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The effect of curing hepatitis C with direct-acting antiviral treatment on endothelial function

Joshua S Davis1,2,3, Melissa Young1, Sandra Lennox1

  • 1Division of Medicine, John Hunter Hospital, Newcastle, NSW, Australia.

Antiviral Therapy
|July 27, 2018
PubMed

Insights

Antiviral treatment for chronic hepatitis C (CHC) improved endothelial function markers, suggesting CHC contributes to cardiovascular risk. However, microvascular reactivity did not change significantly, indicating complex effects on vascular health.

Area of Science:

  • Cardiovascular Health
  • Hepatology
  • Vascular Biology

Background:

  • Chronic hepatitis C (CHC) is linked to increased cardiovascular risk.
  • The association between CHC and endothelial dysfunction remains unclear.
  • This study investigates the impact of antiviral therapy on endothelial function in non-cirrhotic CHC patients.

Purpose of the Study:

  • To assess the effect of antiviral treatment on endothelial function in adults with non-cirrhotic chronic hepatitis C.
  • To determine if viral clearance improves vascular health markers.

Main Methods:

  • A self-controlled, before-and-after study design was employed.
  • 16 non-cirrhotic CHC patients received 12 weeks of paritaprevir/ritonavir, ombitasvir, and dasabuvir (PrOD), with ribavirin for genotype-1a.
  • Endothelial function was measured using reactive hyperaemia peripheral arterial tonometry (RHPAT) and serum angiopoietin-2 (Ang-2) and E-selectin levels before, during, and after treatment.

Main Results:

  • All 16 patients achieved sustained virological response.
  • No significant change was observed in RHPAT index during treatment.
  • Significant improvements were noted in serum Ang-2 and E-selectin levels post-treatment (P<0.001 for both).

Conclusions:

  • Eliminating hepatitis C virus (HCV) viraemia significantly improves endothelial function markers (serum Ang-2, E-selectin).
  • Bedside microvascular reactivity (RHPAT) did not show significant changes.
  • Chronic HCV infection may be associated with endothelial cell dysfunction, contributing to long-term cardiovascular risk.
Abstract

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