[Physiopathology of unstable angina].
The major risk of atherosclerotic disease is the occurrence of an acute coronary syndrome. The pathogenesis of instable angina involves the formation of an arterial thrombus as a consequence of the rupture of an atheromatous plaque. This risk of plaque rupture appears to depend on plaque morphology rather than plaque size or severity of stenosis. Ratio of lipid core to fibrous determined by the balance between smooth muscle cells proliferation and extracellular matrix synthesis stabilizing the plaque and macrophages which degrade collagen, determine the plaque vulnerability. The fibrous cap weakness leads to the plaque activation, plaque fissure or erosion activating a thrombotic cascade. A general inflammation or prothrombotic states are probably involved suggesting the need for a systemic therapeutic in addition with the treatment of the culprit lesion.
Teiger
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Service de physiologie explorations fonctionnelles, fédération de cardiologie, hôpital Henri Mondor, 51, avenue du Maréchal de Lattre de Tassigny, 94010 Créteil, France. teiger@im3.inserm.fr
D000789:Angina, Unstable / Q000150:complications* / Q000503:physiopathology; D001161:Arteriosclerosis / Q000209:etiology; D003329:Coronary Vasospasm / Q000209:etiology; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000209:etiology; D017202:Myocardial Ischemia / Q000209:etiology; D012421:Rupture; D013927:Thrombosis / Q000209:etiology