Why the study?
Thrombus formation commonly complicates LVAD therapy despite anticoagulation with VKA and a platelet inhibitor.
Does left ventricular assist device (LVAD) implantation alter plasma markers of hemostasis and contact activation in adults with end-stage heart failure?
Does left ventricular assist device (LVAD) implantation alter plasma markers of hemostasis and contact activation in adults with end-stage heart failure?
LVAD implantation is associated with continuous low-grade systemic platelet and contact activation despite antithrombotic therapy, potentially explaining the high risk of LVAD-induced thrombosis.
Thrombus formation is a common complication during left ventricular assist device (LVAD) therapy, despite anticoagulation with vitamin K antagonists (VKA) and a platelet inhibitor. Plasma levels of markers for primary and secondary hemostasis and contact activation were determined before LVAD implantation and 6 and 12 months thereafter in 37 adults with end-stage heart failure. Twelve patients received a HeartMate 3, 7 patients received a HeartWare, and 18 patients received a HeartMate II. At baseline, patients had elevated plasma levels of the platelet protein upon activation, β-thromboglobulin, and active von Willebrand factor in thrombogenic state (VWFa), which remained high after LVAD implantation. Von Willebrand factor levels and VWF activity were elevated at baseline but normalized 12 months after LVAD implantation. High D -dimer plasma levels, at baseline, remained elevated after 12 months. This was associated with an increase in plasma thrombin-antithrombin-complex levels and plasma levels of contact activation marker-cleaved H-kininogen after LVAD implantation. Considering these results it could be concluded that LVAD patients show significant coagulation activation despite antithrombotic therapy, which could explain why patients are at high risk for LVAD-induced thrombosis. Continuous low-grade systemic platelet activation and contact activation may contribute to prothrombotic effects of LVAD.
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Liesdek et al. (2022) studied this question.
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