Jl. Houghton et al., EFFECT OF AFRICAN-AMERICAN RACE AND HYPERTENSIVE LEFT-VENTRICULAR HYPERTROPHY ON CORONARY VASCULAR REACTIVITY AND ENDOTHELIAL FUNCTION, Hypertension, 29(3), 1997, pp. 706-714
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.