title: Effects of HeartWare ventricular assist device on the von Willebrand factor: results of an academic Belgian center.
abstract: Left Ventricular Assist Device (LVAD) is a promising therapy for patients with advanced heart failure (HF), but bleeding complications remain an important issue. Previous series show that acquired von Willebrand syndrome was present in up to 100 % of first generation LVAD recipients. We report the effects of new generation LVADs on vW factor (vWF) metabolism and activity in our center.
  
  
  
  Fifteen LVAD recipients (HeartWare®, Framingham, MA, USA) were compared to 12 HF patients, matched for age and body mass index. vWF antigen and activity, as well as D-dimers, were measured on hemostasis analyzers. A vWF LVAD-induced alteration was evocated when the [vWF activity]/[vWF antigen] ratio was <0.6. ADAMTS13 and high molecular weight multimers of vWF were also assessed.
  
  
  
  LVAD recipients had similar levels of endothelial vWF production than the HF subjects (137 ± 14.5 vs. 147 ± 11.7 %; respectively, p = 0.611) but a decreased vWF activity (90 ± 11 vs. 132.6 ± 13 %; respectively, p = 0.017). [vWF activity]/[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). ADAMTS13 activity was 80.3 ± 4.7 % in LVAD recipients and 96.2 ± 3.5 % in the HF patients (p = 0.016). LVAD patients disclosed markedly elevated D-dimers (3217.7 ± 735 vs. 680.6 ± 223.2 ng/mL FEU in the HF patients, p = 0.006). The LVAD patients experienced one major hemorrhagic event and one systemic thrombotic event during the median follow-up of 345 days.
  
  
  
  LVAD recipients achieved a new hemostatic equilibrium characterized by infrequent major hemorrhagic and thrombotic events, despite a mildly impaired vWF function and a markedly enhanced thrombin formation.
  
  
  
  ISRCTN39517567.
authors.affiliation: Department of Cardiology, Université Libre de Bruxelles (ULB), 808 Lennik Street, 1070, Brussels, Belgium. Fatemeh.EsmaeilZadeh@erasme.ulb.ac.be.
authors.forename: Fatemeh
authors.initials: F
authors.lastname: Esmaeilzadeh
authors.affiliation: Department of Cardiology, Université Libre de Bruxelles (ULB), 808 Lennik Street, 1070, Brussels, Belgium.
authors.forename: Aurélien
authors.initials: A
authors.lastname: Wauters
authors.affiliation: Laboratory of Haemostasis, Erasme Hospital, Université Libre de Bruxelles (ULB), Brussels, Belgium.
authors.forename: Walter
authors.initials: W
authors.lastname: Wijns
authors.affiliation: Department of Cardiology, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel (VUB), Brussels, Belgium.
authors.forename: Jean-François
authors.initials: JF
authors.lastname: Argacha
authors.affiliation: Department of Cardiology, Université Libre de Bruxelles (ULB), 808 Lennik Street, 1070, Brussels, Belgium.
authors.forename: Philippe
authors.initials: P
authors.lastname: van de Borne
mesh_terms: D000071120:ADAMTS13 Protein / Q000097:blood; D000046:Academic Medical Centers; D000328:Adult; D001530:Belgium; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy*; D006353:Heart-Assist Devices / Q000009:adverse effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D011474:Prosthesis Design; D012307:Risk Factors; D013917:Thrombin / Q000378:metabolism; D013927:Thrombosis / Q000097:blood / Q000209:etiology; D013997:Time Factors; D016896:Treatment Outcome; D016277:Ventricular Function, Left; D014842:von Willebrand Diseases / Q000097:blood / Q000209:etiology; D014841:von Willebrand Factor / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D014841:von Willebrand Factor; D013917:Thrombin; D000071120:ADAMTS13 Protein; C099604:ADAMTS13 protein, human
keywords: ADAMTS13; Bleeding; HeartWare; Left ventricle assist device; von Willebrand factor