Heart failure is more common in African Americans and appears to be of worse severity. At the time of diagnosis, left ventricular function is more severely impaired and the clinical class is more advanced. The strongest risk factor for heart failure in African Americans appears to be hypertension, which is both more prevalent and more pathologic in African Americans. It is likely that heart failure represents an important end organ effect of hypertension. When affected by heart failure, African Americans experience a greater rate of hospitalization and may be exposed to a higher mortality risk as well. Genomic medicine has yielded a number of candidate single nucleotide polymorphisms that might contribute to the excess pathogenicity of heart failure in African Americans, but much more work needs to be done in larger cohorts. Effective therapy of heart failure must start with the recognition of the different manifestations of heart failure in African Americans. An increased awareness of the risk of hypertension followed by early and effective intervention may reduce the risk of heart failure in this population.

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The treatment of heart failure with angiotensin-converting enzyme inhibitors has resulted in substantial improvements in morbidity and mortality due to heart failure. Varying reports in the literature have suggested that African Americans respond less well to angiotensin-converting enzyme inhibitors, but careful reanalysis of major clinical trials in heart failure, especially the Studies of Left Ventricular Dysfunction (SOLVD), demonstrates a similar mortality benefit for African Americans as for whites. Morbidity, measured as hospitalizations, may not be as favorably impacted. African Americans do respond to angiotensin-converting enzyme inhibitors as a preemptive strategy to prevent heart failure, but the incidence of heart failure is still higher in this population. Mechanisms for these potential nuances in the response to angiotensin-converting enzyme inhibitors are not yet clear. The exaggerated benefit of nitrates and hydralazine implicates alterations in nitric oxide homeostasis. Race is an inadequate model to explain the observed differences. Careful translational research focusing on genetic patterns of disease may help resolve these outstanding questions.