Although studies with a sufficient number of minority patients are sparse, those available suggest that black Americans have a higher case fatality from coronary heart disease, but lesser amounts of atherosclerotic coronary artery disease. A possible explanation for this apparent paradox is that myocardial ischemia may be more prevalent with less coronary artery atherosclerosis in black Americans because of comorbid diseases or differences in coronary physiology. This could be secondary to excess hypertension and left ventricular hypertrophy in black Americans but may also be related to intrinsic or acquired differences in coronary artery autoregulation and vasoreactivity leading to depression in coronary blood flow and reserve. The proposed research will study mechanisms of excess coronary ischemia secondary to alterations in autoregulation and arteriolar vasoreactivity in black Americans with hypertension, varying degree of left ventricular hypertrophy and angiographically normal or mildly diseased coronary arteries. The intracoronary Doppler flow velocity guidewire together with quantitative coronary angiography will be used to study changes in coronary blood flow in man secondary to pharmacologic provocateurs known to induce arteriolar vasodilation. White Americans with similar demographic characteristics and equivalent amount of ventricular hypertrophy and coronary disease will be similarly studied in a parallel fashion for comparison. A control group of normal white and black Americans will be studied to detect unexpected intrinsic differences. Both endothelium dependent and independent induction of coronary arteriolar vasodilation will be studied. In 25% of patients with endothelium dependent defects in arteriolar vasodilation, retesting will be performed after intracoronary infusion of L-arginine, the precursor of endothelium dependent relaxing factor. Finally, the possibility of a rightward shift in coronary artery autoregulation in chronic hypertension will be investigated. This finding would necessitate that the lower limit of autoregulation occur at higher diastolic pressures, resulting in a drop-off of coronary perfusion at normal physiologic pressures and ischemia.
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