Left ventricular assist devices (LVAD) have been used to "bridge" patients with end-stage heart failure to transplantation. Although several reports have suggested that the native ventricular function recovers after long-term LVAD support, a process called "reverse remodeling", the underlying biological mechanisms are still unclear. Various molecular pathways of the human myocardium associated with apoptosis, response to stress, or matrix changes are known to be altered under conditions of heart failure, and some have been shown to be reversibly regulated during left ventricular mechanical support, suggesting that the descriptive term "reverse remodeling" is, at least in parts, a reversible mechanism. The reduction of volume and pressure overload with a decrease of ventricular wall stress leading to an improvement of myocardial blood supply under mechanical circulatory assistance, may be one explanation for the molecular myocardial changes and may reflect one possible cause for the phenomenon of "reverse remodeling".