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

Figure 1 Thrombotic risk development in hepatitis C virus infection. Viral inflammation is driven by elevated interleukin-6 and tumor necrosis factor-α, promoting immune activation. Endothelial dysfunction results from increased vascular endothelial growth factor and reduced nitric oxide bioavailability, favoring a procoagulant state. Mixed cryoglobulinemia contributes through immune complex deposition and vascular injury. Comorbidities, including diabetes, human immunodeficiency virus, and chronic kidney disease, further amplify risk. Host factors, such as genetic predisposition and baseline cardiovascular disease, modulate susceptibility. HCV: Hepatitis C virus; IL-6: Interleukin-6; TNF-α: Tumor necrosis factor-α; VEGF: Vascular endothelial growth factor; NO: Nitric oxide; HIV: Human immunodeficiency virus; CKD: Chronic kidney disease; CVD: Cardiovascular disease.

Figure 2 Biomarkers and risk stratification in hepatitis C virus-associated thrombosis. Candidate biomarkers - including interleukin-6, tumor necrosis factor-α, high-sensitivity C-reactive protein, D-dimer, von Willebrand factor, N-terminal pro-B-type natriuretic peptide, and factor VIII - may provide prognostic value for assessing cardiovascular and thrombotic risk in patients with chronic hepatitis C virus infection. HCV: Hepatitis C virus; IL-6: Interleukin-6; TNF-α: Tumor necrosis factor-α; hs-CRP: High-sensitivity C-reactive protein; NT-proBNP: N-terminal pro B-type natriuretic peptid.

Figure 3 Potential benefits of anticoagulation in hepatitis C virus cirrhosis. Anticoagulation in patients with hepatitis C virus-related cirrhosis may reduce portal vein thrombosis, limit hepatic decompensation, and improve survival. HCV: Hepatitis C virus; PVT: Portal vein thrombosis.