冠心病知识（阿斯利康培训）.pptVIP

* 先看一下动脉粥样硬化的形成过程。 动脉粥样硬化是一个慢性炎症过程，内皮功能异常是这个过程的起始。很多因素都可导致血管内皮功能异常，如高胆固醇、高血压、糖尿病、感染等。内皮功能异常时，LDL-C穿过内皮进入动脉壁，引发炎症反应，继而LDL-C被氧化，氧化的LDL-C被巨噬细胞吞噬。之后，吞噬有氧化LDL-C的巨噬细胞转变成泡沫细胞，泡沫细胞在动脉壁中聚集，死亡后细胞内脂质释放，大量脂质堆积形成脂肪纹。随着这种过程的进行，脂质核心越来越大，逐渐形成动脉粥样硬化斑块。 * HMG-CoA还原酶是胆固醇合成途径中最重要的限速酶。 瑞舒伐他汀是具有高度选择性的HMG-CoA还原酶竞争性抑制剂，对于HMG-CoA还原酶的抑制作用显著强于其他他汀类药物，可抑制循环中超过90％的HMG-CoA还原酶活性。 * 他汀的抗动脉粥样硬化价值，经历了14年的循证历程锤炼。 * This slide shows the relationship between LDL-C levels and CV event rate in a number of large statin clinical trials and demonstrates that the lower the level of LDL-C observed, the lower the CV event rate. This observation supports the NCEP recommendations to treat to a goal LDL-C concentration.1,2 However, although substantial reductions in LDL-C were obtained with statins (by 23-37%) they do not entirely eliminate events, suggesting that lipid parameters besides LDL-C, such as HDL-C, triglyceride, lipoprotein (a), and LDL particle size and susceptibility to oxidation as well as other risk factors and pleiotropic effects of these drugs, influence CHD risk. The results from on-going trials should answer questions of whether further reductions in LDL-C will provide additional benefit. References Rosenson RS. Exp Opin Emerg Drugs 2004;9(2):269–279. LaRosa JC, Grundy SM, Waters DD et al. N Engl J Med 2005;352:1425-1435. Adapted from Rosenson RS. Statins: can the new generation make an impression? Expert Opin Emerg Drugs 2004;9(2):269–279, with permission from Ashley Publications. Reproduced from LaRosa JC et al. N Engl J Med 2005;352:1425-1435 with permission. Copyright (c) 2005 Massachusetts Medical Society. All rights reserved. * 《中国血脂异常防治指南》结合中国的实际情况，改进了NCEP ATPIII提出的极高危患者LDL-C70mg/dL(2.0mmol/L)的治疗目标。建议高危患者将LDL-C降低至小于100mg/dL(2.59mmol/L)，而极高危患者，应该使LDL-C降至 80mg/dL(2.07mmol/L)。 * * * Using a guidewire and balloon catheter. Wire-guided balloon angioplasty. 四、心律失常的治疗 1.室早和非持续性室速：可不用抗心律失常药物；持续单形室速：利多卡因、胺碘酮、同步电复律 2.持续多形性室速或室颤：非同步直流电除颤 3.缓慢的心律失常：阿托品0.5～1mg，iv 4.Ⅱ°或Ⅲ°AVB伴血流动力学障碍：起搏