Long-term cigarette smoking impairs endothelium-dependent coronary arterial vasodilator function.
Long-term cigarette smoking impairs endothelium-dependent coronary arterial vasodilator function.
复制标题
长期吸烟会损害内皮依赖性冠状动脉血管舒张功能。
DOI：
10.1161/01.cir.92.5.1094
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发表时间：
1995
期刊：
影响因子：
37.8
通讯作者：
Jan Minners
中科院分区：
文献类型：
--
作者：
A. Zeiher;V. Schächinger;Jan Minners
背景
BACKGROUND
Smoking is a primary risk factor for coronary and peripheral vascular disease. Because the endothelium is a principal target for the effects of risk factors early in the pathogenesis of atherosclerosis, we investigated whether long-term smoking is associated with impaired endothelial vasodilator function of epicardial conductance vessels regardless of the presence or absence of atherosclerotic lesions.
METHODS AND RESULTS
Using quantitative coronary angiography, we measured epicardial artery diameter at baseline, after maximal increases in coronary blood flow that caused flow-mediated dilation (which is strictly endothelium dependent), and after intracoronary injection of nitroglycerin (an endothelium-independent dilator) in 96 patients. Endothelium-dependent, flow-mediated dilation was significantly (P < .0001) blunted in smokers (n = 46) compared with non-smokers (n = 50). The ratio of flow-dependent dilation to nitroglycerin-induced dilation was significantly (P < .001) lower in smokers (0.34 +/- 0.32) compared with nonsmokers (0.59 +/- 0.23), indicating that the blunted dilator response to increased blood flow was out of proportion to the mildly impaired dilator response to nitroglycerin in smokers. In the presence of angiographically visible atherosclerosis, flow-dependent dilation was essentially absent (3.0 +/- 6.5%) in smokers. Multivariate analysis revealed that luminal irregularities by angiography (P < .0001) and smoking (P < .001) were the only variables to be independently associated with a reduced flow-dependent dilator response of epicardial arteries. Intracoronary ultrasound demonstrated that flow-dependent dilation progressively decreased with increasing atherosclerotic plaque load (r = -.82, P < .0001; n = 24). However, over the entire range of wall thickening, segments from smokers exhibited a significantly (P < .01) impaired flow-dependent dilator response compared with those of nonsmokers.
CONCLUSIONS
Long-term cigarette smoking is associated with impaired endothelium-dependent coronary vasodilation regardless of the presence or absence of coronary atherosclerotic lesions.
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影响因子：
--
作者：
COOKE, JP;STAMLER, J;LOSCALZO, J
通讯作者：
LOSCALZO, J
影响因子：
37.8
作者：
VITA, JA;TREASURE, CB;GANZ, P
通讯作者：
GANZ, P
影响因子：
158.5
作者：
LUDMER, PL;SELWYN, AP;GANZ, P
通讯作者：
GANZ, P
人类的大冠状动脉对血流变化有反应：这是一种内皮依赖性机制，在动脉粥样硬化患者中失效。
影响因子：
24
作者：
Nabel,EG;Selwyn,AP;Ganz,P
通讯作者：
Ganz,P
影响因子：
56.9
作者：
FRANGOS, JA;ESKIN, SG;IVES, CL
通讯作者：
IVES, CL