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Link between plasminogen activator inhibitor-1 and cardiovascular risk in chronic hepatitis C after viral clearance

Ming-Ling Chang1,2, Yu-Sheng Lin3,4, Li-Heng Pao5,6

  • 1Liver Research Center, Division of Hepatology, Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Taoyuan, Taiwan.

Scientific Reports
|February 18, 2017
PubMed

Insights

Hepatitis C virus (HCV) therapy increases plasminogen activator inhibitor-1 (PAI-1) levels and cardiovascular risk in patients with sustained virological response (SVR). Platelet count and specific genetic factors influence PAI-1 levels during and after treatment.

Area of Science:

  • Hepatology
  • Cardiovascular Medicine
  • Genetics

Background:

  • The role of plasminogen activator inhibitor-1 (PAI-1) in Hepatitis C Virus (HCV) infection pathophysiology is not well understood.
  • PAI-1 is a key regulator of fibrinolysis and has been implicated in cardiovascular disease.

Purpose of the Study:

  • To investigate the association between PAI-1 levels, HCV infection, anti-HCV therapy, and cardiovascular events.
  • To explore the influence of genetic polymorphisms (PAI-1-rs1799889 and interferon-λ3-rs12979860) on PAI-1 levels.

Main Methods:

  • Prospective evaluation of 669 HCV patients, with detailed measurements before, during, and after anti-HCV therapy for 536 patients.
  • Multivariate analysis and Generalized Estimating Equations (GEE) were used to analyze PAI-1 levels, platelet counts, and genetic factors.
  • Cardiovascular events were monitored within 24 weeks post-therapy.

Main Results:

  • Before therapy, platelet count and PAI-1-rs1799889 genotype correlated with PAI-1 levels.
  • In patients achieving sustained virological response (SVR), platelet count remained associated with PAI-1 levels post-therapy.
  • PAI-1-rs1799889 and interferon-λ3-rs12979860 genotypes influenced PAI-1 levels longitudinally.
  • SVR patients showed increased PAI-1 levels, lipids, homocysteine, and PAI-1 activity post-therapy, correlating with accelerated cardiovascular risk.

Conclusions:

  • Platelet count consistently correlates with PAI-1 levels in HCV patients.
  • Specific genetic polymorphisms significantly impact PAI-1 levels over the course of HCV therapy.
  • SVR patients exhibit elevated PAI-1 levels and increased cardiovascular risk post-treatment, particularly vulnerable individuals.

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