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动脉粥样硬化的发病原理尚未完全明了,目前仍以脂质浸润及血栓形成和血小板聚集学说为主。急性心肌梗塞的发生,尽管因素很多,其基本的病理过程是由于冠状动脉血栓的形成。近年来,亦有一些学者对此传统的观点提出异议,其主要根据如下:(1)心性猝死的血栓发生率仅占10％,且随着梗塞病程的延长而增加。(2)致死的穿壁性心肌梗塞者血栓发生率达55％,而死于心内膜下心肌梗塞者却很少发生血栓;(3)伴有心原性休克的心肌梗塞患者中,血栓发生率超过70％。从而提示梗塞区的血流缓慢或淤滞与发病有一定的关系。众所周知,血小板无论在形成血栓或粥样硬化方面都起着重要作用。由于血小板的致活释放血栓素A(T×A_2)能引起冠状动脉的痉挛;同时还可抑制腺
The pathogenesis of atherosclerosis is not yet fully understood, is still based on lipid infiltration and thrombosis and platelet aggregation theory. The occurrence of acute myocardial infarction, despite many factors, is due to the formation of coronary thrombosis. In recent years, some scholars have also raised objections to this traditional view. The main reasons are as follows: (1) The incidence of thrombosis in sudden cardiac death accounts for only 10%, and increases with the duration of the infarction. (2) Thrombosis occurred in 55% of those who died of transmyocardial infarction, whereas those who died of subendocardial myocardial infarction seldom experienced thrombosis. (3) Thrombosis occurred in patients with myocardial infarction with cardiogenic shock Rate more than 70%. Thus suggesting that the blood flow in the infarct area is slow or stasis has a certain relationship with the incidence. It is well-known that platelets play an important role both in the formation of thrombus and atherosclerosis. Due to the release of thromboxane A (T × A_2) induced by platelet can cause coronary spasm; also inhibit the gland