Increased carbon monoxide production by hemeoxygenase-1 caused by device-mediated hemolysis: Thrombotic phantom menace?

Vance G. Nielsen, Ellen C. Pearson, M. Cristina Smith

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Replacement of key components of the circulatory system with artificial devices has become the mainstay of therapy for conditions such as end-stage valvular disease or congestive heart failure. Unfortunately, device thrombosis and thromboembolic morbidity persist despite optimized anticoagulation. This work reviews the commonly known causes of device-associated thrombophilia, introduces recent literature concerning the effect of carbon monoxide on coagulation, and presents new patient data linking endogenously produced carbon monoxide with device-associated thrombosis. A new paradigm involving the interaction of red blood cell lysis-induced upregulation of hemoxygenase-1, increased endogenous carbon monoxide, hyperfibrinogenemia, and contact protein/microparticle-induced thrombin generation is presented.

Original languageEnglish (US)
Pages (from-to)1008-1014
Number of pages7
JournalArtificial Organs
Volume37
Issue number11
DOIs
StatePublished - Nov 2013

Keywords

  • Carbon monoxide
  • Hemeoxygenase-1
  • Hemolysis
  • Prosthetic heart valve
  • Thromboembolism
  • Total artificial heart
  • Ventricular assist device

ASJC Scopus subject areas

  • Bioengineering
  • Medicine (miscellaneous)
  • Biomaterials
  • Biomedical Engineering

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