From the National Heart and Lung Institute, Imperial College, Institute of Cardiovascular Medicine and Science, Royal Brompton Hospital, London (K.F., P.G.S.), and the Robertson Centre for Biostatistics, University of Glasgow, Glasgow (I.F.) - both in the United Kingdom; Département Hospitalo-Universitaire Fibrosis Inflammation Remodeling, Hôpital Bichat, Assistance Publique-Hôpitaux de Paris, INSERM Unité 1148, and Université Paris-Diderot, Sorbonne Paris Cité - all in Paris (P.G.S.); the Montreal Heart Institute Coordinating Centre, Université de Montréal, Montreal (J.-C.T.); the Third Division of Cardiology, Medical University of Silesia, Katowice, Poland (M.T.); and the Department of Cardiology and Laboratory for Technologies of Advanced Therapies Center, University Hospital of Ferrara and Maria Cecilia Hospital, GVM Care and Research, Ettore Sansavini Health Science Foundation, Cotignola, Italy (R.F.).
N Engl J Med. 2014 Sep 18;371(12):1091-9. doi: 10.1056/NEJMoa1406430. Epub 2014 Aug 31.
An elevated heart rate is an established marker of cardiovascular risk. Previous analyses have suggested that ivabradine, a heart-rate-reducing agent, may improve outcomes in patients with stable coronary artery disease, left ventricular dysfunction, and a heart rate of 70 beats per minute or more.
We conducted a randomized, double-blind, placebo-controlled trial of ivabradine, added to standard background therapy, in 19,102 patients who had both stable coronary artery disease without clinical heart failure and a heart rate of 70 beats per minute or more (including 12,049 patients with activity-limiting angina [class ≥II on the Canadian Cardiovascular Society scale, which ranges from I to IV, with higher classes indicating greater limitations on physical activity owing to angina]). We randomly assigned patients to placebo or ivabradine, at a dose of up to 10 mg twice daily, with the dose adjusted to achieve a target heart rate of 55 to 60 beats per minute. The primary end point was a composite of death from cardiovascular causes or nonfatal myocardial infarction.
At 3 months, the mean (±SD) heart rate of the patients was 60.7±9.0 beats per minute in the ivabradine group versus 70.6±10.1 beats per minute in the placebo group. After a median follow-up of 27.8 months, there was no significant difference between the ivabradine group and the placebo group in the incidence of the primary end point (6.8% and 6.4%, respectively; hazard ratio, 1.08; 95% confidence interval, 0.96 to 1.20; P=0.20), nor were there significant differences in the incidences of death from cardiovascular causes and nonfatal myocardial infarction. Ivabradine was associated with an increase in the incidence of the primary end point among patients with activity-limiting angina but not among those without activity-limiting angina (P=0.02 for interaction). The incidence of bradycardia was higher with ivabradine than with placebo (18.0% vs. 2.3%, P<0.001).
Among patients who had stable coronary artery disease without clinical heart failure, the addition of ivabradine to standard background therapy to reduce the heart rate did not improve outcomes. (Funded by Servier; SIGNIFY Current Controlled Trials number, ISRCTN61576291.).
心率升高是心血管风险的既定标志物。先前的分析表明,一种降低心率的药物伊伐布雷定可能改善心率为 70 次/分钟或更高、患有稳定型冠状动脉疾病、左心室功能障碍的患者的结局。
我们对 19102 例同时患有稳定型冠状动脉疾病(无临床心力衰竭)且心率为 70 次/分钟或更高(包括 12049 例因心绞痛而活动受限的患者[加拿大心血管学会分级为 II 级及以上,该分级范围为 I 至 IV 级,级别越高表明因心绞痛导致的体力活动受限越严重])的患者进行了一项随机、双盲、安慰剂对照的伊伐布雷定加标准基础治疗试验。我们将患者随机分配至安慰剂组或伊伐布雷定组,剂量为每日两次,每次 2.5 至 10mg,调整剂量以达到目标心率 55 至 60 次/分钟。主要终点为心血管原因死亡或非致死性心肌梗死的复合终点。
在 3 个月时,伊伐布雷定组的平均(±SD)心率为 60.7±9.0 次/分钟,安慰剂组为 70.6±10.1 次/分钟。中位随访 27.8 个月后,伊伐布雷定组和安慰剂组主要终点的发生率无显著差异(分别为 6.8%和 6.4%,危险比为 1.08;95%置信区间为 0.96 至 1.20;P=0.20),心血管原因死亡和非致死性心肌梗死的发生率也无显著差异。伊伐布雷定与活动受限性心绞痛患者的主要终点发生率增加相关,但与无活动受限性心绞痛患者无关(交互检验 P=0.02)。伊伐布雷定组的心动过缓发生率高于安慰剂组(18.0% vs. 2.3%,P<0.001)。
在无临床心力衰竭的稳定型冠状动脉疾病患者中,将伊伐布雷定加用至标准基础治疗以降低心率并未改善结局。(由 Servier 资助;SIGNIFY 当前对照试验注册号,ISRCTN61576291。)