Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Preserved Vasodilator Response to Acetylcholine in Atherosclerotic Coronary Arteries Before and After PTCA

Preserved Vasodilator Response to Acetylcholine in Atherosclerotic Coronary Arteries Before and... The vascular response to local administration of acetylcholine is used, clinically, to assess endothelial function in vivo. However, whether this response predominantly reflects the functional state of the vascular endothelium, or rather results from smooth muscle reactivity per se is not clear. In 15 patients with chronic stable angina and angiographically significant coronary disease, we studied the effects of increasing doses of intracoronary acetylcholine (5, 10, 30, 50, and 80 μg) and nitroglycerin (200 μg) on coronary vascular tone. In three patients the protocol was perfrnned at the time of diagnostic coronary angiographv and 7 and 24 hours after angioplasty. The remaining five underwent acetylcholine administration before and after percutaneous transluminl coronary angioplasty (PTCA). We quantitatively assessed the diameter of 54 coronary arterial segments; 12 stenotic segments, 13 post‐PICA segments with residual irregularities, 18 reference segments of the ranee arteries taken proximal to the stenosis or to the dilatation site, and II remote segments ofnonstenotic vessels. They all showed a bimodal response to acetylcholine. At the lowest concentration (5 μg) the agent invariably caused dilatation (9.22 ± 6.55%), which was not significantly different in the various segments and was always less than that induced by nitroglycerin (24.56 ± 12.82%, P < 0.0001). At the highest doses (50 or 80 μg) acetylcholine always induced vasoconstriction, which was significantly more pronounced in the post‐PTCA (‐31.54 ± 10.65%) and stenotic segments (‐23.08 ± 11.88%) than in the reference and remote segments (respectively, ‐14.88 + 7.63% and ‐ 18.67 + 8.37%, P < 0.05). We conclude that: (l) some degree of endothelial dependent vasodilatation is preserved even in the presence of atheroma and intimal injury induced by angioplasty; (2) atheroma and especially acute intimal injury augment the vasoconstrictor response to high dose acetylcholine, the effect being most probably mediated by primary smooth muscle supersensivity: (3) since acetylcholine has direct and endothelium‐mediated vasoactive effects, this agent may not be the ideal one for testing endothelial integrity. (J Interven Cardiol 1994; 7:57–64) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Interventional Cardiology Wiley

Preserved Vasodilator Response to Acetylcholine in Atherosclerotic Coronary Arteries Before and After PTCA

Download PDF
8 pages

Loading next page...
 
/lp/wiley/preserved-vasodilator-response-to-acetylcholine-in-atherosclerotic-oqRcmka8dF

References (23)

Publisher
Wiley
Copyright
Copyright © 1994 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0896-4327
eISSN
1540-8183
DOI
10.1111/j.1540-8183.1994.tb00890.x
Publisher site
See Article on Publisher Site

Abstract

The vascular response to local administration of acetylcholine is used, clinically, to assess endothelial function in vivo. However, whether this response predominantly reflects the functional state of the vascular endothelium, or rather results from smooth muscle reactivity per se is not clear. In 15 patients with chronic stable angina and angiographically significant coronary disease, we studied the effects of increasing doses of intracoronary acetylcholine (5, 10, 30, 50, and 80 μg) and nitroglycerin (200 μg) on coronary vascular tone. In three patients the protocol was perfrnned at the time of diagnostic coronary angiographv and 7 and 24 hours after angioplasty. The remaining five underwent acetylcholine administration before and after percutaneous transluminl coronary angioplasty (PTCA). We quantitatively assessed the diameter of 54 coronary arterial segments; 12 stenotic segments, 13 post‐PICA segments with residual irregularities, 18 reference segments of the ranee arteries taken proximal to the stenosis or to the dilatation site, and II remote segments ofnonstenotic vessels. They all showed a bimodal response to acetylcholine. At the lowest concentration (5 μg) the agent invariably caused dilatation (9.22 ± 6.55%), which was not significantly different in the various segments and was always less than that induced by nitroglycerin (24.56 ± 12.82%, P < 0.0001). At the highest doses (50 or 80 μg) acetylcholine always induced vasoconstriction, which was significantly more pronounced in the post‐PTCA (‐31.54 ± 10.65%) and stenotic segments (‐23.08 ± 11.88%) than in the reference and remote segments (respectively, ‐14.88 + 7.63% and ‐ 18.67 + 8.37%, P < 0.05). We conclude that: (l) some degree of endothelial dependent vasodilatation is preserved even in the presence of atheroma and intimal injury induced by angioplasty; (2) atheroma and especially acute intimal injury augment the vasoconstrictor response to high dose acetylcholine, the effect being most probably mediated by primary smooth muscle supersensivity: (3) since acetylcholine has direct and endothelium‐mediated vasoactive effects, this agent may not be the ideal one for testing endothelial integrity. (J Interven Cardiol 1994; 7:57–64)

Journal

Journal of Interventional Cardiology – Wiley

Published: Feb 1, 1994

There are no references for this article.