Hepatitis C virus and cardiovascular disease: Current knowledge and unmet needs

The relationship between hepatitis C virus (HCV) infection and cardiovascular disease (CVD) is increasingly recognized, with studies indicating elevated CVD prevalence and mortality among individuals with HCV. Chronic HCV patients exhibit a higher CVD risk, especially in the population of end-stage renal disease on hemodialysis. Pathogenic mechanisms may include oxidative stress, endothelial damage, metabolic dysregulation, and chronic inflammation. These factors enhance vascular damage, promoting plaque formation and instability. Direct-acting antivirals (DAAs), which have revolutionized HCV treatment by achieving sustained virologic response rates of over 95%, significantly mitigate CVD risk. DAA therapy improves endothelial function, reduces inflammatory biomarkers, and lowers the incidence of CVD events. However, lipid profiles may paradoxically increase following HCV clearance. In addition, the contrasting outcomes between DAA treatment and arrhythmia risk remain elusive. Potential epigenetic changes for CVD risk may persist after successful viral eradication. The elucidation of unmet needs is critical for solidifying screening guidelines for HCV patients with CVD and for exploration of the long-term CVD outcome in the DAA era.