Clyde W. Yancy, MD, Guest Editor Medical Director, Heart Failure/Heart Transplantation, University of Texas Southwestern Medical Center, Dallas, TX Address for correspondence: Clyde W. Yancy, MD, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9047 E-mail: clyde.yancy@utsouthwestern.edu Medical therapy for heart failure has been one of the great clinical success stories in contemporary cardiovascular therapeutics. The introduction of effective treatment strategies, including angiotensin-converting enzyme inhibitors, β-adrenergic receptor antagonists, angiotensin II receptor antagonists, aldosterone antagonists, and potent diuretics, has resulted in a remarkable decrement in the mortality risk of heart failure. Recently completed clinical trials have experienced much lower annual mortality rates than expected or have noted a lower risk of death despite more advanced heart failure. For example, despite recruiting a patient population with classic New York Heart Association class III symptoms, the recently reported Valsartan Heart Failure Trial (Val-HeFT) realized an annual placebo mortality risk of only 9%, 25% less than was expected by the investigators.1 Even the Carvedilol Prospective Randomized Cumulative Survival (COPERNICUS) trial, which evaluated patients with advanced heart failure, had a placebo mortality risk of 19% compared with the nearly 50% mortality risk noted in the original Cooperative New Scandinavian Enalapril Survival Study (CONSENSUS) trial.2 The influence of the addition of β-blocker therapy to standard treatment regimens for heart failure has resulted in a nearly 50% decrease in overall mortality risk compared with historical controls treated with digoxin and diuretics only. The most compelling evidence of improved outcomes in heart failure is the noteworthy observation by the Framingham investigators that heart failure mortality has decreased by 12% each decade since the 1950s and this does not include the impact of β-blocker therapy.3 Thus, appropriate medical interventions in patients with heart failure can lead to substantial improvements in the probability of survival and the need for hospitalization. However, this seemingly beneficial validation of the results of evidencebased treatment are beset by a major issue. There is growing concern that the salutary benefits of medical therapy cannot be reasonably extrapolated to the population at large. Further, there is a question of whether significant patient groups exist in which successful therapies for heart failure are lacking or perhaps even harmful. Nowhere is this concern greater than in the African-American cohort. Because of the unique influence of hypertension and a complex interplay of socioeconomic and genomic factors, the expression of cardiovascular disease within patients who are self-described as African American appears in some cases to be in variance from what has been traditionally described. In particular, for this heart failure phenotype there appears to be a more worrisome natural history, a peculiar epidemiology with a unique emphasis on hypertension, a more worrisome prognosis, and potentially important differences in response to medical therapy. In this edition of Congestive Heart Failure, members of the Heart Failure and Hypertension Groups at University of Texas Southwestern Medical Center in Dallas, TX, address important observations from the medical literature describing the state of the art of the status of heart failure in African Americans. An initial review of the natural history, epidemiology, and prognosis of heart failure begins the discussion. It is followed by a description of the burden of hypertension in African Americans. Discussions on African-American persons’ response to medical therapy of heart failure follow, focusing on the use of angiotensin-converting enzyme inhibitors and β blockers. The final discussion describes a unique experience regarding care for heart failure in an urban setting. Virtually all of the data sources used in the articles are from retrospective reviews and post hoc analyses of data sets that were not intended to specifically address either the natural history of heart failure or African Americans’ response to medical therapy for heart therapy. Thus, the authors’ comments reflect the limitations of the data sources and at best should be regarded as hypothesis generating. Limited data are available from small, single-center studies and/or observational studies, yet a growing base of data that yields important information helpful in clinical decision making is developing and will, we hope, form the basis for further thought and investigations. www.lejacq.com ID:0306