Abstract 3003: Coronary Autoregulation is Shifted Rightward in African Americans With Left Ventricular Hypertrophy
Previously, we reported that African Americans (AA) with hypertensive LVH demonstrate depressed sensitivity of the coronary microcirculation to stimulated relaxation with the endothelium-dependent agent acetylcholine. We further hypothesized that coronary autoregulation, manifested by the linear coronary pressure-flow relation exhibited during mid and late diastole, is shifted rightward in AA with LVH leading to an increase in the extrapolated coronary closing (zero-flow) pressure. In order to investigate this, the instantaneous coronary pressure-flow relationship was analyzed in diastole using simultaneous measurements of coronary blood flow velocity and arterial pressure at baseline and during peak hyperemia induced by adenosine. A 0.018 Doppler wire (Flo Wire) was used to record flow velocity. After converting flow velocity to flow, diastolic flow-pressure loops were digitized and linear regression analysis utilized to extrapolate zero- flow pressure averaged over 3 cardiac cycles. Groups analyzed included 18 AA and 39 Caucasians (CA) who were normotensive and 27 AA and 42 CA with hypertensive LVH. All had angiographically normal coronary arteries. For normotensive subjects; age, BMI, indexed LV mass, and coronary flow reserve (CFR) were similar among AA and CA. Closing pressures at baseline and during peak hyperemia were also similar (58 +/−3 vs. 53 +/− 2 mmHg, p=0.18 and 44 +/− 3 vs 42 +/− 2 mmHg, p=0.6). For subjects with LVH; age, BMI, indexed LV mass, and CFR were also similar among AA and CA. However, closing pressures at baseline and during peak hyperemia were significantly different (62 +/−3 vs 53 +/− 2 mmHg, p=0.033 and 52 +/− 3 vs 41 +/− 3 mmHg, p=0.033). Thus, we found that AA with LVH have significantly elevated zero-flow closing pressures both at baseline and during peak hyperemia when compared with similar CA. This suggests a deficiency in autoregulatory reserve which could affect microvascular perfusion despite borderline normal diastolic pressures. Depressed autoregulatory reserve may play a role in increased cardiovascular mortality rates among AA and warrants further investigation.