CORONARY ANGIOPLASTY AMELIORATES HYPOPERFUSION-INDUCED ENDOTHELIAL DYSFUNCTION IN PATIENTS WITH STABLE ANGINA-PECTORIS

Citation
T. Komaru et al., CORONARY ANGIOPLASTY AMELIORATES HYPOPERFUSION-INDUCED ENDOTHELIAL DYSFUNCTION IN PATIENTS WITH STABLE ANGINA-PECTORIS, Journal of the American College of Cardiology, 27(1), 1996, pp. 30-37
Citations number
47
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
07351097
Volume
27
Issue
1
Year of publication
1996
Pages
30 - 37
Database
ISI
SICI code
0735-1097(1996)27:1<30:CAAHED>2.0.ZU;2-Y
Abstract
Objectives. This study sought to investigate the effect of coronary an gioplasty on chronic hypoperfusion-induced endothelial dysfunction in patients with coronary heart disease. Background. The endothelium is a n important component for organ how regulation. Ischemia with or witho ut reperfusion is known to cause endothelial dysfunction. We tested th e hypothesis that chronic hypoperfusion impairs endothelial function i n the angiographically normal coronary artery segment distal to stenos is and that the impairment by chronic hypoperfusion is reduced by coro nary angioplasty. Methods. In 13 patients with stable angina pectoris, substance P (10, 30 and 100 pmol) and nitroglycerin (200 mu g) were s equentially infused into the coronary artery in a cumulative manner on the day after coronary angioplasty. In 10 of these patients, vascular responses to these agents were again investigated 3 months after angi oplasty. Changes in vascular diameter were evaluated in vessels locate d proximal and distal to the target lesion, both of which were angiogr aphically normal, by performing computer-assisted quantitative coronar y angiography. In five patients, the transstenotic pressure gradient w as also measured with a pressure sensor-mounted guide wire before angi oplasty. Results. On the day after angioplasty, the magnitude of dilat ion by substance P in distal segments was significantly less than that in proximal segments and inversely correlated with the transstenotic pressure gradient (p < 0.05) and lesion stenosis (p < 0.05). There was no difference in nitroglycerin induced vasodilation between the two v essel segment groups. Three months later, the impaired response to sub stance P in the distal segment was restored to normal. Conclusions. We conclude that chronic hypoperfusion impairs endothelium dependent dil ation of coronary artery distal to critical stenosis in patients with ischemic heart disease and that coronary angioplasty ameliorates the e ndothelial dysfunction within 3 months.