Hepatitis C virus-associated cardiomyopathy: A review of pathogenesis

Abstract

BACKGROUND

Hepatitis C virus (HCV) affects millions of individuals globally and is linked to dilated cardiomyopathy and hypertrophic cardiomyopathy via complex direct viral, immune, and metabolic mechanisms, often exacerbated by cirrhosis, increasing cardiovascular morbidity.

AIM

To review the pathogenesis of cardiomyopathy in patients infected with HCV and investigate its clinical implications.

METHODS

A narrative literature review (PubMed, Scopus, Google Scholar; 1990–2024) focused on English-language studies examining the HCV–cardiomyopathy link, pathophysiology, and treatment. The findings were qualitatively synthesized.

RESULTS

HCV drives cardiomyopathy through direct viral toxicity, immune damage, genetic factors, and apoptosis. The associated cirrhosis contributes via cirrhotic cardiomyopathy mechanisms. Clinically, HCV increases cardiovascular events. Direct-acting antivirals (DAAs) generally improve cardiovascular outcomes by reducing adverse events and enhancing cardiac function.

CONCLUSION

HCV is a significant cardiomyopathy risk factor involving diverse pathways, including cirrhosis. DAA therapy offers cardiovascular benefits. Further research on the underlying mechanisms, biomarkers (e.g., M2BPGi, Ang-2), and global DAA access is warranted.

Keywords: Hepatitis C virus; Cardiomyopathy; Direct-acting antivirals; Cirrhosis; Cardiotropic

Core Tip: Chronic hepatitis C virus (HCV) infection is emerging as a significant contributor to cardiomyopathy, including dilated, hypertrophic, and arrhythmogenic subtypes. This review synthesizes evidence outlining complex pathogenic mechanisms: Direct viral toxicity via HCV core protein-mediated cytokine release (e.g., tumor necrosis factor alpha), immune-mediated damage, genetic predispositions, apoptotic pathways, and cirrhotic cardiomyopathy from HCV-induced liver disease. Notably, direct-acting antiviral (DAA) therapies not only achieve high cure rates but also improve cardiac function, although potential cardiotoxic effects require vigilance. The study underscores the need for further research into mechanistic insights, biomarker validation, and expansion of global DAA access to mitigate cardiovascular risks and improve patient outcomes.