PROSPECTIVE RANDOMIZED AMLODIPINE SURVIVAL EVALUATION

PROSPESS(前瞻性随机氨氯地平生存评估)是一个 多中心随机、安慰剂对照、双盲、平行试验 这是在105个中心进行的。其目的是评价其疗效。 氨氯地平，一种长效二氢吡啶钙通道阻滞剂 与安慰剂相比，合并死亡率(心脏和非心脏) 死亡)和危及生命的心脏事件 (IIIb-IV级心力衰竭。所有患者均接受安慰剂治疗。 血管紧张素转换酶抑制剂、地高辛和利尿剂。按心分层随机 衰竭病因，缺血性或非缺血性心肌病， 预先指定的。主要终点是死亡和 心脏病态事件。次要终点是全因死亡率。 在缺血层，猝死和泵衰竭是相似的。 在两个治疗臂上。相比之下，猝死人数减少了 38%，泵故障减少45% 非缺血层。虽然死亡方式并没有因治疗而不同 在缺血患者中，氨氯地平似乎同样降低了这两个指标 9例脑缺血患者猝死和泵衰竭死亡。 普赖斯证明氨氯地平是一种安全的钙拮抗剂。 对于任何病因的左心功能不全患者，都会有所裨益 对于非缺血性病因的患者。Praise-2将是一项设计的研究 进一步研究氨氯地平对患者死亡率的影响 充血性心力衰竭，NYHA III-IV，非缺血性病因。

PRAISE (Prospective Randomized Amlodipine Survival Evaluation) was a multicenter, randomized, placebo-controlled, double-blind, parallel trial which was conducted at 105 centers. Its purpose was evaluate the efficacy of amlodipine, a long acting dihydropyridine calcium channel blocker compared with placebo on combined mortality (cardiac and non-cardiac deaths) and life-threatening cardiac events in patients with severe (class IIIb-IV heart failure. All patients were treated with an Ace-Inhibitor, digoxin, and diuretic. Stratified randomization by heart failure etiology, ischemic or nonischemic cardiomyopathy, was prespecified. The primary endpoint was a combination of death and cardiac morbid events. The secondary endpoint was all-cause mortality. In the ischemic stratum, sudden deaths and pump failures were comparable in the two treatment arms. In contrast, sudden deaths were reduced by 38% and pump failures were reduced by 45% by amlodipine in the nonischemic stratum. While the mode of death did not differ by treatment in the ischemic patients, amlodipine appeared to comparably reduce both sudden death and death from pump failure in the ninischemic patients. PRAISE demonstrates that amlodipine is a safe calcium antagonist to use in patients with LV dysfunction of any etiology, and will be of benefit to patients with non-ischemic etiology. PRAISE-2 will be a study designed to examine further the effects of amlodipine on mortality in patients with congestive heart failure, NYHA III-IV, of nonischemic etiology.