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研究表明动脉粥样硬化是在内皮损伤、脂质代谢异常、血流动力学损伤、遗传、感染、物理化学等损伤刺激下启动的,多种炎症因子、免疫机制及相关细胞因子网络交叉样作用于血管壁,动脉粥样硬化逐渐形成和发展同时伴随不稳定斑块的破裂、血栓形成,导致慢性和急性缺血或闭塞性临床事件。不论何种机制,血管壁动脉粥样硬化必须通过血液来介导和促进,易损血液包括血液的成分和状态异常,血液易损程度与动脉粥样硬化性临床事件正相关。
Studies have shown that atherosclerosis is initiated by a number of inflammatory and endothelial cell damage, lipid metabolism, hemodynamic damage, heredity, infection, physical and chemical damage, and a variety of inflammatory factors, immune mechanisms and related cytokines network cross-like effect In the vascular wall, the progressive formation and development of atherosclerosis accompanied by the rupture of unstable plaque, thrombosis, leading to chronic and acute ischemic or occlusive clinical events. Regardless of the mechanism, atherosclerosis of the vessel wall must be mediated and facilitated by the blood, components and abnormalities of the bloodstream, including blood, and blood vulnerability are positively correlated with atherosclerotic clinical events.