Background: Left Ventricular Assist Device (LVAD) is a promising therapy for patients with advanced heart failure\n(HF), but bleeding complications remain an important issue. Previous series show that acquired von Willebrand\nsyndrome was present in up to 100 % of first generation LVAD recipients. We report the effects of new generation\nLVADs on vW factor (vWF) metabolism and activity in our center.\nMethods: Fifteen LVAD recipients (HeartWare�®, Framingham, MA, USA) were compared to 12 HF patients, matched\nfor age and body mass index. vWF antigen and activity, as well as D-dimers, were measured on hemostasis\nanalyzers. A vWF LVAD-induced alteration was evocated when the [vWF activity]/[vWF antigen] ratio was <0.6.\nADAMTS13 and high molecular weight multimers of vWF were also assessed.\nResults: LVAD recipients had similar levels of endothelial vWF production than the HF subjects (137 �± 14.5 vs. 147 �±\n11.7 %; respectively, p = 0.611) but a decreased vWF activity (90 �± 11 vs. 132.6 �± 13 %; respectively, p = 0.017). [vWF\nactivity]/[vWF antigen] ratio was 0.65 �± 0.02 in the LVAD recipients and 0.92 �± 0.06 in the subjects with HF (p = 0.001).\nADAMTS13 activity was 80.3 �± 4.7 % in LVAD recipients and 96.2 �± 3.5 % in the HF patients (p = 0.016). LVAD patients\ndisclosed markedly elevated D-dimers (3217.7 �± 735 vs. 680.6 �± 223.2 ng/mL FEU in the HF patients, p = 0.006). The\nLVAD patients experienced one major hemorrhagic event and one systemic thrombotic event during the median\nfollow-up of 345 days.\nConclusions: LVAD recipients achieved a new hemostatic equilibrium characterized by infrequent major hemorrhagic\nand thrombotic events, despite a mildly impaired vWF function and a markedly enhanced thrombin formation.
Loading....