冠心病治疗策略的演变.ppt

This is a key slide to focus on the whole issue of vulnerable plaque, plaque rupture and resulting MI. Also point out, first manifestation of CAD, can be the last: 50% MI 10% sudden heart death 30% angina pectoris At present, there is ongoing research which appears to confirm that the process of lowering cholesterol levels using statins has the additional benefit of stabilising vulnerable plaque. Ask to what extent they agree with this theory. If they agree, ask if they consider, as a logical consequence, that statins should be prescribed earlier in the CAD cycle of development! 30 30 新近在美国心脏病学院（ACC）学术会上公布，新英格兰医学杂志电子版同日全文发表了对比经皮冠状动脉血管重建和根据指南强化药物治疗改善稳定性冠心病患者的预后（COURAGE）试验的结果，引起医学界与社会的关注。研究入选2,287例严重但稳定的冠心病患者，均有心绞痛症状和心肌缺血的客观证据，冠状动脉造影显示在冠状动脉近端至少70%狭窄。 在COURAGE试验中，2,287例患者均依据指南，接受理想的药物治疗，包括他汀类药物、抗血小板治疗（阿司匹林81～325mg，若不耐受阿司匹林则应用氯吡格雷75mg/d，PCI治疗组为阿司匹林和氯吡格雷联用）、血管紧张素转化酶抑制剂或血管紧张素拮抗剂（ACEI/ARB）和β阻滞剂。所有患者应用强化降脂治疗使低密度脂蛋白胆固醇（LDL-C）达到60～85mg。在此基础上，患者被随机接受（n=1149）或不接受PCI（n=1138）治疗。随访2.5～7年，随访的中位数时间4.6年。预先设计的预后终点为总死亡率，严重心血管事件（死亡、非致命心肌梗死或卒中），单独计算非致命性心肌梗死或因急性冠状动脉综合征住院。 一旦出现内皮细胞的激活，趋化因子、选择素和粘附分子的表达，这个阶段就会成为粥样硬化的一个启动机制——微小炎症。当白细胞尤其是单核细胞侵入到血管壁，它们将释放更多的趋化因子，这样又吸引了更多的白细胞加入进来。它们还可以释放生长因子来刺激血管平滑肌细胞增殖和泡抹细胞形成。总之，这一切最终将会导致粥样硬化的形成。 动脉壁内脂质浸润导致粥样斑块形成的“脂质浸润”学说提出已有一百余年的历史，其提出基于高脂血症与AS的因果关系，因而长期以来在AS发生机制中占主导地位。 A famous pathologist Several biochemical markers have been identified as predictors of future cardiovascular (CV) events. In the past, cholesterol levels have been used in various patient populations to assess the risk for future CV events and guide physicians in the treatment of high-risk patients. Recently, high-sensitivity C-reactive protein (hs-CRP) has been identified as a strong predictor of CV events. Rifai and Ridker constructed an algorithm for CV risk prediction using cholesterol measurements along with hs-CRP. Combining the risk associated with hs-CRP measurements and the risk associated with the total ratio of cholesterol to high-density lipoprotein cholesterol is th