Normalization of abnormal coronary vasomotion by calcium antagonists in patients with hypertension

• Published in: Circulation (New York, N.Y.) N.Y.), 1996-04, Vol.93 (7), p.1380-1387
• Main Authors: FRIELINGSDORF, J, SEILER, C, KAUFMANN, P, VASSALLI, G, SUTER, T, HESS, O. M
• Format: Article
• Language: English
• Subjects: Antihypertensive agents; Biological and medical sciences; Calcium Channel Blockers - pharmacology; Calcium Channel Blockers - therapeutic use; Cardiovascular system; Coronary Angiography; Coronary Vessels - drug effects; Coronary Vessels - physiopathology; Exercise Test; Female; Hemodynamics; Humans; Hypertension - drug therapy; Hypertension - physiopathology; Male; Medical sciences; Middle Aged; Nitric Oxide - metabolism; Pharmacology. Drug treatments; Prospective Studies; Retrospective Studies; Vasomotor System - drug effects; Vasomotor System - physiopathology
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.CIR.93.7.1380

Endothelial dysfunction with a loss of endothelium-dependent vasodilation has been reported in patients with arterial hypertension. The purpose of the present study was to evaluate coronary vasomotor response to dynamic exercise in patients with coronary artery disease with and without arterial hypertension and to determine the effect of calcium antagonists on coronary vasomotion. Cross-sectional areas of a normal and a stenotic coronary vessel segment were examined in 79 patients with coronary artery disease at rest and during supine bicycle exercise (Ex). Change in luminal area after acute administration of a calcium antagonist (diltiazem or nicardipine), during exercise, and after sublingual nitroglycerin (percent change compared with rest = 100%) was assessed by biplane quantitative coronary arteriography. Patients were divided into two groups: Group 1 (control) consisted of 48 patients without (normotensive subjects, n = 30; hypertensive subjects, n = 18) and group 2 of 31 patients with (normotensive subjects, n = 15; hypertensive subjects, n = 16) pretreatment with a calcium antagonist immediately before exercise. The groups did not differ with regard to clinical characteristics or hemodynamic data measured during exercise. Mean aortic pressure at rest, however, was significantly increased in hypertensive patients compared with normotensive subjects in group 1 (103 mm Hg versus 92 mm Hg, P < .01) and group 2 (110 mm Hg versus 98 mm Hg, P < .025). In group 1, exercise-induced vasomotor response was significantly different between normotensive and hypertensive patients in normal (+20% versus +1%, P < .003) and stenotic vessels (-5% versus -20%, P < .025). However, in group 2 there was coronary vasodilation in normotensive and hypertensive patients for both normal (delta Ex +23% versus +21%, P = NS) and stenotic vessel segments (+24% versus +26%, P = NS). Abnormal coronary vasomotion during exercise can be observed in hypertensive patients with reduced vasodilator response in normal arteries and enhanced vasoconstrictor response in stenotic arteries. Calcium antagonists prevent the abnormal response of normal and stenotic coronary arteries to exercise in hypertensive patients and thus may compensate for endothelial dysfunction with reduced vasodilator response to exercise.