Heart failure etiology and response to milrinone in decompensated heart failure - Results from the OPTIME-CHF study
Heart failure etiology and response to milrinone in decompensated heart failure - Results from the OPTIME-CHF study
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DOI：
10.1016/s0735-1097(02)02968-6
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发表时间：
2003-03-19
影响因子：
24
通讯作者：
O'Connor, CM
中科院分区：
文献类型：
--
作者：
Felker, GM;Benza, RL;O'Connor, CM
本研究的目的是评估心力衰竭（HF）病因学和失代偿性HF对米力农的反应之间的相互作用。背景病因学对HF具有预后和治疗意义，但其与变力性治疗反应的关系尚不清楚。方法：（OPTIME-CHF）研究将949名患有收缩功能障碍和失代偿性HF的患者随机分为两组，分别接受48至72小时的静脉注射米力农或安慰剂。主要终点是60天内因心血管原因住院的天数。在事后分析中，我们评估了对米力农的反应和HF病因之间的相互作用。结果缺血性患者的主要终点为13.0天，非缺血性患者为11.7天（p = 0.2）。缺血组和非缺血组的60天死亡率分别为11.6%和7.5%（p = 0.03）。校正基线差异后，病因和米力农的作用之间存在显著的相互作用。在主要终点（米力农组13.6天vs安慰剂组12.4天，相互作用p = 0.055）和死亡或再住院复合终点（42% vs安慰剂组36%，相互作用p = 0.01）方面，米力农治疗的缺血性病因患者的结局往往比安慰剂治疗的患者更差。相比之下，米力农治疗的非缺血性患者的主要终点（10.9天与安慰剂12.6天）和死亡或再住院的复合终点（28%与安慰剂35%）方面的结果往往得到改善。米力农对缺血性心力衰竭可能有害，但对非缺血性心肌病可能有益。(C)2003年由美国心脏病学会基金会。
OBJECTIVES The goal of this study was to assess the interaction between heart failure (HF) etiology and response to milrinone in decompensated HF.BACKGROUND Etiology has prognostic and therapeutic implications in HF, but its relationship to response to inotropic therapy is unknown.METHODS The Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) study randomized 949 patients with systolic dysfunction and decompensated HF to receive 48 to 72 h of intravenous milrinone or placebo. The primary end point was days hospitalized from cardiovascular, causes within 60 days. In a post-hoc analysis, we evaluated the interaction between response to milrinone and etiology of HF.RESULTS The primary end point was 13.0 days for ischemic patients and 11.7 days for nonischemic patients (p = 0.2). Sixty-day mortality was 11.6% for the ischemic group and 7.5% for the nonischemic group (p = 0.03). After adjustment for baseline differences, there was a significant interaction between etiology and the effect of milrinone. Milrinone-treated patients with ischemic etiology tended to have worse outcomes than those treated with placebo in terms of the primary end point (13.6 days for milrinone vs. 12.4 days for placebo, p = 0.055 for interaction) and the composite of death or rehospitalization (42% vs. 36% for placebo, p = 0.01 for interaction). In contrast, outcomes in nonischemic patients treated with milrinone tended to be improved in terms of the primary end point (10.9 vs. 12.6 days placebo) and the composite of death or rehospitalization (28% vs. 35% placebo).CONCLUSIONS Milrinone may have a bidirectional effect based on etiology in decompensated HF. Milrinone may be deleterious in ischemic HF, but neutral to beneficial in nonischemic cardiomyopathy. (C) 2003 by the American College of Cardiology Foundation.