洛汀新早联行动—培训课件.pptVIP

* 可以看出应用洛汀新联合CCB组的，对意向治疗人群24小时动态血压监测收缩压/舒张压距基线的变化如图所示，SELECT研究结果提示联合治疗组（贝那普利/氨氯地平）血压显著下降，有统计学意义， P 0.0001。 * 对意向治疗人群的血压反应率及控制率的分析表明，与氨氯地平或贝那普利单药治疗相比，洛汀新? /CCB联合治疗显著改善血压反应率（不同治疗间收缩压降低10 ）与控制率（收缩压140 mm Hg ），P0.0001，这个临床研究证明，联合治疗明显优于单药，对于严重收缩期高血压患者，临床治疗可以选择起始以洛汀新为基础的联合临床方案. * 在研究，我们不仅观察到联合可以得到很好的血压达标率，另外还观察到药品的安全性和副作用，尤其是CCB通常会引起水肿，如果联合是否副作用会增加？ 不良事件结果分析表明，氨氯地平5mg组新发外周水肿的发生率为9.4%，洛汀新? /氨氯地平联合治疗组的发生率为3.8%，降低约60%，这提示，洛汀新?能有效避免CCB引起的水肿。不但没有副作用加倍，相反降低，这样更能增加患者的依从性。作用机制是什么呢? * Short-acting dihydropyridine calcium channel blockers (DHP-CCBs) are associated with various side effects including: flushing, tachycardia, angina, dizziness and headache. The long-acting DHPs, such as amlodipine, tend to avoid these effects, but are associated with dose-dependent peripheral edema. Peripheral edema is caused by a mismatch between arteriolar and venous dilation. Arterial dilation is responsible for the reduction in BP with CCBs. However, without comparable venous dilation, capillary pressure may increase, leading to leakage of fluid into the extracellular space, thereby resulting in edema. References Messerli FH. Vasodilatory edema: a common side effect of antihypertensive therapy. Am J Hypertens 2001;14:978–9. Weir MR. Incidence of pedal edema formation with dihydropyridine calcium channel blockers: issues and practical significance. J Clin Hypertens 2003;5:330–5. CCB(钙通道阻滞剂)相关的外周水肿发生机制是，CCB作为钙通道阻滞剂仅扩张动脉，而没有扩张静脉，由此液体自血管中渗出，最终发生水肿。 * 而ACEI/CCB联合使用时， CCB 和ACEI导致动脉扩张，同时ACEI也导致静脉扩张，从而阻断了水肿发生机制，最终减轻CCB导致水肿的不良反应。这样就可以增加这些老年患者的依从性，加强了患者治疗的信心。 Peripheral edema with calcium channel blockers (CCBs) is explained by a greater dilation of the arteriolar rather than the venous circulation, giving rise to an increased transcapillary gradient and capillary leakage. The addition of a renin angiotensin system blocker, such as an angiotensin receptor blocker, helps negate this effect because they cause dilation of both arterial and venous capillary beds, thus bringing transcapillary pressure