CORONARY-ARTERY CONSTRICTION CAUSED BY THE COLD PRESSER TEST IN HUMANHYPERTENSION

Hypertensive patients with angiographically normal coronary arteries m ay have myocardial ischemia when metabolic demand increases. Abnormal epicardial coronary artery vasomotion in response to sympathetic stimu lation may contribute to ischemia in such patients. We studied the vas omotor response of smooth coronary arteries to a cold presser test in 10 hypertensive patients without other risk factors and in 9 control s ubjects. 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 p resser 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 patien ts (P<.001). Coronary blood flow velocity and blood flow increased 51 +/- 26% (P<.05) and 87 +/- 27% (P<.001), respectively, in control subj ects and 68 +/- 52% (P<.05) and 36 +/- 33% (P<.01) in hypertensive pat ients. At peak cold presser test, despite a significant higher rate-pr essure product in hypertensive patients, blood flow was similar in bat h groups, suggesting an uncoupling between myocardial metabolic demand and supply. Thus, hypertension impairs the vasodilator response of an giographically normal coronary arteries to a cold presser test. This a bnormal response may be due to enhanced catecholamine reactivity and/o r impairment of endothelial flow-mediated vasodilator response.