OP-107: REDUCTION IN SERUM URIC ACID LEVELS AFTER CARDIAC RESYNCHRONIZATION THERAPY CORRELATES WITH LEFT VENTRICULAR REVERSE REMODELING

Abstract

Objective: Levosimendan is a positive inotropic agent used for acute heart failure which exerts positive inotropic effect by increasing the calcium sensitivity of cardiac troponin C without increasing intracellular calcium concentrations. Levosimendan improves, left ventricular systolic and diastolic function as well as neurohormonal and inflammatory activation. Systolic dyssynchrony is an independent predictor of clinical outcome and poor survival in patients with heart failure. Diastolic dyssynchrony is at least as common as systolic dyssynchrony in systolic HF patients, and is often present without a concurrent systolic dyssynchrony in this population. In this study, we aimed to assess the effects of levosimendan infusion on indices of systolic and diastolic dyssynchrony. Methods: A total of 42 patients (mean age: 64.1±12.9, M/F: 32/10) that admitted to our clinic with acute heart failure were enrolled. Exclusion criteria were any acute or chronic infectious or inflammatory diseases, recent myocardial infarction ( 2.5mg/dl), use of anti-inflammatory agents, serious arrhythmias and supine systolic blood pressure <85mmHg. Levosimendan was administered as a 10-min intravenous bolus infusion at 6–12mg/kg, followed by a continuous 24-h infusion at 0.1mg/kg/min. The infusion was maintained at a constant rate for 24 h unless the patient had a major cardiovascular event or had a serious adverse reaction. Echocardiographic examinations were conducted before the drug administration and at the end of the 24 h infusion period. Systolic and diastolic dyssynchrony were defined as maximal time delay in peak systolic and early diastolic velocities of 4 basal LV segments with the color-coded tissue Doppler imaging. Results: Before and after the levosimendan infusion, there was no difference regarding with dosage of furosemide (mean dosage: 133.5±38.1mg vs 138.1±41.0mg, p = 0.257) and use of Angiotensin Converting Enzyme inhibitors (ACEi) (33% vs. 34), Angiotensin receptor blockers (ARBs) (50% vs. 48%) and beta blockers (78%vs 74), respectively. After the levosimendan infusion systolic (69.2±23.4ms vs. 58.9±20.1ms, p = 0.02) and diastolic (68.5±22.0ms vs. 57.0±20.2ms; p =0.01) maximal time delays were decreased significantly. Conclusions: Levosimendan decreases systolic and diastolic dyssynchrony in patients with acute heart failure. Favorable electromechanical effects of levosimendan therapy might be another mechanism of short term clinical improvement.