Hepatitis C virus-associated cardiomyopathy: A review of pathogenesis

Inderjeet Singh Bharaj1, Gurkaranvir Singh2, Ajit Singh Brar3

  • 1Department of Internal Medicine, Abrazo Health Network, Glendale, AZ 85308, United States.

World Journal of Virology
|September 30, 2025
PubMed

Insights

Hepatitis C virus (HCV) causes cardiomyopathy through viral, immune, and metabolic pathways, often worsened by cirrhosis. Direct-acting antiviral (DAA) therapy improves heart health and reduces cardiovascular events in affected patients.

Area of Science:

  • Cardiology
  • Virology
  • Immunology

Background:

  • Hepatitis C virus (HCV) infection is associated with dilated and hypertrophic cardiomyopathy.
  • Pathogenesis involves complex viral, immune, and metabolic mechanisms, exacerbated by cirrhosis.
  • This increases cardiovascular morbidity in infected individuals.

Purpose of the Study:

  • To review the pathogenesis of cardiomyopathy in Hepatitis C virus (HCV) patients.
  • To investigate the clinical implications of HCV-associated cardiomyopathy.
  • To explore the impact of treatment on cardiovascular outcomes.

Main Methods:

  • A narrative literature review was conducted using PubMed, Scopus, and Google Scholar.
  • Searched for English-language studies published between 1990 and 2024.
  • Findings on the HCV-cardiomyopathy link, pathophysiology, and treatment were qualitatively synthesized.

Main Results:

  • HCV induces cardiomyopathy via direct viral toxicity, immune damage, genetic factors, and apoptosis.
  • Cirrhosis contributes through cirrhotic cardiomyopathy mechanisms, increasing cardiovascular events.
  • Direct-acting antivirals (DAAs) improve cardiovascular outcomes by reducing adverse events and enhancing cardiac function.

Conclusions:

  • HCV is a significant risk factor for cardiomyopathy, involving diverse pathways including cirrhosis.
  • DAA therapy demonstrates cardiovascular benefits for patients with HCV.
  • Further research is needed on mechanisms, biomarkers (M2BPGi, Ang-2), and global DAA access.
Abstract

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