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Platelet glycoprotein IIb/IIIa inhibitor attenuates complement activation during in vitro ventricular assist

D L Serna1, J Huh, H Ha

  • 1Division of Cardiothoracic Surgery, University of California Irvine Medical Center, Orange 92868, USA.

ASAIO Journal (American Society for Artificial Internal Organs : 1992)
|November 6, 1998
PubMed

Insights

Protecting platelet glycoprotein IIb/IIIa receptors with an inhibitor reduces complement activation during ventricular assist device use. This finding suggests a method to improve blood compatibility in mechanical circulatory support systems.

Area of Science:

  • Biomedical Engineering
  • Hematology
  • Immunology

Background:

  • Ventricular assist devices (VADs) can cause complement activation and platelet dysfunction.
  • Platelets normally regulate complement via C1 serine protease inhibitor (C1 INH).
  • Platelet dysfunction during VAD circulation may lead to loss of complement regulation.

Purpose of the Study:

  • To evaluate if a platelet glycoprotein IIb/IIIa receptor inhibitor can reduce VAD-associated complement activation.
  • To investigate the role of platelet integrity in complement regulation during VAD support.

Main Methods:

  • In vitro simulation of eight centrifugal VAD circuits using human whole blood for 4 days.
  • Maintenance of physiological conditions (temperature, pH, blood gases, etc.).
  • Measurement of C1 INH and C3a levels with and without a glycoprotein IIb/IIIa inhibitor (MK-383).

Main Results:

  • Circulating C1 INH levels initially increased then decreased within 12 hours in VAD circuits.
  • Pre-treatment with MK-383 attenuated the decrease in unbound C1 INH.
  • C3a levels increased significantly (34-fold with inhibitor, 22-fold without) within 4 hours.

Conclusions:

  • Protection of the platelet GP IIb/IIIa complex appears to delay complement activation during in vitro VAD circulation.
  • Targeting platelet function may be a strategy to mitigate complement-mediated adverse effects of VADs.

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