Racial Differences in the Coronary Microcirculation
Racial Differences in the Coronary Microcirculation
To 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.
BACKGROUND:

 Although studies in 1992 with a sufficient number of minority patients were sparse, those
 available suggested that Black Americans had a higher case fatality from coronary heart
 disease, but lesser amounts of atherosclerotic coronary artery disease. A possible
 explanation for this apparent paradox was that myocardial ischemia might 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 might also have been related to intrinsic or
 acquired differences in coronary artery autoregulation and vasoreactivity leading to
 depression in coronary blood flow and reserve.

 DESIGN NARRATIVE:

 The intracoronary Doppler flow velocity guidewire together with quantitative coronary
 angiography was used to study changes in coronary blood flow in blacks secondary to
 pharmacologic provocateurs known to induce arteriolar vasodilation. White Americans with
 similar demographic characteristics and equivalent amount of ventricular hypertrophy and
 coronary disease were similarly studied in a parallel fashion for comparison. A control group
 of normal white and Black Americans were studied to detect unexpected intrinsic differences.
 Both endothelium dependent and independent induction of coronary arteriolar vasodilation were
 studied. In 25 percent of patients with endothelium dependent defects in arteriolar
 vasodilation, retesting was 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 was investigated. This
 finding would necessitate that the lower limit of autoregulation occurred at higher diastolic
 pressures, resulting in a drop-off of coronary perfusion at normal physiologic pressures and
 ischemia.

 The study completion date listed in this record was obtained from the "End Date" entered in
 the Protocol Registration and Results System (PRS) record.
No eligibility criteria