4.6 Article

Contact pathway in surgical and transcatheter aortic valve replacement

Journal

FRONTIERS IN CARDIOVASCULAR MEDICINE
Volume 9, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fcvm.2022.887664

Keywords

contact pathway; aortic valve replacement; thrombosis; factor XI; factor XII; kallikrein

Funding

  1. Sociedad Espanola de Cardiologia: Proyecto FEC Investigacion Clinica
  2. CIBERCV [CB16/11/00385]
  3. Fundacion Seneca [19873/GERM/15]
  4. CIBERER [ACCI18-04, ER19P5AC765/2019]
  5. Instituto de Salud Carlos III [PI21/00137]
  6. Sociedad Espanola de Trombosis y Hemostasia (SETH: grupos emergentes)
  7. University of Murcia, Spain

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In this study, the factors involved in the contact pathway during aortic valve replacement were analyzed, and their impact on the development of thromboembolic complications was assessed. The results showed that TAVR or SAVR did not significantly activate the contact pathway. However, there was a significant reduction in FXI levels during the SAVR procedure, which was associated with a lower incidence of thrombotic events.
BackgroundAortic valve replacement is the gold standard treatment for severe symptomatic aortic stenosis, but thrombosis of bioprosthetic valves (PVT) remains a concern. ObjectiveTo analyze the factors involved in the contact pathway during aortic valve replacement and to assess their impact on the development of thromboembolic complications. MethodsThe study was conducted in 232 consecutive patients who underwent: transcatheter aortic valve replacement (TAVR, N = 155), and surgical valve replacement (SAVR, N = 77) (MUVITAVI project). Demographic and clinical data, outcomes including a combined end point (CEP) of thrombotic events, and imaging controls were recruited. Samples were collected 24 h before and 48 h after valve replacement. FXII, FXI and (pre)kallikrein were evaluated by Western Blot and specific ELISA with nanobodies. ResultsThe CEP of thrombotic events was reached by 19 patients: 13 patients presented systemic embolic events and 6 patients subclinical PVT. Valve replacement did not cause FXII activation or generation of kallikrein. There was a significant reduction of FXI levels associated with the procedure, which was statistically more pronounced in SAVR than in TAVR. Cases with reductions of FXI below 80% of basal values had a lower incidence of embolic events during the procedure than patients in whom FXI increased above 150%: 2.7 vs. 16.7%; p: 0.04. ConclusionTAVR or SAVR did not significantly activate the contact pathway. A significant reduction of FXI, was observed, particularly in SAVR, associated with lower incidence of thrombotic events. These results encourage evaluating the usefulness and safety of FXI-directed antithrombotic treatments in these patients.

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