Levosimendan--an inoprotective drug or much ado about nothing?

摘要

Levosimendan is a unique drug with a dual mechanism of action. First, it exerts positive inotropic effects by binding calcium dependent to troponin C during systole only. Levosimendan prolongs the cross-bridging time of actin-myosin filaments. It acts on troponin C only when intracellular calcium levels are high, i.e., during systole. During diastole, when intracellular calcium levels are low, it has no effect on troponin C. Thus it improves systolic and diastolic myocardial function. Unlike the catecholamines and the phosphodiesterase II inhibitors, levosimendan does not increase the level of intracardiomyocyte calcium (1). Positive inotropy with normal levels of intracellular calcium avoids the undesired side effects of increased intracellular calcium, like an increase in oxygen consumption (1) and the risk for fatal arrhythmia (1, 2).