Heme oxygenase derived carbon monoxide and iron mediated plasmatic hypercoagulability in a patient with calcific mitral valve disease

Jess L Thompson, Vance G Nielsen, Allison R. Castro, Andrew Chen

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

We present a case of a patient with calcific mitral valve stenosis and plasmatic hypercoagulability. Using thrombelastography, the patient was determined to have an abnormally large velocity of plasma thrombus growth and strength with reduced vulnerability to lysis. Critically, increased carboxyhemoglobin concentration (2.4 %) was present, likely secondary to hemolysis from mitral stenosis and engagement of systemic heme oxygenase. It was determined that the patient’s plasmatic hypercoagulability was in part due to carboxyhemefibrinogen formation and iron-enhancement of coagulation via two thrombelastographic methods. In conclusion, future investigation of the involvement of both carbon monoxide and iron mediated hypercoagulability in the setting of stenotic valve disease is warranted.

Original languageEnglish (US)
Pages (from-to)532-535
Number of pages4
JournalJournal of Thrombosis and Thrombolysis
Volume39
Issue number4
DOIs
StatePublished - May 1 2015

Fingerprint

Heme Oxygenase (Decyclizing)
Thrombophilia
Carbon Monoxide
Mitral Valve
Iron
Mitral Valve Stenosis
Thrombelastography
Carboxyhemoglobin
Hemolysis
Thrombosis
Growth

Keywords

  • Carbon monoxide
  • Fibrinogen
  • Heme oxygenase
  • Iron
  • Mitral valve stenosis
  • Thrombelastography

ASJC Scopus subject areas

  • Hematology
  • Cardiology and Cardiovascular Medicine

Cite this

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AU - Thompson, Jess L

AU - Nielsen, Vance G

AU - Castro, Allison R.

AU - Chen, Andrew

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