Clinical-pathological correlations of coronary disease progression and regression.
Clinical-pathological correlations of coronary disease progression and regression.
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DOI：
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发表时间：
1992-12
期刊：
影响因子：
37.8
通讯作者：
V. Fuster;J. Badimón;L. Badimón
中科院分区：
文献类型：
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作者：
V. Fuster;J. Badimón;L. Badimón
动脉粥样硬化的发生可能是由于某些血管部位（弯曲点、分叉点等）的血流振荡剪切应力所致。产生慢性轻微损伤，导致动脉内皮I型损伤的功能改变;实验上，这被致动脉粥样硬化危险因素如高胆固醇血症、高血压、免疫复合物、病毒感染和烟草烟雾增强。这种最小的损伤导致脂质和单核细胞的积累（巨噬细胞），并且随后，由巨噬细胞释放的毒性产物产生内膜表面的损伤，具有剥脱内皮II型损伤或损伤，其吸引血小板;所有这些细胞释放生长因子，促进平滑肌细胞的迁移和增殖，并产生“纤维内膜损伤”或主要的“内膜损伤”的囊外。脂质损害“被薄囊包围的脂质病变往往很小，容易破裂，引起III型损伤或损害;也就是说，它们柔软而脆弱，含有大量的巨噬细胞，这些巨噬细胞可能释放胶原酶和弹性蛋白酶形成肿胀，并且通过它们的位置，受到流动剪切力的影响。斑块破裂后有血栓形成;当血栓较小时，它们可以变得机化并有助于动脉粥样硬化斑块的生长;当血栓较大且闭塞时，它们导致急性冠状动脉综合征。新的数据表明，在斑块破裂时，某些“血栓形成”风险因素调节血栓形成的程度，从而调节斑块与各种急性冠状动脉综合征的生长。除了需要更好地了解动脉粥样硬化形成的基础生物学，重点是确定和修改原发性动脉粥样硬化和血栓形成的危险因素应继续作为一级预防。此外，新的方法应该集中在识别，稳定和小的“脂质斑块”容易破裂（这些不一定是血管造影明显），以及使用更好的和更安全的抗血栓药物，以防止进展的消退。
The initiation of atherosclerosis may result from blood flow oscillatory shear stress in certain vascular sites (bending points, bifurcations, etc.) producing chronic minimal injury resulting in functional alteration of the arterial endothelium type I injury; experimentally, this is potentiated by atherogenic risk factors such as hypercholesterolemia, hypertension, immunocomplexes, viral infections, and tobacco smoke. Such minimal injury leads to accumulation of lipid and monocytes (macrophages), and subsequently, toxic products released by the macrophages produce damage of the intimal surface with denuding endothelium type II injury or damage, which attracts platelets; all of these cells release growth factors, prompting migration and proliferation of smooth muscle cells and producing a "fibro-intimal lesion" or the outside of the capsule of a predominant "lipid lesion." The lipid lesions surrounded by a thin capsule tend to be small and rupture easily, causing type III injury or damage; that is, they are soft and weak, contain large numbers of macrophages, which may release collagenase and elastase to form abscesses, and by their location, are under the effect of flow shear forces. After plaque disruption there is thrombus formation; when thrombi are small, they can become organized and contribute to the growth of the atherosclerotic plaque; when thrombi are large and occlusive, they lead to the acute coronary syndromes. New data suggest that, at the time of plaque disruption, certain "thrombogenic" risk factors modulate the degree of thrombogenicity and, thereby, the growth of the plaque versus the various acute coronary syndromes. Aside from the need for better understanding of the basic biology of atherogenesis, emphasis on identifying and modifying the primary atherogenic and thrombogenic risk factors should continue for primary prevention. Also, new approaches should focus on the identification, stabilization, and regression of the small "lipid plaques" prone to rupture (these are not necessarily angiographically apparent), as well as on the use of better and safer antithrombotic agents for prevention of progression.