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Chronic hepatitis C infection: An independent risk factor for subclinical atheromatosis.
Revista Clínica Española 2019 Februrary 15
BACKGROUND: The association between subclinical atheromatosis and chronic hepatitis C virus (HCV) infection is unknown but is relevant now that antivirals are improving the survival of patients with the infection.
OBJECTIVES: To determine whether HCV is an independent risk factor for subclinical atheromatosis and to analyse the changes in lipid profiles according to viral RNA levels and hepatic fibrosis.
PATIENTS AND METHODS: We conducted an observational, cross-sectional study that included 102 HCV-positive patients and 102 HCV-negative patients with parity in terms of sex and age, with no history of cardiovascular or kidney disease or diabetes. Atheromatosis (the presence of atheromatous plaques) and the carotid intima-media thickness (CIMT) were assessed using ultrasonography of the carotid and femoral arteries.
RESULTS: There was a greater presence of atheromatosis in any vascular territory in HCV-positive patients than in the patients without infection (58.8% vs. 28.4%, p<.0001). In the multivariate analysis, the factors significantly associated with atheromatosis included HCV infection (OR, 14.37 [5.5-37.3]; p<.001), age (OR, 1.12 [1.1-1.2]; p<.001), male sex (OR, 4.32 [1.9-9.5]; p<.001) and the triglyceride/HDL cholesterol coefficient (TG/HDL-indirect indicator of insulin resistance) (OR, 1.34 [1.1-1.6]; p=.007). The HCV-positive patients with atheromatous plaques had a higher TG/HDL coefficient but no significant differences in terms of the viral load or degree of hepatic fibrosis and with a 'low risk' lipid profile.
CONCLUSIONS: HCV infection is an independent risk factor for subclinical atheromatosis. Systemic arterial ultrasonography for this population improves the cardiovascular risk assessment beyond lipid profile abnormalities and the risk calculation using SCORE tables.
OBJECTIVES: To determine whether HCV is an independent risk factor for subclinical atheromatosis and to analyse the changes in lipid profiles according to viral RNA levels and hepatic fibrosis.
PATIENTS AND METHODS: We conducted an observational, cross-sectional study that included 102 HCV-positive patients and 102 HCV-negative patients with parity in terms of sex and age, with no history of cardiovascular or kidney disease or diabetes. Atheromatosis (the presence of atheromatous plaques) and the carotid intima-media thickness (CIMT) were assessed using ultrasonography of the carotid and femoral arteries.
RESULTS: There was a greater presence of atheromatosis in any vascular territory in HCV-positive patients than in the patients without infection (58.8% vs. 28.4%, p<.0001). In the multivariate analysis, the factors significantly associated with atheromatosis included HCV infection (OR, 14.37 [5.5-37.3]; p<.001), age (OR, 1.12 [1.1-1.2]; p<.001), male sex (OR, 4.32 [1.9-9.5]; p<.001) and the triglyceride/HDL cholesterol coefficient (TG/HDL-indirect indicator of insulin resistance) (OR, 1.34 [1.1-1.6]; p=.007). The HCV-positive patients with atheromatous plaques had a higher TG/HDL coefficient but no significant differences in terms of the viral load or degree of hepatic fibrosis and with a 'low risk' lipid profile.
CONCLUSIONS: HCV infection is an independent risk factor for subclinical atheromatosis. Systemic arterial ultrasonography for this population improves the cardiovascular risk assessment beyond lipid profile abnormalities and the risk calculation using SCORE tables.
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