Cellular and biomolecular mechanisms in dilated cardiomyopathy

Abstract

Dilated cardiomyopathy (DCM) is a primary myocardial disease, characterized by unior biventricular dilation associated with a generally progressive contractile dysfunction . It is predominantly diagnosed in the advanced stage, in which it manifests itself by cardiomegaly and heart failure, causing significant morbidity and mortality . Less frequently, it is identified in the initial stage, in which the congestive signals are absent but ventricular dilation and dysfunction in a mild or moderate degree are evident . At first, DCM was considered a disease of obscure etiology. Several decades after being identified as an entity, its complex pathogenesis has gradually become better understood. Systematic studies generated in immunology, genetics, and cellular and molecular biology have contributed to the understanding of the disease mechanism. However, the heterogeneous character of DCM, coupled with the multiplicity of pathologic processes involved, has made this task difficult. DCM is currently understood as a multifactorial disease, in which viral infections, immunologic mechanisms and genetic factors, acting individually or together, result in a definitive myocardial lesion (fig. 1).