Zeiher A M, Schächinger V, Saurbier B, Just H
Department of Internal Medicine III, University of Freiburg.
Basic Res Cardiol. 1994;89 Suppl 1:115-28. doi: 10.1007/978-3-642-85660-0_11.
The endothelium plays a major role in modulating vascular smooth muscle tone by synthesizing and metabolizing a number of vasoactive substances. Since the endothelium is both a target for and a mediator of vascular disease, functional alterations in coronary vascular reactivity due to endothelial dysfunction might play an important integral part in the clinical presentation of coronary artery disease. Recent advances in interventional techniques including intracoronary instrumentation by Doppler catheters to measure blood flow velocities and 2-D-ultrasound catheters to evaluate arterial wall architecture during coronary angiography provided the diagnostic tools to assess endothelial vasodilator function and its relation to atherosclerotic disease. The current weight of evidence suggests that disturbances of vasomotor function of epicardial conductance vessels are fundamental to the development of atherosclerosis, and impaired endothelial vasodilation is the predominant mechanism underlying inappropriate vasoconstriction in atherosclerosis. However, endothelial vasodilator dysfunction is not only confined to atherosclerotic epicardial vessels, but may also extend into the coronary microcirculation, which does not develop overt atherosclerotic lesions, but determines coronary blood flow in the absence of hemodynamically significant stenoses. The most important factors associated with impaired endothelium-mediated dilation of the coronary microcirculation are hypercholesterolemia and advanced age. With respect to the clinical presentation of coronary artery disease, endothelial vasodilator dysfunction appears to play a causative role for triggering myocardial ischemia in stable angina pectoris, to aggravate the sequelae of acute ischemic syndromes, and might be the primary underlying mechanism in some patients with syndrome X, whereas variant angina appears to be related to a hyperreactivity of the vascular smooth muscle layer. Thus, the assessment of endothelium-mediated modulation of coronary vasomotor tone in the clinical setting offers unique and important insights into mechanisms leading to ischemic manifestations of coronary artery disease.
内皮通过合成和代谢多种血管活性物质，在调节血管平滑肌张力方面发挥主要作用。由于内皮既是血管疾病的靶点，又是血管疾病的介质，内皮功能障碍导致的冠状动脉血管反应性的功能改变可能在冠状动脉疾病的临床表现中起重要的整体作用。介入技术的最新进展，包括通过多普勒导管进行冠状动脉内检测以测量血流速度，以及在冠状动脉造影期间使用二维超声导管评估动脉壁结构，为评估内皮舒张功能及其与动脉粥样硬化疾病的关系提供了诊断工具。目前的证据表明，心外膜传导血管的血管舒缩功能紊乱是动脉粥样硬化发生发展的根本原因，内皮舒张功能受损是动脉粥样硬化中不适当血管收缩的主要潜在机制。然而，内皮舒张功能障碍不仅局限于心外膜动脉粥样硬化血管，还可能延伸至冠状动脉微循环，冠状动脉微循环虽未形成明显的动脉粥样硬化病变，但在无血流动力学显著狭窄的情况下决定冠状动脉血流量。与冠状动脉微循环内皮介导的舒张功能受损相关的最重要因素是高胆固醇血症和高龄。就冠状动脉疾病的临床表现而言，内皮舒张功能障碍似乎在稳定型心绞痛中触发心肌缺血起致病作用，在急性缺血综合征的后遗症中起加重作用，并且可能是某些X综合征患者的主要潜在机制，而变异型心绞痛似乎与血管平滑肌层的高反应性有关。因此，在临床环境中评估内皮介导的冠状动脉血管舒缩张力调节，为了解导致冠状动脉疾病缺血表现的机制提供了独特而重要的见解。
