Effect of ivabradine on left ventricular remodelling after reperfused myocardial infarction: A pilot study

Background. - Heart rate is a major determinant of myocardial oxygen demand; in ST-segment elevation myocardial infarction (STEM!), patients treated with primary percutaneous intervention (PPCI), heart rate at discharge correlates with mortality. Ivabradine is a pure heart rate-reducing agent that has no effect on blood pressure and contractility, and can reverse left ventricular (LV) remodelling in patients with heart failure. Aims. To evaluate whether ivabradine, when added to current guideline-based therapy, improves LV remodelling in STEMI patients treated with PPCI. Methods. This paired-cohort study included 124 patients between June 2011 and July 2012. Ivabradine (5 mg twice daily) was given promptly after PPCI, along with beta-blockers, to obtain a heart rate < 60 beats per minute (ivabradine group). This group was matched with STEMI patients treated in line with current guidelines, including beta-blockers (bisoprolol), according to age, sex, infarct-related coronary artery, ischaemia time and infarct size determined by initial cardiac magnetic resonance imaging (CMR) (control group). Statistical analyses were performed according to an intention-to-continue treatment principle. CMR data at 3 months were available for 122 patients. Results. Heart rate was lower in the ivabradine group than in the control group during the initial CMR (P=0.02) and the follow-up CMR (P=0006). At the follow-up CMR, there was a smaller increase in LV end-diastolic volume index in the ivabradine group than in the control group (P= 0.04). LV end-systolic volume index remained unchanged in the ivabradine group, but increased in the control group (P=0.01). There was a significant improvement in LV ejection fraction in the ivabradine group compared with in the control group (P=0.04). Conclusions. In successfully reperfused STEMI patients, ivabradine may improve LV remodelling when added to current guideline-based therapy. (C) 2013 Elsevier Masson SAS. All rights reserved.