The cardiac resynchronization therapy (CRT) is a relatively new option for the treatment of heart failure patients with intraventricular conduction disturbances (i.e. QRS wider than 130 ms), especially with dyssynchronous heart failure (left bundle branch block). From pathophysiological point of view it restores simultaneous depolarization of heart ventricles and optimizes the heart function which provides clinical benefits. On molecular level, the CRT leads to the restoration of disturbances caused during dyssynchronous heart failure development and progression, related to electrophysiology (potassium and sodium currents, connexin-43 localization), structure (α-actinin organization, α-Myosin Heavy Chain protein expression), apoptosis, oxygen consumption and inflammation. One of the most important benefits of CRT is its ability to increase the efficiency of heart work without enhancement of oxygen consumption. In this review we aimed to summarize the principal alterations caused by the CRT on molecular level.