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Acute effects of levosimendan and dobutamine on QRS duration in patients with heart failure.

Author(s): Yontar OC, Yilmaz MB, Yalta K, Erdem A, Tandogan I

Affiliation(s): Cumhuriyet University, Faculty of Medicine, Department of Cardiology, Sivas - Turkey. drcanyontar@gmail.com

Publication date & source: 2010-12, Arq Bras Cardiol., 95(6):738-42. Epub 2010 Nov 12.

Publication type: Randomized Controlled Trial

BACKGROUND: Levosimendan is a novel inotropic agent that enhances cardiac contractility without increasing cellular calcium intake, so that it is not supposed to cause intracellular calcium overload and related arrhythmias. In patients with heart failure, prolonged QRS duration is associated with increased risk of mortality and sudden cardiac death. Structural changes in the left ventricle may lead to asynchronous contraction, causing conduction delay and a prolonged QRS on the surface electrocardiogram. OBJECTIVE: We aimed to compare the acute effects of levosimendan and dobutamine on QRS duration in patients with severe heart failure and sinus rhythm. METHODS: Sixty consecutive patients with ischemic heart failure were enrolled for the study and randomized into two groups for levosimendan (n=37) or dobutamine (n=23) infusions. 67.2 % were male; mean age was 66.4 +/- 9.2 years for all patients. Baseline QRS durations in levosimendan and dobutamine groups were, 120.44 +/- 23.82 ms vs 116.59 +/- 13.80 ms respectively. Baseline ejection fractions were both depressed (23.15 +/- 8.3% vs 24.56 +/- 7.5%). RESULTS: In the levosimendan group, QRS duration shortened from baseline value to 116.47 +/- 24.56 msec (p=0.006), whereas dobutamine group showed no significant change (p=0.605). Both drugs caused an increase in ejection fraction, but only the levosimendan group showed significance (27.95 +/- 8.9% p=0.003 vs 26.67 +/- 7.6%, p=0.315). CONCLUSION: We suggest that the administration of levosimendan, not dobutamine, shortens QRS duration on the surface ECG, possibly by means of providing collective contraction in the left ventricle muscle fibers. The molecular basis of this effect remains to be clarified.

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