By Michael B. Gravanis (auth.), Peter W. F. Wilson MD (eds.)

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N Eng/ JMed 1991, 325:1551-1556. 18. : Patients with evidence of coronary endothelial dysfunction as assessed by acetylcholine infusion demonstrate marked increase in sensitivity to constrictor effects of catecholamines. Circulation 1992, 85:1390-1397. 19. Bogaty P, Hackett D, Davies G, Maseri A: Vasoreactivity of the culprit lesion in unstable angina. Circulation 1994, 90:5-11. 20. : Evidence of impaired endothelium-dependent coronary vasodilatation in patients with angina pectoris and normal coronary angiograms.

Interestingly, these are the very same interventions that attenuate atherosclerosis and improve morbidity and mortality outcomes from cardiovascular disease, suggesting a mechanistic link between endothelial dysfunction and atherosclerosis. The simple presence or anatomic severity of fixed atherosclerotic lesions is not necessarily predictive of cardiac events. nal thrombosis, and vasospasm. The morphologic ATLAS OF ATHEROSCLEROSIS: RISK FACTORS AND TREATMENT 22 characteristics of vulnerable plaques relate to their structural and physiologic features that are largely influenced by neighboring endothelial cells.

Normal endothelium provides a fluid antiatherogenic environment that inhibits platelet and leukocyte adhesion, prevents vasospasm, promotes fibrinolysis, and inhibits vascular smooth muscle cell growth. Under pathologic conditions when homeostatic mechanisms are altered, the phenotypic changes that occur in endothelial cells support a vasospastic, prothrombotic, and proinflammatory milieu, and play a central role in the pathophysiology and clinical manifestations of cardiovascular disease [1]. A critical homeostatic function of normal endothelium involves control of vascular tone, determined by a dynamic balance of endothelium-derived vasoactive mediators.

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Atlas of Atherosclerosis: Risk Factors and Treatment by Michael B. Gravanis (auth.), Peter W. F. Wilson MD (eds.)
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