CORONARY-ARTERY CONSTRICTION CAUSED BY THE COLD PRESSER TEST IN HUMAN HYPERTENSION

Hypertensive patients with angiographically normal coronary arteries may have myocardial ischemia when metabolic demand increases. Abnormal epicardial coronary artery vasomotion in response to sympathetic stimulation may contribute to ischemia in such patients. We studied the vasomotor response of smooth coronary arteries to a cold presser test in 10 hypertensive patients without other risk factors and in 9 control subjects. Vessel dimensions were measured by quantitative angiography, and blood flow was calculated using an intracoronary Doppler catheter in the left anterior descending coronary artery. In response to cold presser stimulation, arteries of control subjects dilated 13.0 +/- 5.9% (P<.001), and they constricted 8.2 +/- 8.5% in hypertensive patients (P<.001). Rate-pressure product increased from 9466 +/- 1677 to 12547 +/- 2367 beats per minute (bpm).mm Hg in control subjects (P<.001) and from 13720 +/- 1823 to 17353 +/- 2037 bpm.m Hg in hypertensive patients (P<.001). Coronary blood flow velocity and blood flow increased 51 +/- 26% (P<.05) and 87 +/- 27% (P<.001), respectively, in control subjects and 68 +/- 52% (P<.05) and 36 +/- 33% (P<.01) in hypertensive patients. At peak cold presser test, despite a significant higher rate-pressure product in hypertensive patients, blood flow was similar in bath groups, suggesting an uncoupling between myocardial metabolic demand and supply. Thus, hypertension impairs the vasodilator response of angiographically normal coronary arteries to a cold presser test. This abnormal response may be due to enhanced catecholamine reactivity and/or impairment of endothelial flow-mediated vasodilator response.