, and problems that confound our ability to adequately address the cardiovascular health needs of African‐American patients.
The increase in CVD in African Americans has traditionally been attributed to the high prevalence of hypertension. The group of authors presented here embraces this observation as one of paramount importance. However, newer perspectives, primarily from the field of genomic medicine, have emerged that also appear to be important if we are to fully understand the burden of CVD in this population. Given the number of described polymorphisms in the renin‐angiotensin‐aldosterone, sympathetic nervous, cytochrome P450, nitric oxide, and inflammatory cytokine systems, it is plausible that a genotype of risk that contributes to CVD in African Americans will ultimately emerge.
It should be noted, however, that the interpretation of genomic markers of disease is contextual; that is, gene‐environment interactions will ultimately serve as a better platform to explain CVD. Thus, obesity, dietary preferences, and other lifestyle issues remain important. In addition, ongoing care and caution must be exercised as we continue to explore not only gene‐environment interactions, but also any specific race‐based reference to CVD. The assignment of race is self‐selected, nonphysiologic, arbitrary, and heterogeneous. Race cannot be a proxy for genetics or disease.
Despite these cautionary statements, it is clear that those who may be described as African American are indeed at increased risk for CVD. The prevalence of hypertension in African Americans is the highest in the world and 80% of persons in this group are likely to become hypertensive. CVD is the most common cause of death in African Americans and they experience death due to CVD and stroke at rates higher than other groups in the United States. Long‐held beliefs regarding best treatment strategies for hypertension in African Americans are largely rhetorical and not well grounded in evidence‐based medicine. The more contemporary databases (the Antihypertensive and Lipid‐Lowering Treatment to Prevent Heart Attack Trial [ALLHAT] 1 and the African American Study of Kidney Disease and Hypertension [AASK], 2 for example) demonstrate that thiazide diuretics are preferred agents for all patients with hypertension and when other compelling indications exist, the use of neurohormonal antagonists (e.g., angiotensin‐converting enzyme [ACE] inhibitors, angiotensin‐receptor antagonists, and β blockers) is preferred. The treatment algorithm generated by the Working Group on Hypertension in African Americans 3 is embraced by the authors in this publication as an appropriate and effective means of treating this population and reducing morbidity and mortality due to CVD and stroke. Although not stated as such by the guidelines of the seventh report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure, 4 we suggest that African Americans with hypertension should be treated aggressively with targeted, tighter blood pressure control.
The approach to therapy needs to take important comorbidities and confounders into consideration. Multiple‐drug regimens are often required and, if diuretics are utilized, potassium repletion is required in addition to careful surveillance of renal function. Concomitant diabetes, obstructive pulmonary disease, ischemic heart disease, and heart failure will further modify treatment strategies. Designing a regimen that promotes compliance is likewise critically important. Peculiar side effect concerns include the risk for angioedema with ACE inhibitors, which may be more frequently seen in African Americans.
Diabetes further contributes to the CVD risk profile in African Americans. The prevalence of diabetes is disproportionately high among African Americans and younger persons are developing diabetes at an alarming rate. This is likely related to the climbing rates of obesity and is similarly associated with dyslipidemia. The prevalence of diabetes in African Americans is at least 20% and the incidence of the entire cascade of diabetes‐related complications is higher in this group. It has been suggested that physiologic nuances exist that account for the higher rate of diabetes in African Americans—the principle culprit being increased insulin resistance. It is not yet clear whether this is simply due to obesity or the result of a unique gene‐environment interaction. Glycemic control is accomplished less frequently in these patients, but to date there are no concerns that either of the recommended treatment strategies, including thiazolidinediones, are less effective in African Americans than in non‐Hispanic whites.
When risk factors affecting African Americans continue in an unabated manner, overt CVD occurs, including angina, myocardial infarction (MI), and heart failure. Although the number of reported MIs in African Americans is seemingly lower than in non‐Hispanic whites, population data, vis‐`‐vis causes of death, suggest that CVD results in death in a disproportionate number of African Americans. When affected by acute coronary syndromes, these patients should be treated in a manner that is identical to others. Vigorous use of reperfusion strategies; antiplatelet agents; statins; β blockers; and, where applicable, renin‐angiotensin‐aldosterone antagonists should drive all treatment decisions. In the setting of left ventricular dysfunction after an MI, adherence to accepted evidence‐based treatment strategies is critical.
The natural history of hypertensive heart disease and left ventricular dysfunction after MI is the eventual development of heart failure. When heart failure impacts African‐American patients, it does so more frequently, at an earlier age, with more left ventricular dysfunction, and with more advanced symptoms. Despite ongoing concerns, there are no compelling data that support a different treatment strategy for established heart failure due to systolic dysfunction in African Americans. Moreover, the best available data suggest that the combination of ACE inhibitors and β blockers, especially carvedilol, is as effective in African Americans as in all others. 5 Practitioners should be admonished to adhere to published treatment guidelines for heart failure in all patients, irrespective of race. The ongoing African‐American Heart Failure Trial (A‐HeFT) 6 represents the first prospective study designed to elucidate the natural history of heart failure in African Americans, test the adjunctive benefit of nitric oxide enhancing therapy in chronic heart failure, and identify genetic markers of risk in African Americans with heart failure.
The diagnosis and treatment of CVD in African Americans is not only confounded by subtle differences in pathophysiology, natural history, and drug responsiveness, but also by disparate delivery of care within our health care system. The Institute of Medicine and Kaiser Family Foundation reports clearly identify gaps in care that are not attributable to different indications for care or patient preference. These gaps that are devoid of reasonable explanation are known as disparities 7 (Figure). Efforts are required to raise the awareness of risk factors and to establish the critical need for appropriate intervention to address the burden of CVD in African Americans.
The goal of this initiative is not race‐based care. Such a model would do all a great disservice. The nonphysiologic nature of race makes the concept of race‐based care untenable. Rather, the focus of this and similar efforts is to sensitize the medical community to the CVD burden in all segments of our population and to strive for the most effective management of CVD.
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