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Prevalent platelet dysfunction in patients with aortic valve disease

Wolfgang Prohaska1, Armin Zittermann, Jan U Lüth

  • 1Institute for Laboratory and Transfusion Medicine, Heart and Diabetes Center North Rhine Westfalia, University Hospital of the Ruhr, University Bochum, Bad Oeynhausen, Germany. wprohaska@hdz-nrw.de

The Journal of Heart Valve Disease
|November 5, 2008
PubMed

Insights

Patients undergoing aortic valve replacement (AVR) show significantly higher platelet dysfunction compared to coronary artery bypass graft (CABG) candidates. This dysfunction may contribute to microvascular issues in AVR patients.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Biomedical Engineering

Background:

  • Heart valve disease, particularly aortic valve disease, leads to rough, calcified valve leaflets.
  • This surface irregularity disrupts normal blood flow and is suspected to activate the hemostasis system.
  • The precise mechanisms underlying this activation remain incompletely understood.

Purpose of the Study:

  • To investigate platelet function in patients with heart valve disease undergoing aortic valve replacement (AVR).
  • To compare platelet function in AVR candidates with patients undergoing coronary artery bypass graft (CABG) surgery.
  • To explore the potential role of platelet dysfunction in the pathogenesis of microvascular complications in AVR.

Main Methods:

  • Platelet function was assessed preoperatively in 660 CABG and 421 AVR candidates using the platelet function analyzer (PFA-100).
  • PFA results were reported as closure time.
  • Subgroups of 40 AVR and 50 CABG patients also had von Willebrand factor antigen and collagen-binding activity measured.

Main Results:

  • Platelet dysfunction was significantly more prevalent in AVR candidates (83%) compared to CABG candidates (22%).
  • Mean PFA closure time was markedly higher in AVR patients (231 ± 59 s) than in CABG patients (153 ± 60 s; p < 0.01).
  • No significant differences were observed in mean platelet volume, platelet distribution width, or von Willebrand factor levels between the groups.

Conclusions:

  • Disturbed blood flow and shear stress in aortic valve disease likely lead to platelet activation, degranulation, and microparticle shedding.
  • These altered platelet characteristics may contribute to microvascular dysfunction and thrombotic events in patients with aortic valve disease.
  • Platelet dysfunction is a key finding in AVR patients, suggesting a potential mechanism for associated complications.
Abstract

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