Endothelial dysfunction correlates with liver fibrosis in chronic HCV infection
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 ( versus , ). FMD values were inversely related to liver elastomeric values. c-IMT values were normal. The risk for endothelial dysfunction development in the third tertile () 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.
Autore Pugliese
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DI LEO A.;AMORUSO A.;ZITO A.;DEVITO F.;CORTESE F.;CICCONE M.M.;VIGGIANI M.T.;GESUALDO M.;BARONE M.;BRUNETTI N.D.;SCICCHITANO P.;SCHIRALDI S.
Titolo volume/Rivista
Non Disponibile
Anno di pubblicazione
2015
ISSN
1687-6121
ISBN
Non Disponibile
Numero di citazioni Wos
Nessuna citazione
Ultimo Aggiornamento Citazioni
Non Disponibile
Numero di citazioni Scopus
12
Ultimo Aggiornamento Citazioni
Non Disponibile
Settori ERC
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Codici ASJC
Non Disponibile
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