Mokuno H, Daida H, Yamaguchi H
Juntendo University, Division of Cardiology.
Nihon Rinsho. 1993 Aug;51(8):2132-8.
During the progression of early atherosclerotic lesions, atherosclerotic plaque rupture, with intraluminal thrombosis superimposed, which is one of the principle mechanisms of evolving atherosclerosis, may lead to thrombotic occlusion and ischemic coronary syndrome. Pathologic studies suggest that plaque rupture and overlying thrombi, which are dynamic and repetitive may frequently occur. In most cases, healed ruptures and incorporation of thrombi produce plaque progression without manifestation of clinical symptoms. However, acute mural occlusive thrombi, overlying plaque ruptures, cause unstable angina and acute myocardial infarction. The different pathogenesis between unstable angina and acute myocardial infarction might depend on the composition and stability of the thrombus resulting from the degree of vessel injury and blood flow. Soft lipid-rich plaques appear more prone to rupture, particularly when the lipid pool is localized eccentrically within the intima. Macrophages in the plaque may also facilitate plaque rupture by releasing proteases.
在早期动脉粥样硬化病变进展过程中，动脉粥样硬化斑块破裂并伴有管腔内血栓形成，这是动脉粥样硬化发展的主要机制之一，可能导致血栓性阻塞和缺血性冠状动脉综合征。病理研究表明，斑块破裂和覆盖其上的血栓是动态且反复发生的，可能频繁出现。在大多数情况下，愈合的破裂和血栓的融合会导致斑块进展而无临床症状表现。然而，覆盖在斑块破裂处的急性壁内闭塞性血栓会引发不稳定型心绞痛和急性心肌梗死。不稳定型心绞痛和急性心肌梗死之间不同的发病机制可能取决于由血管损伤程度和血流导致的血栓的组成和稳定性。富含脂质的软斑块似乎更容易破裂，尤其是当脂质池偏心地位于内膜内时。斑块中的巨噬细胞也可能通过释放蛋白酶促进斑块破裂。
