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| |  Ivabradine Improves Heart Rate and Left-Ventricular Function in Patients With Severe Systolic Chronic Heart Failure on Beta-Blockers: Presented at HF2008 By Chris Berrie MILAN, Italy -- June 19, 2008 -- Addition of the novel agent ivabradine to beta-blocker treatment of patients with severe chronic systolic heart failure (CSHF) significantly and safely reduces heart rate and improves left ventricular (LV) function, according to a multicentre, open-label, phase 2 study. The findings were presented in a poster session here on June 16 at the Heart Failure 2008 (HF2008) Congress. Ivabradine's effect on heart rate is via selective inhibition of the If current in the pacemaking activity of sinoatrial node cells. Unlike beta-blockers, ivabradine does not affect myocardial contractility and intracardiac conduction. "Ivabradine is a drug that just lowers heart rate without any inotropic positive or negative effects," said principal investigator Guillaume Jondeau, MD, PhD, Cardiology Department, Hôpital Bichat, Paris, France. The drug has also shown antianginal and anti-ischaemic efficacy, with beneficial effects on LV function in patients with systolic LV dysfunction. Dr. Jondeau and colleagues conducted their study to evaluate the effects of ivabradine on heart rate and LV function and its safety in patients with severe CSHF receiving conventional therapy. Entry criteria were severe CSHF, New York Heart Failure (NYHF) class III/IV, hospitalisation for HF within prior 12 months, LV ejection fraction (LVEF) <=35% (ischaemic or nonischaemic origin), heart rate >=60 beats/min, and current beta-blocker therapy. Patients received treatment with oral ivabradine for 6 weeks, with uptitration according to heart rate and clinical tolerability every 2 weeks from 2.5 mg BID to 5 mg BID, to a final dose of 7.5 mg BID. A total of 87 patients were enrolled; mean age was 62 years and 75% were male; 44% of patients had ischaemic HF; and mean disease duration was 44 months. Additional therapy included angiotensin-converting enzyme (ACE) inhibitors/angiotensin-receptor blockers (99%), diuretics (94%), and cardiac glycosides (25%). Of the overall group, 65% were titrated to the highest dose and 17.2% to the intermediate dose. Mean heart rate significantly improved from baseline to week 6 (74.1 vs 64.0; P < .001), with greater improvement seen for patients with higher baseline heart rates. LV function improved significantly, with a 5.3% increase in LVEF from the 28.6% rate at baseline (P < .001); LV end systolic volume decreased by 18.5 mL from the 161.7 mL value at baseline (P < .001); and LV end diastolic volume showed an improvement trend, with an 8.2 mL decrease from 223.8 mL at baseline (P = .053). There were negligible effects on blood pressure. Investigator-determined clinical symptoms improved in 66.7% of patients; 52% showed improvement from NYHA class IV to class III. Five patients experienced bradycardia (symptomatic in 2 patients). Four serious adverse events were seen and were not considered to be treatment related. Dr. Jondeau added, "These are significant effects, which also suggest that the more you decrease the heart rate, the greater is your improvement in [LV] ejection fraction." Funding for this study was provided by Servier.
[Presentation title: Haemodynamic Effects of Ivabradine, a Pure Heart Rate Lowering Agent, in Patients With Severe Systolic Chronic Heart Failure Receiving Beta-Blockers. Abstract P738]
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