A 2004 paper in the New England Journal of Medicine provided a rationale for studying BiDil only in blacks in the A-HeFT trial, by indicating that there were racial differences in the prevalence, risk factors, causation, disease severity, outcomes and response to therapy between black and white patients with heart failure.132 Accordingly, the authors argued, studying only blacks would avoid the “substantial variation in genetic and environmental factors that influence disease progression and the response to therapy.” They hypothesized that blacks were biologically different from whites due to lower levels of nitric oxide in the blood or other unspecified biological characteristics. Importantly, the study made no effort to measure these characteristics but used self-identified race as the marker of genetics.127 Another example of the misuse of genetics is a 2001 New England Journal of Medicine study that claimed to demonstrate a greater response to angiotensin-converting enzyme inhibitor therapy in white compared to black patients with left ventricular dysfunction.133 In his detailed critique of this study, Kaufman134 notes that it has been highly cited as evidence for a differential response to
