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Accelerated activation of the coagulation pathway during cardiopulmonary bypass in aortic replacement surgery: a prospective observational study

BACKGROUND: Any form of surgery or tissue damage causes release of tissue factor into the circulation. This may lead to the accelerated consumption of coagulation factors, resulting in severe consumptive coagulopathy. In this study, we compared the molecular markers involved in coagulation activatio...

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Detalles Bibliográficos
Autores principales: Sato, Hideo, Yamamoto, Koji, Kakinuma, Akihito, Nakata, Yoshinori, Sawamura, Shigehito
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4477500/
https://www.ncbi.nlm.nih.gov/pubmed/26099510
http://dx.doi.org/10.1186/s13019-015-0295-9
Descripción
Sumario:BACKGROUND: Any form of surgery or tissue damage causes release of tissue factor into the circulation. This may lead to the accelerated consumption of coagulation factors, resulting in severe consumptive coagulopathy. In this study, we compared the molecular markers involved in coagulation activation during cardiopulmonary bypass (CPB) between patients who underwent aortic replacement surgery and those who underwent valve surgery. METHODS: This prospective observational study was performed in each 14 patients who underwent aortic replacement surgery or valve surgery. We evaluated the differences in the levels of fibrinogen, activated factor VII (FVIIa), thrombin–antithrombin complex (TAT), and soluble fibrin monomer complex (SFMC) during surgery between these two groups. RESULTS: The change in fibrinogen levels showed no difference between the groups. The magnitude of increase in TAT was much larger in patients who underwent aortic replacement surgery than in those who underwent valve surgery (173.6 vs. 49.4 ng/mL; p = 0.0001). More importantly, the elevation of FVIIa was significantly higher in patients who underwent aortic replacement (28.5 vs. 19.0 mU/mL; p = 0.0122). The magnitude of increase in SFMC was also larger in the aortic replacement surgery. CONCLUSIONS: The activation of coagulation during CPB was dramatically higher in the aortic replacement surgery compared with the valve surgery, probably owing to the activation of the extrinsic coagulation pathway in the former. This could potentially exacerbate consumptive coagulopathy after CPB termination in patients who underwent aortic replacement, possibly resulting in massive hemorrhage due to impaired hemostasis.