In 80 subjects with normal coronary arteries, African American race was not associated with excess depression in coronary vascular relaxation after adjusting for left ventricular hypertrophy.
Observational (n=80)
Does African-American race affect coronary vascular reactivity and endothelial function independently of hypertensive left ventricular hypertrophy in patients with normal coronary arteries?
Racial differences in coronary vascular reactivity and endothelial function between black and white subjects appear to be driven by the presence of hypertensive left ventricular hypertrophy rather than intrinsic racial differences.
Excess cardiovascular morbidity and mortality among African (black) Americans remains an important yet unexplained public health problem. One possible explanation proposes that intrinsic or acquired abnormalities 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 testing of coronary artery and microvascular relaxation using intracoronary infusions of acetylcholine and adenosine, a Doppler tipped intracoronary guide wire, and quantitative coronary angiography. We measured the percent increase in coronary blood flow and epicardial diameter after graded infusion of intracoronary acetylcholine and in coronary blood flow after intracoronary adenosine in 31 normotensive subjects (10 black, 21 white) and 49 hypertensive subjects with left ventricular hypertrophy (25 black, 24 white). Categorical and multivariate analyses revealed that in response to intracoronary adenosine and acetylcholine, the depression in endothelium-independent and -dependent microvascular relaxation during peak agonist effect was largely related to the presence of chronic hypertension and left ventricular hypertrophy. Normotensive subjects demonstrated no intrinsic racial differences in conduit and resistance vessel vasoreactivity. In response to maximal infusion of acetylcholine, epicardial coronary arteries constricted similarly in black and white subjects with hypertensive left ventricular hypertrophy and dilated similarly in normotensive black and white subjects. Thus, our study shows that in a cohort of black and white subjects referred for coronary arteriography because of chest pain, African American race is not associated with excess intrinsic or acquired depression in coronary vascular relaxation during the peak effect of the endothelium-dependent and -independent agonists acetylcholine and adenosine, after adjustment for the presence of left ventricular hypertrophy.
Houghton et al. (Sat,) conducted a observational in Chest pain with normal coronary arteries (n=80). African-American race vs. White race was evaluated on Percent increase in coronary blood flow and epicardial diameter after intracoronary acetylcholine and adenosine. In 80 subjects with normal coronary arteries, African American race was not associated with excess depression in coronary vascular relaxation after adjusting for left ventricular hypertrophy.