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Endothelial dysfunction correlates with liver fibrosis in chronic HCV infection

Michele Barone1, Maria Teresa Viggiani2, Annabianca Amoruso1

  • 1Gastroenterology Unit, Department of Medical and Surgical Science, University of Foggia, OO. RR. Foggia, Viale Pinto 1, 71122 Foggia, Italy.

Gastroenterology Research and Practice
|May 23, 2015
PubMed

Insights

Hepatitis C virus (HCV) infection with advanced liver fibrosis promotes atherosclerosis by causing endothelial dysfunction. This occurs independently of traditional cardiovascular risk factors, highlighting a key link between liver health and heart disease.

Area of Science:

  • Cardiovascular Disease
  • Hepatology
  • Virology

Background:

  • Hepatitis C virus (HCV) infection is linked to proatherogenic activities.
  • HCV may directly affect vessel walls or induce chronic inflammation.
  • The role of HCV in atherosclerosis, particularly in relation to liver fibrosis, requires further clarification.

Purpose of the Study:

  • To investigate the role of HCV in atherosclerosis development.
  • To assess HCV's impact in patients with varying degrees of liver fibrosis and no traditional cardiovascular risk factors.

Main Methods:

  • Forty-five patients with HCV infection were evaluated.
  • Assessed parameters included liver fibrosis (FibroScan, APRI), carotid intima-media thickness (c-IMT), and brachial artery flow-mediated vasodilatation (FMD).
  • Patients were stratified into three groups based on FibroScan values.

Main Results:

  • Patients with advanced fibrosis (FibroScan >11.5 KPa) exhibited significantly lower FMD values compared to those with less fibrosis.
  • FMD values showed an inverse correlation with liver elastomeric values.
  • A FibroScan value >11.5 KPa predicted endothelial dysfunction with 79% accuracy.

Conclusions:

  • Advanced liver fibrosis in Hepatitis C virus infection promotes atherosclerosis.
  • Endothelial dysfunction is a key mechanism, independent of common cardiovascular risk factors.
  • HCV-induced liver fibrosis is a significant contributor to cardiovascular risk.

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