Genetic polymorphisms and oxidative stress in heart failure.

Abstract

Heart failure results from various known cardiovascular diseases, such as coronary artery disease, or can be the result of an idiopathic dilated cardiomyopathy. It is of utmost importance for diagnostic, preventive, and therapeutic purposes to understand the cellular events that trigger the cascade of functional and structural changes that result in the development and progression of heart failure. Progress in unraveling the genetic background in both ischemic and nonischemic cardiomyopathies has been slow compared with that for monogenic diseases, such as some forms of hypertrophic cardiomyopathy or familial dilated cardiomyopathies. It is likely that susceptibility to and risk of progression of heart failure are both influenced by many genes acting in concert or independently. Among the diverse subcellular mechanisms implicated in the pathogenesis and progression of heart failure, reactive oxygen species play a major role. The search for genetic polymorphisms in clinical association studies in order to identify genotypes susceptible to develop and affect the progression to heart failure has been the focus of many investigations over the past several years. In this review, the authors summarize the current data in support of the role of various polymorphisms of genes related to oxidative stress in the susceptibility to develop heart failure, and its progression.