A Six-Year Experience with the Omnicarbon Valve in North American Patients

Carrier, Julie; Teijeira, J; Greentree, David; Gagnon, Sylvie; Brochu, Marie-Claude; Paulin, Chantal; Lepage, Serge; Côté, Michel

doi:10.1111/j.0886-0440.2004.04086.x

Cited by 2 publications

(2 citation statements)

References 15 publications

(24 reference statements)

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“…PHVs produce varying amounts of RBC lysis as measured by increased circulating LDH activity that can vary between an average of 225 to greater than 600 U/L . Similarly, LVADs and TAHs increase circulating LDH activity, varying between as little as 205 U/L to >4500 U/L .…”

Section: Phvs Lvads and Tahs Cause Hemolysis And Engage The Hemeoxymentioning

confidence: 99%

“…In addition to suffering the consequences of either insufficient (thrombosis) or excessive (bleeding) anticoagulant therapy, patients with circulatory devices experience red blood cell (RBC) lysis secondary to the shear forces of blood flow across device surfaces/impellers . Such lysis is measured a number of ways, but increased circulating lactate dehydrogenase (LDH) activity released from RBCs is a commonly used marker of hemolysis in these settings . In sum, patients with circulatory devices suffer a device‐dependent incidence of thromboembolism and increased release of heme into the systemic circulation during device‐induced hemolysis despite anticoagulation .…”

mentioning

confidence: 99%

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Increased Carbon Monoxide Production by Hemeoxygenase‐1 Caused by Device‐Mediated Hemolysis: Thrombotic Phantom Menace?

2013

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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.

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Section: Phvs Lvads and Tahs Cause Hemolysis And Engage The Hemeoxymentioning

confidence: 99%

mentioning

confidence: 99%