全面干预动脉粥样硬[到1]...ppt

* 关键信息：大家都知道冠脉痉挛是无器质性冠脉狭窄病人发生急性心梗的重要原因。这项研究表明氟伐他汀可以通过改善内皮功能而降低冠脉痉挛的发生率。可见他汀改善内皮功能的作用在减少急性事件的发生中有着非常重要的作用。 背景：前瞻、随机研究。64名患者无器质性冠脉狭窄，但冠脉内注射乙酰胆碱可诱发冠脉痉挛。随机分为接受氟伐他汀30 mg/日＋Ca离子拮抗剂 (31 病人缓释地尔硫卓100-200mg或缓释硝苯地平20-40mg）治疗或单独Ca离子拮抗剂 (33个病人)治疗。 6个月后，再次冠脉内注射乙酰胆碱，观察冠脉痉挛发生情况。氟伐他汀组31例病人中16例患者（51.5%）冠脉痉挛被抑制，非他汀组， 33例病人中7例患者（21.2%）冠脉痉挛被抑制，结果证实在原来传统钙离子拮抗剂的基础上加用氟伐他汀会更好的改善冠脉痉挛。其机制可能为应用氟伐他汀后，内皮细胞产生一氧化氮增多。 * 下面我们来看动脉粥样硬化形成过程中的另一个重要因素：炎症反应。 * 关键信息：这是在动脉粥样硬化起始阶段，炎症促进粥样硬化斑块形成的示意图。 LDL-C进入动脉壁，沉积于动脉内膜，并被氧化，氧化的LDL-C容易被巨噬细胞吞噬，形成泡沫细胞，同时引发炎症反应。巨噬细胞可分泌包括CD40/CD40L, TNF-α, IL-1, IL-6 ，CRP等在内的多种炎症成分，CRP只是其中一种。在这些炎症物质的作用下，内皮功能降低。背景：在动脉粥样硬化的进展阶段，炎症反应也发挥着巨大作用。随着LDL-C不断进入，泡沫细胞不断形成，大量泡沫细胞破裂释放脂质，堆积成脂质核心。炎症反应的持续进展，刺激平滑肌细胞增殖并纤维化，包裹在脂质核心外，形成纤维帽。 The major risk factors that promote atherogenesis — cigarette smoking, hypertension, atherogenic lipoproteins, and hyperglycemia — are well established and are known to give rise to a variety of injurious stimuli that activate the inflammatory process. The majority of acute coronary events arise from plaque rupture and thrombosis. The fibrous cap is not a static structure and is constantly being remodeled. Smooth muscle cells and collagenous fibrils are important structural components of the cap. CRP is one of a number of markers (others include CD40/CD40L, TNF-α, IL-1, IL-6 ) which increase dramatically during the inflammatory mechanisms that promote atherosclerosis process through the inhibition of collagen synthesis and the stimulation of collagenase secretion. Such processes result in making the fibrous cap vulnerable and susceptible to rupture. These events are thought to contribute not only to the formation of plaque but may also contribute to its disruption resulting in the formation of a blood clot. Thus, virtually every step in atherogenesis is believed to involve substances involved in the inflammatory response and cells that are characteristic of inflammation. * 关键信息：炎症不但促进了斑块进展，还促进了斑块的破裂。研究发现斑块破裂部位有炎症细胞的聚集，并且炎症细胞可释放基质金属蛋白酶使纤维帽降解，最终导致斑块破裂。 当LDL-C不