Cardiac Biomedicine: Cardiac Hypertrophy and Failure Draft - Research Proposal Example

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). Review of Literature 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.

Sebastiani 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 remodeling 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.

It has been postulated that cardiomyocyte apoptosis has been implicated in the pathogenesis of heart failure, and this pathophysiological process has been conceived to be central in the causation of congestive heart failure (Moorjani et al., 2006). An exhaustive literature review of available literature on the molecular mechanism of cardiac failure will be done to update the current knowledge and identify the gap in research. Methodology The study will be done in an experimental design. A series of 50 patients with hypertrophic cardiomyopathy with and without congestive heart failure with increased left ventricular afterload and sizes measured by echocardiography will be subjected to serial left ventricular endomyocardial biopsy samples at each echocardiographically defined stages such as left ventricular hypertrophy, dilation, and failure.

Caspase 3, 8, and 9 activities will be measured by specific fluorogenic peptide substrates and immunohistochemistry and cardiomyocyte DNA fragmentation will be determined by immunohistochemical assays. Data Analysis The data will be analyzed in suitable statistical software. The correlation between the severity of the disease and Caspase activities will be determined to reach a conclusion about the molecular mechanism of congestive heart failure in hypertrophic cardiomyopathy.