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@article{1227620,
author = {Fox, K and Ford, I and Steg, PG and Tardif, JC and Tendera, M and Ferrari, R and Siegelová, Jarmila and Špinar, Jindřich},
article_location = {USA},
article_number = {12},
doi = {http://dx.doi.org/10.1056/NEJMoa1406430},
language = {eng},
issn = {0028-4793},
journal = {New England Journal of Medicine},
note = {Paní prof. Siegelová a pan prof. Špinar vyjmenováni jako jedni z "Investigators" z ČR. Do is.muni zaevidováno na základě žádosti pana prof. Dobšáka.},
title = {Ivabradine in Stable Coronary Artery Disease without Clinical Heart Failure},
volume = {371},
year = {2014}
}
TY - JOUR
ID - 1227620
AU - Fox, K - Ford, I - Steg, PG - Tardif, JC - Tendera, M - Ferrari, R - Siegelová, Jarmila - Špinar, Jindřich
PY - 2014
TI - Ivabradine in Stable Coronary Artery Disease without Clinical Heart Failure
JF - New England Journal of Medicine
VL - 371
IS - 12
SP - 1091-1099
EP - 1091-1099
PB - MASSACHUSETTS MEDICAL SOC
SN - 00284793
N1 - Paní prof. Siegelová a pan prof. Špinar vyjmenováni jako jedni z "Investigators" z ČR. Do is.muni zaevidováno na základě žádosti pana prof. Dobšáka.
N2 - 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.
ER -
FOX, K, I FORD, PG STEG, JC TARDIF, M TENDERA and R FERRARI. Ivabradine in Stable Coronary Artery Disease without Clinical Heart Failure. \textit{New England Journal of Medicine}. USA: MASSACHUSETTS MEDICAL SOC, 2014, vol.~371, No~12, p.~1091-1099. ISSN~0028-4793. Available from: https://dx.doi.org/10.1056/NEJMoa1406430.
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