In many cases, however, it is not possible to arrive at a specific etiologic diagnosis, and thus it is often more desirable to classify the cardiomyopathies into one of three types dilated, restrictive, hypertrophic on the basis of differences in their pathophysiology and clinical presentation (Braunwald, 2005, 13-78).
Current literature concerning the molecular mechanism of this disease and attendant cardiac failure will be searched to find out the gap in the current knowledge. Sebastini et al. in their 2009 article, discusses the molecular events linking mtDNA defects to cardiac hypertrophy as the cause of congestive heart failure. It has been suggested that the cellular and molecular mechanism of cardiac dysfunction is related to energy derangements and increase of mitochondrial derived reactive oxygen species. There is a continuous cardiomyopathic remodelling in the pathogenesis of congestive heart failure has been attributed to mitochondrial proliferation and the factor of mechanical dysfunction (Sebastini et al., 2009). Moorjani et al. (2006) investigated the phenomenon of activation of apoptotic Caspase cascade during the transition to pressure overload induced heart failure.