Key result
Advanced liver fibrosis (fibroscan >11.5 KPa) in HCV patients was associated with lower flow-mediated vasodilatation (4.7% vs 7.1%, p=0.03) and a 6.9-fold higher risk of endothelial dysfunction.
Cross-Sectional (n=45)
Absolute Event Rate: 4.7% vs 7.1%
p-value: p=0.03
Advanced liver fibrosis in chronic HCV infection is associated with endothelial dysfunction, suggesting a proatherogenic role independent of traditional cardiovascular risk factors.
Suggests heightened CV risk in HCV with advanced fibrosis; hypothesis-generating and requires prospective confirmation before practice implications.
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.
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Barone et al. (2015) conducted a cross-sectional in Chronic HCV infection (n=45). Advanced liver fibrosis (fibroscan >11.5 KPa) vs. Lower degrees of liver fibrosis (first and second tertiles) was evaluated on Brachial artery flow-mediated vasodilatation (FMD) (p=0.03). Advanced liver fibrosis (fibroscan >11.5 KPa) in HCV patients was associated with lower flow-mediated vasodilatation (4.7% vs 7.1%, p=0.03) and a 6.9-fold higher risk of endothelial dysfunction.
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