(国)冠心病.ppt

起始 5 mg 美托洛尔 /安慰剂静注 HR49bpm, SBP99 mmHg, P-Q 0.26s, 无呼吸困难/冷汗 ＋5＋5 ，间隔2min 15min后 HR49bpm, SBP99 mmHg, P-Q 0.26s, 无呼吸困难/冷汗 50mg美托洛尔/安慰剂口服，q6h x 48h 3-15天 剂量减半/不服 100mg 美托洛尔/安慰剂，bid口服 随机 双盲 安慰剂 对照 研究 入选/排除标准与哥德堡研究相似 European Heart Journal 1985;6:199-226 MIAMI研究 美托洛尔显著减少急性期（15天）高危组的死亡率 减少急性期室上速的发生 显著缩小梗死面积 European Heart Journal 1985;6:199-226 MIAMI研究  大型、多中心、共计1250家医院的45852名发病24小时内的急性心梗病人入选，治疗组方案：第一天: 倍他乐克静注5mgx3，平片50mg Q6h 第二天: 倍他乐克平片50mg Q6h(口服一天四次)第三天开始:倍他乐克缓释片200mg 一天一次四星期后结束观察 Lancet 2005;366:1622–32. COMMIT/CCS-2研究 Lancet 2005;366:1622–32. COMMIT/CCS-2研究 与原来?受体阻滞剂在急性心梗的应用试验比较，本研究入选患者范围扩大(如SBP100mg,HR50bpm) 在目前处方信息及ACC/AHA指南中，血流动力学不稳定患者使用?受体阻滞剂属禁忌， COMMIT试验中5%的患者中-重度心力衰竭。心源性休克增加29%，抵消了 早期?受体阻滞剂使用的益处 Lancet 2005;366:1622–32. COMMIT/CCS-2研究 Lancet 2005;366:1622–32. 急性心梗患者建立稳定的血流动力学情况后，开始?受体阻滞剂治疗可预防再梗和猝死 如果院内开始更广泛的?受体阻滞剂治疗，使得出院时更多患者长期使用?受体阻滞剂治疗，则获益更大 COMMIT/CCS-2研究 Thanks * LDL和VLDL，尤其是氧化修饰的LDL，经损伤的内皮细胞或内皮细胞裂隙→中膜，平滑肌细胞增殖、吞噬脂质→泡沫细胞，脂蛋白又降解而释出各种脂质，刺激纤维组织增生，共同构成粥样斑块 * There is now a strong body of evidence supporting the role played by CRP in driving many stages of the atherosclerotic process. This slide is a brief summary of the major mechanisms, however there is a large and growing body of literature on the subject. CRP is thought to be a marker of vascular inflammation, and plays a synergistic role with other traditional risk factors such as elevated LDL-C in promoting atherosclerotic progression. In all stages of the process, elevated levels of CRP seem to be pro-atherogenic. In the earliest stages of endothelial dysfunction, elevated CRP levels reduce levels of nitric oxide to the unstable plaque. In the later stages of atherosclerosis, elevated CRP causes the caps of plaques to thin and become more unstable. Bisoendial RJ, Kastelein JJP, Stroes ESG. Atherosclerosis 2007; 195:e10-18 Packard RRS, Libby P. Clin Chem 2008; 54:24-38 *