EFFECT OF AFRICAN-AMERICAN RACE AND HYPERTENSIVE LEFT-VENTRICULAR HYPERTROPHY ON CORONARY VASCULAR REACTIVITY AND ENDOTHELIAL FUNCTION

Excess cardiovascular morbidity and mortality among African (black) Am ericans remains an important yet unexplained public health problem. On e possible explanation proposes that intrinsic or acquired abnormaliti es in coronary vascular reactivity and endothelial function result in excess ischemia among black Americans. To examine this hypothesis, we subjected 80 individuals with normal coronary arteries to invasive tes ting of coronary artery and microvascular relaxation using intracorona ry infusions of acetylcholine and adenosine, a Doppler tipped intracor onary guide wire, and quantitative coronary angiography. We measured t he percent increase in coronary blood flow and epicardial diameter aft er graded infusion of intracoronary acetylcholine and in coronary bloo d flow after intracoronary adenosine in 31 normotensive subjects (10 b lack, 21 white) and 49 hypertensive subjects with left ventricular hyp ertrophy (25 black, 24 white). Categorical and multivariate analyses r evealed that in response to intracoronary adenosine and acetylcholine, the depression in endothelium-independent and -dependent microvascula r relaxation during peak agonist effect was largely related to the pre sence of chronic hypertension and left ventricular hypertrophy. Normot ensive subjects demonstrated no intrinsic racial differences in condui t and resistance vessel vasoreactivity. In response to maximal infusio n of acetylcholine, epicardial coronary arteries constricted similarly in black and white subjects with hypertensive left ventricular hypert rophy and dilated similarly in normotensive black and white subjects. Thus, our study shows that in a cohort of black and white subjects ref erred for coronary arteriography because of chest pain, African Americ an race is not associated with excess intrinsic or acquired depression in coronary vascular relaxation during the peak effect of the endothe lium-dependent and -independent agonists acetylcholine and adenosine, after adjustment for the presence of left ventricular hypertrophy.