Increased Cardiovascular Mortality in African Americans: Can We Turn the Tide?

May 1, 2006

What factors are causing the increased incidence of hypertension and cardiovascular mortality in African Americans, and what can be done to counteract them?

Q: The incidence of hypertension and cardiovascular mortality is higher in African Americans than in other racial groups. What factors are driving this increased risk, and what measures can be taken to counteract them?

A: According to the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), blood pressure (BP) remains largely uncontrolled across all racial and ethnic groups.1 However, the prevalence of hypertension is almost 40% higher in blacks than in whites. The Hypertension Detection and Follow-up Program reported that severe hypertension (diastolic pressures higher than 150 mm Hg) was 5 to 7 times more common in blacks than in whites in all age groups except the very elderly.

Stroke mortality rates are 80% higher and cardiac mortality rates are 50% higher among African Americans. Most notably, hypertension-related end-stage renal disease rates are 320% higher in African Americans than in patients of other races.2 How can these strikingly higher rates of target-organ disease, morbidity, and mortality be explained?


Lifestyle factors. Although numerous biochemical and endocrine mechanisms have been suggested as causes, these genetic elements appear to be less important than lifestyle factors. Although these factors are not unique to African Americans, their effects are compounded by a number of important social problems that continue to affect cardiovascular outcomes in this group.3 In disadvantaged communities, often located in inner cities, the failure or delay in diagnosing hypertensionmay result from inadequate patient education. Patients in these communities often mistrust the medical profession and may be unaware of the potential benefits of pharmacologic treatment. Diets are likely to contain insufficient amounts of healthful foods, such as fresh produce, whole grains, lean meats, and fish. Many inner-city food stores often do not carry such items, and resources may not be available to educate patients and support healthy lifestyle choices.

Even when adequate resources are available, inadequate patient adherence to medication regimens and insufficient follow-up contribute to poor control rates. Although lack of adherence is not related solely to the cost of medications, cost certainly can be an obstacle to BP control for many patients.

Physician-related barriers. These obstacles to BP control are not restricted to minority groups.4 Practitioners are frequently insufficiently aggressive in their management of hypertension; they often delay the initiation of therapy and do not aggressively titrate drug dosages to achieve goal BP. Despite the clear association between elevated systolic BP and cardiovascular disease, many physicians are unconvinced of the importance of elevated systolic BP. They often do not educate patients adequately about the risks of uncontrolled BP and the importance of long-term adherence to a treatment regimen.

Other factors. The increased prevalence of type 2 diabetes mellitus among African Americans-together with a higher prevalence of cigarette smoking, obesity, and lipid disorders-contributes to the increased cardiovascular risk and underscores the need for aggressive control not only of BP but of other risk factors.


Thiazidediuretics appear to be appropriate for initial therapy in all patients with uncomplicated hypertension, including African Americans. When thiazide diuretics are added to other classes of antihypertensive agents-such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), or β-blockers-they enhance the efficacy of these agents and negate any racial or ethnic differences in BP response.

Calcium antagonists effectively lower BP in African Americans and may be more effective than ACE inhibitors, ARBs, or β-blockers as monotherapy.In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), 35% of whose participants were black, the risk of stroke was significantly greater in black patients treated with lisinopril than in black patients treated with amlodipine or chlorthalidone.5 The data suggested that the difference may have been related in part to a 4-mm Hg systolic BP elevation in the lisinopril group. ALLHAT confirmed the benefits of diuretic therapy for BP reduction and cardiovascular risk reduction in African Americans.

In the African American Study of Kidney Disease and Hypertension (AASK), all patients were hypertensive at entry and had a glomerular filtration rate between 20 and 65 mL/min.6 The patients were randomized to different BP goals: the usual goal was a mean arterial pressure of 102 to 107 mm Hg; the lower goal was a mean arterial pressure of 92 mm Hg or lower. In patients without significant proteinuria, the decline in renal function was comparable in all treatment groups, whereas in patients with significant proteinuria, the rate of renal function deterioration was significantly slowed with the ACE inhibitor ramipril. This suggests that in patients with established chronic renal disease, inhibitors of the renin-angiotensin system can provide significant renoprotection.

In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) trial, more than 9000 patients with hypertension and left ventricular hypertrophy were randomly assigned to losartan or atenolol, with a diuretic added as needed.7 Although patients in the losartan group demonstrated a reduction in cardiovascular disease end points, primarily because of a decrease in stroke, these apparent benefits were not observed in a small subgroup of African Americans (533 patients).However, the authors suggest that the subanalysis was limited by the relatively small number of events. Monotherapy with agents that modulate the renin-angiotensin-aldosterone system appears to reduce BP less effectively in African Americans than in other groups.

One potential barrier to the use of ACE inhibitors in blacks is the increased risk of angioedema, which occurs 2 to 5 times more frequently than in whites and may relate to an increased sensitivity to bradykinin. Although this complication is rare, it has led to the discontinuation of ACE inhibitor therapy in many black patients. ARBs are not associated with angioedema.

Finally, evidence from a recent meta-analysis of trials in which β-blockers were used as monotherapy suggests that, compared with other agents, β-blockers are less effective in reducing cardiovascular risk in patients with uncomplicated hypertension and that they may increase the risk of stroke.8 The authors recommended that β-blockers not be considered as initial monotherapy in patients with uncomplicated hypertension. These observations do not negate the value of β-blockers in patients with established coronary disease and/or tachyarrhythmias.




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