J 2014

Ivabradine in Stable Coronary Artery Disease without Clinical Heart Failure

FOX, K, I FORD, PG STEG, JC TARDIF, M TENDERA et. al.

Basic information

Original name

Ivabradine in Stable Coronary Artery Disease without Clinical Heart Failure

Authors

FOX, K, I FORD, PG STEG, JC TARDIF, M TENDERA and R FERRARI

Edition

New England Journal of Medicine, USA, MASSACHUSETTS MEDICAL SOC, 2014, 0028-4793

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

30200 3.2 Clinical medicine

Country of publisher

United States of America

Confidentiality degree

není předmětem státního či obchodního tajemství

Impact factor

Impact factor: 55.873

Organization unit

Faculty of Medicine

DOI

UT WoS

000341687300004
Změněno: 23/2/2015 15:15, Ing. Mgr. Věra Pospíšilíková

Abstract

V originále

BACKGROUND 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. METHODS 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. RESULTS 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). CONCLUSIONS 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.