Abstract
Background. Hepatitis C virus (HCV) infection can exert proatherogenic activities due to its direct action on vessel walls and/or via the chronic inflammatory process involving the liver. Aims. To clarify the role of HCV in atherosclerosis development in monoinfected HCV patients at different degrees of liver fibrosis and with no risk factors for coronary artery disease. Methods. Forty-five patients were included. Clinical, serological, and anthropometric parameters, liver fibrosis (transient liver elastometry (fibroscan) and aspartate aminotransferase to platelet ratio index (APRI)), carotid intima-media thickness (c-IMT), and brachial artery flow-mediated vasodilatation (FMD) were assessed. Patients were divided into 3 tertiles according to fibroscan values. Results. Patients in the third tertile (fibroscan value >11.5 KPa) showed FMD values were significantly lower than second and first tertiles (4.7 ± 1.7% versus 7.1 ± 2.8%, p = 0.03). FMD values were inversely related to liver elastomeric values. c-IMT values were normal. The risk for endothelial dysfunction development in the third tertile (p = 0.02) was 6.9 higher than the first tertile. A fibroscan value >11.5 KPa had a positive predictive power equal to 79% for endothelial dysfunction. Conclusions. HCV advanced liver fibrosis promotes atherosclerosis by inducing endothelial dysfunction independently of common cardiovascular risk factors.
Highlights
Despite significant advances in the treatment of coronary artery disease (CAD), this condition remains the leading cause of death worldwide [1]
Conflicting data are on the relationship between CAD and hepatitis C virus- (HCV-) related chronic hepatitis
No difference was observed according to sex, age, systolic blood pressure, waist circumference, total cholesterol, triglycerides, alanine aminotransferase (ALT), Hepatitis C virus (HCV)-RNA quantization, and prevalence of genotype 1
Summary
Despite significant advances in the treatment of coronary artery disease (CAD), this condition remains the leading cause of death worldwide [1]. A cross-sectional study and three casecontrol researches found an increased risk for atherosclerosis (assessed by means of carotid intima-media thickness (CIMT)) in HCV patients [9,10,11,12]. To clarify the role of HCV in atherosclerosis development in monoinfected HCV patients at different degrees of liver fibrosis and with no risk factors for coronary artery disease. Serological, and anthropometric parameters, liver fibrosis (transient liver elastometry (fibroscan) and aspartate aminotransferase to platelet ratio index (APRI)), carotid intima-media thickness (c-IMT), and brachial artery flow-mediated vasodilatation (FMD) were assessed. A fibroscan value >11.5 KPa had a positive predictive power equal to 79% for endothelial dysfunction. HCV advanced liver fibrosis promotes atherosclerosis by inducing endothelial dysfunction independently of common cardiovascular risk factors
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