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Monocyte tissue factor expression and ongoing complement generation in ventricular assist device patients

C R Wilhelm1, J Ristich, R L Kormos

  • 1Department of Surgery and Artificial Heart Program, University of Pittsburgh Medical Center, Pennsylvania 15213, USA.

The Annals of Thoracic Surgery
|May 16, 1998
PubMed
Summary
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Complement activation in ventricular assist device patients drives hemostatic issues. This study links complement system activation to leukocyte-platelet aggregates and thrombin generation.

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Hematology

Background:

  • Ventricular assist device (VAD) use is associated with hemostatic abnormalities and cellular aggregation.
  • Ongoing complement activation is a potential mediator of these VAD-related complications.

Purpose of the Study:

  • To investigate the role of complement activation in VAD patients.
  • To examine the relationship between complement activation and leukocyte-platelet aggregate formation and thrombin generation.

Main Methods:

  • Blood samples were collected from 30 patients pre- and post-VAD implantation.
  • Plasma levels of thrombin-antithrombin III complexes, C3a, and SC5b-9 were quantified.
  • Flow cytometry assessed monocyte tissue factor expression and monocyte-platelet/granulocyte-platelet conjugates.

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Main Results:

  • Complement markers (C3a, SC5b-9) were significantly elevated throughout the study period.
  • Monocyte tissue factor expression and thrombin-antithrombin III complexes peaked postoperatively.
  • Elevated granulocyte-platelet conjugates correlated with complement activation (SC5b-9).

Conclusions:

  • Complement activation plays a significant role in VAD patients.
  • Complement mediates the formation of leukocyte-platelet aggregates.
  • Complement may indirectly promote thrombin generation via monocyte tissue factor expression.