By Michael B. Gravanis (auth.), Peter W. F. Wilson MD (eds.)
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Additional resources for Atlas of Atherosclerosis: Risk Factors and Treatment
Restoring vascular nitric oxide formation by L-arginine improves the symptoms of intermittent claudication in patients with peripheral arterial occlusive disease. JAm Coll Cardiol1998, 2:1336-1344. Pepine CJ: The effects of angiotensin-converting enzyme inhibition on endothelial dysfunction: potential role in myocardial ischemia. Am J Cardiol1998, 82(10[A]):235-275. THEROSCLEROSIS: RISK FACTORS AND TREATMENT 40 THE MACROPHAGE AND ATHEROSCLEROTIC PROCESS Peter Libby C HA PTE R Data from pathologic studies and clinical trials over the past decade have led to a reassessment of the pathogenesis and treatment of atherosclerotic disease.
Under pathologic conditions when homeostatic mechanisrns 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 rnanifestation of cardiovascular disease . A critical homeostatic function of normal endothelium involves control of vascular tone, determined by a dynamic balance of endothelium-derived vasoactive mediators. Dilator substances include prostacyclin, bradykinin, endotheliurnderived hyperpolarizing factor (EDHF), and , importantly, nitric oxide (NO) .
M0-macrophage; PMN-polymorphonuclear leukocyte. ) NDOTHELIAL DYSFUNCTION AND ATHEROTHROMBOSIS 33 lntra lu mi nal thrombus Propagation of th rombus Lipidpool Intraplaque thromus Vessel injury FIGURE 2-24. Pathologie studies have shown that rupture of atherosclerotic plaques and subsequent luminal thrombosis underlies the etiology of acute ischemic coronary syndromes, including myocardial infarction and unstable angina. A lipid-rich core (particularly in the shoulder regions of lesions), abundance of inflammatory cells, a thin fibrous cap, and dysfunctional overlying endothelium characterize morphologic features of lesions prone to rupture.