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.