| Abstract [eng] |
Despite intensive search for new therapeutic interventions, dilated cardiomyopathy (DCM) remains the major cause of heart failure in the patients of relatively young age who eventually require heart transplantation, however many patients parish before a donor heart becomes available. The common proof of presence of the virus in the DCM myocardium is polymerase chain reaction analysis, whereas the inflammatory infiltrates in endomyocardial biopsy (EMB) supports the inflammatory origin of the disease. However, the data about the molecular mechanisms playing a key role in the pathogenesis of development of various origins of DCM are still missing. Therefore, the main goal of this study was to investigate in more details the molecular mechanisms in virus-positive and inflammatory-positive myocardiums by application of molecular-biological, histological and immunohistochemical techniques. As progression of heart failure is closely linked to fibrosis, the development of tool to quantify the cardiac fibrosis and to evaluate the immunohistochemical stainings of the EMB was an integral part of this study. The most important findings of this study showed that both types of investigated chronic DCM have different dominant molecular mechanism suggesting more options for further DCM treatment. Conventional therapeutic agents for chronic DCM and heart failure can be combined with others such as collagen I metabolism regulating (in case of chronic viral DCM) and anti-apoptotics (in case of idiopathic chronic inflammatory DCM). The application of digital Genie method for the quantification of fibrosis can be more accurate and substitute the hard work of the pathologist. |
