Congestive heart failure (CHF) is a complicated pathophysiological syndrome, leading cause of hospitalization as well as mortalities in developed countries wherein an irregular function of the heart leads to the insufficient blood supply to the body organs. It is an accumulative slackening of various complications including myocardial infarction (MI), coronary heart disease (CAD), hypertension, valvular heart disease (VHD) and cardiomyopathy; its hallmarks include hypertrophy, increased interstitial fibrosis and loss of myocytes. The etiology of CHF is very complex and despite the rapid advancement in pharmacological and device-based interventional therapies still, a single therapy may not be sufficient to meet the demand for coping with the diseases. Total artificial hearts (TAH) and ventricular assist devices (VADs) have been widely used clinically to assist patients with severe HF. Unfortunately, direct contact between the patient’s blood and device leads to thromboembolic events, and then coagulatory factors, as well as, infection contribute significantly to complicate the situation. There is no effective treatment of HF except cardiac transplantation, however, genetic variations, tissue mismatch; differences in certain immune response and socioeconomic crisis are an important concern with cardiac transplantation suggesting an alternate bridge to transplant (BTT) or destination therapies (DT). For these reasons, researchers have turned to mechanically driven compression devices, ventricular restraint devices (VRD) and heart patches. The ASD is a combination of all operational patches and cardiac support devices (CSD) by delivering biological agents and can restrain or compress the heart. Present study summarizes the accessible peer-reviewed literature focusing on the mechanism of Direct Cardiac Compression (DCC) devices, VRD and patches and their acquaintance to optimize the therapeutic efficacy in a synergistic way.