Zaman A G, Helft G, Worthley S G, Badimon J J
Cardiovascular Biology Research Laboratory, Zena and Michael A. Wiener Cardiovascular Institute (Box 1030), Mount Sinai School of Medicine, New York, NY 10029, USA.
Atherosclerosis. 2000 Apr;149(2):251-66. doi: 10.1016/s0021-9150(99)00479-7.
Atherosclerosis and its thrombotic complications are the major cause of morbidity and mortality in the industrialized world. The progression of atherosclerotic plaques in the coronary circulation is dependent on several risk factors. It is now clear that plaque composition is a major determinant of the risk of subsequent plaque rupture and superimposed thrombosis. The vulnerability of plaques to rupture is further determined by extrinsic triggering factors. Following rupture, the fatty core of the plaque and its high content of tissue factor provide a powerful substrate for the activation of the coagulation cascade. Plaque rupture can be clinically silent or cause symptoms of ischaemia depending on thrombus burden and the degree of vessel occlusion. In addition, plaque rupture and subsequent healing is recognized to be a major cause of further rapid plaque progression. This review looks at the mechanisms underlying the development and progression of atherosclerotic plaques, factors leading to plaque rupture and subsequent thrombosis and their clinical consequences. Finally, we speculate on targets for future research.
动脉粥样硬化及其血栓形成并发症是工业化国家发病和死亡的主要原因。冠状动脉循环中动脉粥样硬化斑块的进展取决于多种危险因素。现在已经清楚，斑块成分是随后斑块破裂和叠加血栓形成风险的主要决定因素。斑块破裂的易损性进一步由外在触发因素决定。破裂后，斑块的脂质核心及其高含量的组织因子为凝血级联反应的激活提供了强大的底物。根据血栓负荷和血管阻塞程度，斑块破裂在临床上可能无症状，也可能导致缺血症状。此外，斑块破裂及随后的愈合被认为是斑块进一步快速进展的主要原因。本综述探讨了动脉粥样硬化斑块发生和进展的潜在机制、导致斑块破裂及随后血栓形成的因素及其临床后果。最后，我们推测了未来研究的靶点。
