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Effect of African-American race and hypertensive left ventricular hypertrophy on coronary vascular reactivity and
J L Houghton1, V E Smith, D S Strogatz
1Department of Medicine, Albany Medical College, NY 12208, USA.
Insights
African American race does not inherently cause reduced coronary vascular relaxation. Hypertension and left ventricular hypertrophy, not race, significantly impact coronary artery and microvascular function in patients with chest pain.
Area of Science:
- Cardiovascular Medicine
- Public Health
- Vascular Biology
Background:
- Cardiovascular disease disproportionately affects African Americans, with underlying causes often unclear.
- Endothelial dysfunction and impaired coronary vascular reactivity are hypothesized contributors to excess cardiovascular events in Black Americans.
Purpose of the Study:
- To investigate racial differences in coronary vascular and endothelial function between Black and White individuals.
- To determine if intrinsic or acquired abnormalities in coronary vasoreactivity contribute to cardiovascular disparities.
Main Methods:
- Invasive testing using intracoronary infusions of acetylcholine and adenosine in 80 individuals (35 Black, 45 White).
- Assessment of coronary artery diameter and blood flow using Doppler-tipped guide wire and quantitative coronary angiography.
- Analysis stratified by hypertensive status and left ventricular hypertrophy.
Main Results:
- Hypertension and left ventricular hypertrophy, not race, were associated with impaired endothelium-independent and -dependent microvascular relaxation.
- Normotensive Black and White subjects showed no intrinsic racial differences in vasoreactivity.
- Epicardial coronary artery responses to acetylcholine were similar across racial groups within hypertensive and normotensive categories.
Conclusions:
- African American race is not independently associated with reduced coronary vascular relaxation.
- Chronic hypertension and left ventricular hypertrophy are key determinants of impaired coronary vasoreactivity, irrespective of race.
- Findings suggest that disparities in cardiovascular outcomes may be linked to factors beyond intrinsic racial differences in coronary vascular function.
Abstract:
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.