BACKGROUND:Levosimendan is a calcium sensitizer that increases the contractility of the myofilaments and is considered not to affect cardiac electrophysiology. We assessed its potential to generate cardiac arrhythmias by analysing ECG recordings from clinical studies on intravenously administered levosimendan in heart failure patients. METHODS AND RESULTS: The database consisted of continuous 1-day recordings, of which 366 were during levosimendan and 142 during placebo comparison. Supraventricular (SVT) and ventricular tachycardia (VT) were defined as > or =3 premature complexes at a rate > or = 120/min. No difference appeared between levosimendan and control groups in the occurrence of atrial fibrillation (12% vs 13%), SVT (28% vs 30%), or VT (41% vs 44% of all recordings; all p = NS). Also the frequency of VT was similar (0.55 +/- 3.89 vs 0.20 +/- 1.08 episodes/h; p = NS). No torsade de pointes or sustained VT occurred. CONCLUSION: Short-term levosimendan therapy of heart failure showed no tendency to increase cardiac arrhythmias. Although assessing only surrogates of prognostically significant arrhythmias, the findings together with previously observed reduction of mortality in heart failure therapy studies support the presumption that levosimendan has an electrophysiologically neutral profile.
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BACKGROUND:Levosimendan is a calcium sensitizer that increases the contractility of the myofilaments and is considered not to affect cardiac electrophysiology. We assessed its potential to generate cardiac arrhythmias by analysing ECG recordings from clinical studies on intravenously administered levosimendan in heart failurepatients. METHODS AND RESULTS: The database consisted of continuous 1-day recordings, of which 366 were during levosimendan and 142 during placebo comparison. Supraventricular (SVT) and ventricular tachycardia (VT) were defined as > or =3 premature complexes at a rate > or = 120/min. No difference appeared between levosimendan and control groups in the occurrence of atrial fibrillation (12% vs 13%), SVT (28% vs 30%), or VT (41% vs 44% of all recordings; all p = NS). Also the frequency of VT was similar (0.55 +/- 3.89 vs 0.20 +/- 1.08 episodes/h; p = NS). No torsade de pointes or sustained VT occurred. CONCLUSION: Short-term levosimendan therapy of heart failure showed no tendency to increase cardiac arrhythmias. Although assessing only surrogates of prognostically significant arrhythmias, the findings together with previously observed reduction of mortality in heart failure therapy studies support the presumption that levosimendan has an electrophysiologically neutral profile.