Overall, 803 subjects were enrolled: (A) 326 patients with liver biopsy-proven treatment naive CHC (175 with and 151 without steatosis); (B) 477 age and gender matched controls, including 292 healthy subjects without steatosis (B1) and 185 with NAFLD (B2). Carotid atherosclerosis (CA), assessed by high-resolution B-mode ultrasonography, was categorized as either intima-media thickness (IMT: >1 mm) or plaques (?.5 mm).
CHC patients had a higher prevalence of CA than controls (53.7 % vs 34.3 % ; p < 0.0001). Younger CHC (<50 years) had a higher prevalence of CA than controls (34.0 % vs 16.0 % ; p < 0.04). CHC patients without steatosis had a higher prevalence of CA than B1 controls (26.0 % vs 14.8 % ; p < 0.02). CHC with steatosis had a higher prevalence of CA than NAFLD patients (77.7 % vs 57.8 % , p < 0.0001). Viral load was associated with serum CRP and fibrinogen levels; steatosis with metabolic syndrome, HOMA-IR, hyperhomocysteinemia and liver fibrosis. Viral load and steatosis were independently associated with CA. Diabetes and metabolic syndrome were associated with plaques.
HCV infection is a risk factor for earlier and facilitated occurrence of CA via viral load and steatosis which modulate atherogenic factors such as inflammation and dysmetabolic milieu.