课件：抗血小板药和抗凝药的临床合理应用.ppt

* Slide 4 Pathophysiology of ACS Various factors affect the risk that an atherosclerotic plaque will rupture, including the tensile strength of the fibrous cap and the shear stresses to which it is subjected. Unstable plaques at high risk of rupture typically have a large lipid core, a thin cap and contain large numbers of macrophages but relatively few smoothmuscle cells. Rupture or fissure of the plaque exposes the thrombogenic core of the lesion and leads to adhesion and aggregation of platelets and thrombus formation. A large fissure typically results in the formation of a large thrombus that completely occludes the coronary artery, causing acute MI, characterized by persistent ST-segment elevation and subsequent development of new Q-waves on the electrocardiogram (ECG). A smaller fissure may result in a mural thrombus that partially or transiently occludes the artery, causing acute myocardial ischemia without persistent ST-segment elevation. The clinical diagnosis is unstable angina, or if thereis biochemical evidence of myocardial damage, non-Q-wave MI. ACS is a classic example of atherothrombosis (plaque rupture and thrombus formation). References Fuster V, Badimon L, Badimon JJ et al. N Engl J Med 1992;326:310–318. Davies MJ. Circulation 1990;82(Suppl 3):II38–46. * References: 1. Topol EJ, Yadav JS. Circulation 2000; 101: 570–80. 2. Drouet L. Cerebrovasc Dis 2002; 13(suppl 1): 1–6. Through the development of new imaging modalities and specific therapeutics that serve as probes, microvascular obstruction, owing to embolization, has become increasingly recognized as an important sequelae of atherosclerotic and atherothrombotic vascular disease.1 Thrombus formation on an atherosclerotic plaque is a dynamic process in which platelets aggregate but also spontaneously disaggregate, leading to embolization of platelet aggregates from an evolving thrombus, which can lead to inflammation or microvascular obstruction.2 Additionally, particulate matter may a