Thrombotic risk in hepatitis C: Interplay between hepatic dysfunction, viral-driven inflammation, and cardiovascular consequences.

Abstract

Hepatitis C virus (HCV) infection, traditionally regarded as a hepatotropic disease, is increasingly recognized as a systemic condition with significant thrombotic implications. Chronic HCV induces a persistent proinflammatory and prothrombotic state that substantially elevates the risk of both venous and arterial events. Mechanistically, HCV drives endothelial dysfunction, enhances platelet activation, disrupts coagulation and fibrinolytic balance, and promotes immune-mediated vascular injury through cryoglobulinemia and chronic systemic inflammation. Clinical manifestations range from portal vein thrombosis and venous thromboembolism to coronary artery disease and ischemic stroke, highlighting the far-reaching consequences of virus-driven coagulopathy. Emerging evidence challenges the historical view of cirrhosis as a "naturally anticoagulated" state, instead describing a fragile hemostatic balance prone to both bleeding and thrombosis. Direct-acting antiviral therapy has transformed outcomes, not only achieving sustained virological response but also reversing systemic inflammation, improving endothelial function, and reducing thrombotic complications. However, patients with advanced fibrosis and comorbidities remain at elevated risk despite viral clearance, underscoring the need for ongoing surveillance. This minireview highlights the interplay between hepatic dysfunction, viral-induced inflammation, and cardiovascular sequelae in chronic HCV, emphasizing the importance of integrating thrombotic risk assessment into clinical care and research frameworks.