Abstract
Right-sided heart failure (RHF) occurs from impaired contractility of the right ventricle caused by pressure, volume overload, or intrinsic myocardial contractile dysfunction. The development of subclinical right ventricle (RV) dysfunction or overt RHF is a negative prognostic indicator. Recent attention has focused on RV-specific inflammatory growth factors and mediators of myocardial fibrosis to elucidate the mechanisms leading to RHF and potentially guide the development of novel therapeutics. This article focuses on the distinct changes in RV structure, mechanics, and function, as well as molecular and inflammatory mediators involved in the pathophysiology of acute and chronic RHF.
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