Abnormal flow-mediated epicardial vasomotion in human coronary arteries isimproved by angiotensin-converting enzyme inhibition - A potential role ofbradykinin
A. Prasad et al., Abnormal flow-mediated epicardial vasomotion in human coronary arteries isimproved by angiotensin-converting enzyme inhibition - A potential role ofbradykinin, J AM COL C, 33(3), 1999, pp. 796-804
Citations number
46
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
OBJECTIVES. This study nas performed to determine whether angiotensin conve
rting enzyme (ACE) inhibition improves endothelium-dependent flow-mediated
vasodilation in patients with atherosclerosis or its risk factors and wheth
er this is mediated by enhanced bradykinin activity.
BACKGROUND. Abnormal coronary vasomotion due to endothelial dysfunction con
tributes to myocardial ischemia in patients with atherosclerosis, and its r
eversal may have an antiischemic action. Previous studies have shown that A
CE inhibition improves coronary endothelial responses to acetylcholine, but
whether this is accompanied by improved responses to shear stress remains
unknown.
METHODS. In 19 patients with mild atherosclerosis, metabolic vasodilation w
as assessed during cardiac pacing. Pacing was repeated during separate intr
acoronary infusions of low-dose bradykinin (BK) and enalaprilat. Endotheliu
m-dependent and -independent vasodilation was estimated with intracoronary
BK and sodium nitroprusside respectively.
RESULTS. Enalaprilat did not-alter either resting coronary vascular tone or
dilation with sodium nitroprusside, but potentiated BK-mediated dilation.
Epicardial segments that constricted abnormally with pacing (-5 +/- 1%) dil
ated (3 +/- 2%) with pacing in the presence of enalaprilat (p = 0.002). Sim
ilarly, BK at a concentration (62.5 ng/min) that did not alter resting diam
eter in the constricting segments also improved the abnormal response to a
6 +/- 1% dilation (p < 0.001). Cardiac pacing-induced reduction in coronary
vascular resistance of 27 +/- 4% (p < 0.001) remained unchanged after enal
aprilat.
CONCLUSIONS. Thus ACE inhibition: A) selectively improved endothelium-depen
dent but not-independent dilation, and B) abolished abnormal flow-mediated
epicardial vasomotion in patients with endothelial dysfunction, in part; by
increasing endogenous BK activity. (C) 1999 by the American College of Car
diology.