doiSerbia

Levosimendan treatment of severe acute congestive heart failure refractory to dobutamine/milrinone in children

Prijić Sergej (Institut za zdravstvenu zaštitu majke i deteta Srbije „Dr Vukan Čupić“, Odeljenje za kardiologiju i kardiohirurgiju, Beograd)
Rakić Sanja (Institut za zdravstvenu zaštitu majke i deteta Srbije „Dr Vukan Čupić“, Odeljenje za kardiologiju i kardiohirurgiju, Beograd)
Nikolić Ljubica (Institut za zdravstvenu zaštitu majke i deteta Srbije „Dr Vukan Čupić“, Odeljenje za kardiologiju i kardiohirurgiju, Beograd)
Jovičić Bosiljka (Institut za zdravstvenu zaštitu majke i deteta Srbije „Dr Vukan Čupić“, Odeljenje za kardiologiju i kardiohirurgiju, Beograd)
Stajević Mila (Institut za zdravstvenu zaštitu majke i deteta Srbije „Dr Vukan Čupić“, Odeljenje za kardiologiju i kardiohirurgiju, Beograd)
Vukomanović Vladislav (Institut za zdravstvenu zaštitu majke i deteta Srbije „Dr Vukan Čupić“, Odeljenje za kardiologiju i kardiohirurgiju, Beograd)
Košutić Jovan (Institut za zdravstvenu zaštitu majke i deteta Srbije „Dr Vukan Čupić“, Odeljenje za kardiologiju i kardiohirurgiju, Beograd)

Introduction. Levosimendan is a novel positive inotropic agent which, improves myocardial contractility through its calcium-sensitizing action, without causing an increase in myocardial oxygen demand. Also, by opening ATP-sensitive potassium channels, it causes vasodilatation with the reduction in both afterload and preload. Because of the long halflife, its effects last for up 7 to 9 days after 24-hour infusion. Case report. We presented three patients 2, 15 and 17 years old. All the patients had severe acute deterioration of the previously diagnosed chronic heart failure (dilatative cardiomyopathy; univentricular heart with bidirectional Glenn anastomosis and restrictive bulboventricular foramen; bacterial endocarditis on artificial aortic valve with severe stenosis and regurgitation). Signs and symptoms of severe heart failure, cardiomegaly (cardio-thoracic index 0.65) and left ventricular dilatation (end-diastolic diameter z-score 2.6; 4.1 and 4.0) were confirmed on admission. Also, myocardial contractility was poor with ejection fraction (EF - 27%, 25%, 35%), fractional shortening (FS - 13%, 11%, 15%) and stroke volume (SV - 40, 60, 72 mL/m2). The treatment with standard intravenous inotropic agents resulted in no improvement but in clinical deterioration. Thus, standard intravenous inotropic support was stopped and levosimendan treatment was introduced. All the patients received a continuous 24-h infusion 0.1 μg/kg/min of levosimendan. In a single patient an initial loading dose of 11 μg/kg over 10 min was administrated, too. Levosimendan treatment resulted in both clinical and echocardiography improvement with the improved EF (42%, 34%, 44%), FS (21%, 16%, 22%) and SV (59, 82, 93 mL/m2). Hemodynamic improvement was registered too, with the reduction in heart rate in all the treated patients from 134-138 bpm before, to less than 120 bpm after the treatment. These parameters were followed by the normalization of lactate levels. Nevertheless, left ventricular end-diastolic diameter did not change after the levosimendan treatment. Conclusion. Our initial experience demonstrates that administration of levosimendan in patients with severe chronic heart failure not responsive to standard intravenous inotropic treatment might result in a significant clinical and hemodynamic improvement and that, in selected patients, it might be life saving. According to our best knowledge patients presented are the first pediatric patients treated with levosimendan in our country.

Keywords: phosphodiesterase inhibitors, hart failure, child, hemodynamics, treatment outcome