Coronary atherosclerosis: determinants of plaque rupture.
Coronary atherosclerosis: determinants of plaque rupture.
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DOI：
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发表时间：
1998-04
影响因子：
39.3
通讯作者：
M. Grønholdt;S. Dalager-Pedersen;E. Falk
中科院分区：
文献类型：
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作者：
M. Grønholdt;S. Dalager-Pedersen;E. Falk
急性冠状动脉综合征的突发和不可预测的发病机制是冠状动脉斑块破裂，血栓形成和血管痉挛叠加。斑块破裂的风险取决于斑块类型（成分）而不是斑块大小（体积）;大多数破裂发生在含有柔软、富含脂质的核心的斑块中，该核心被薄且发炎的纤维组织帽覆盖。与完整的帽相比，破裂的帽通常更薄，含有更少的胶原（负责拉伸强度），更少的平滑肌细胞（smc;胶原合成细胞）和更多的巨噬细胞（胶原降解细胞）。因此，斑块脆弱性和破裂的主要决定因素是进行性脂质积聚（核心形成）和帽弱化，这是由于持续的炎症伴胶原降解（巨噬细胞相关）和受损的愈合和修复（SMC相关）。这些内在的斑块变化使斑块易于破裂，而施加在斑块上的外力，如生物力学和血液动力学应力，可能通过沉淀或“触发”它来决定破裂的实际时间。幸运的是，最近对冠状动脉疾病患者的研究表明，斑块脆弱性和破裂触发因素都可以通过治疗进行有益的修改。
The most important mechanism responsible for the sudden and unpredictable onset of acute coronary syndromes is coronary plaque rupture with thrombosis and vasospasm superimposed. The risk of plaque rupture depends on plaque type (composition) rather than plaque size (volume); most ruptures occur in plaques containing a soft, lipid-rich core that is covered by a thin and inflamed cap of fibrous tissue. Compared with intact caps, the ruptured ones usually are thinner and contain less collagen (responsible for tensile strength), fewer smooth muscle cells (smc; collagen synthesizing cells), and many more macrophages (collagen degrading cells). Therefore, major determinants of plaque vulnerability and rupture are progressive lipid accumulation (core formation) and cap weakening due to ongoing inflammation with collagen degradation (macrophage-related) and impaired healing and repair (smc-related). These intrinsic plaque changes predispose plaques to rupture whereas extrinsic forces imposed on plaques, such as biomechanical and haemodynamic stresses, may determine the actual time of rupture by precipitating or 'triggering' it. Luckily, recent research in patients with coronary artery disease indicates that both plaque vulnerability and rupture triggers may be modified beneficially by treatment.