Chronic hepatitis C and the risk for atherosclerotic and cardiomyopathic heart disease

Abstract

Hepatitis C virus (HCV) infection has been increasingly associated with cardiovascular complications, particularly atherosclerosis and cardiomyopathy, in addition to its primary hepatic effects. Studies indicate a higher prevalence of carotid atherosclerosis in patients with chronic hepatitis C infection, with viral load and steatosis emerging as independent risk factors. HCV-related atherosclerosis appears to develop through complex processes involving endothelial dysfunction, inflammation, oxidative stress, and immune dysregulation. Key cytokines, including tumor necrosis factor-alpha and interleukin-6, increase inflammatory responses, while oxidative stress markers, such as malondialdehyde, are associated with an increased risk of atherogenesis. In addition, HCV infection has been linked to cardiomyopathy. Direct viral effects, including HCV replication within cardiomyocytes and cytotoxicity induced by viral proteins, lead to myocardial injury and functional decline. Indirectly, HCV triggers immune-mediated damage, with heightened pro-inflammatory cytokines exacerbating cardiomyocyte apoptosis and fibrosis. Furthermore, HCV infection promotes a procoagulant imbalance, as evidenced by elevated factor VIII levels and thrombin potential, contributing to the increased cardiovascular risk. While substantial evidence indicates a relationship between HCV and cardiovascular disease, further research is needed to establish causality and guide therapeutic interventions.

Keywords: Cardiomyopathy; Cardiovascular disease; Carotid atherosclerosis; Chronic hepatitis C; Hepatitis C virus; Immune dysregulation; Myocarditis.

Figure 1

Overview of the pathogenesis of chronic hepatitis C and how it contributes to atherosclerosis and cardiomyopathy. HCV: Hepatitis C virus; TNF-α: Tumor necrosis factor-alpha; IL: Interleukin-6.