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Clinical and In Vitro Evidence That Subclinical Hemolysis Contributes to LVAD Thrombosis  Carlo R. Bartoli, MD, PhD, David Zhang, BSE, Jooeun Kang, BA,

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Presentation on theme: "Clinical and In Vitro Evidence That Subclinical Hemolysis Contributes to LVAD Thrombosis  Carlo R. Bartoli, MD, PhD, David Zhang, BSE, Jooeun Kang, BA,"— Presentation transcript:

1 Clinical and In Vitro Evidence That Subclinical Hemolysis Contributes to LVAD Thrombosis 
Carlo R. Bartoli, MD, PhD, David Zhang, BSE, Jooeun Kang, BA, Samson Hennessy-Strahs, BA, David Restle, BSE, Jessica Howard, BS, Gretchen Redline, PharmD, Christian Bermudez, MD, Pavan Atluri, MD, Michael A. Acker, MD  The Annals of Thoracic Surgery  Volume 105, Issue 3, Pages (March 2018) DOI: /j.athoracsur Copyright © 2018 The Society of Thoracic Surgeons Terms and Conditions

2 The Annals of Thoracic Surgery 2018 105, 807-814DOI: (10. 1016/j
The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur ) Copyright © 2018 The Society of Thoracic Surgeons Terms and Conditions

3 Fig 1 (A) Continuous-flow left ventricular assist device (LVAD) patient outcomes (n = 30). (B, C) LVAD support caused subclinical hemolysis as measured by plasma free hemoglobin (pfHgb). In patients that did not develop LVAD thrombosis, pfHgb increased early but decreased over time. In patients that did develop LVAD thrombosis, pfHgb was significantly elevated versus patients without thrombosis before and after 3 months of LVAD support. The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur ) Copyright © 2018 The Society of Thoracic Surgeons Terms and Conditions

4 Fig 2 In a ex vivo model of left ventricular assist device blood trauma, supraphysiologic shear stress caused significant degradation of von Willebrand factor (vWF). Free hemoglobin (Hgb, 30 mg/dL) partially reversed this effect by reducing the activity of ADAMTS-13 the vWF-specific protease. (A) Agarose immunoblotting demonstrated that shear stress eliminated high-molecular-weight vWF multimers and increased low-molecular-weight vWF multimers. The addition of free Hgb increased high-molecular-weight vWF multimers and decreased low-molecular-weight vWF multimers. (B) Polyacrylamide immunoblotting demonstrated that shear stress increased vWF degradation fragments. The addition of free Hgb partially reversed this effect (C). (D) Shear stress significantly increased ADAMTS-13 activity. The addition of free Hgb partially reversed this effect. The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur ) Copyright © 2018 The Society of Thoracic Surgeons Terms and Conditions

5 Fig 3 Shear stress significantly reduced von Willebrand factor (vWF)/collagen binding. Free hemoglobin (Hgb) (30 mg/dL) partially reversed this effect. The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur ) Copyright © 2018 The Society of Thoracic Surgeons Terms and Conditions

6 Fig 4 Proposed mechanism by which left ventricular assist device (LVAD)–associated subclinical hemolysis and elevated plasma free hemoglobin lead to the accumulation of activated von Willebrand factor (vWF) multimers, which are the initial building blocks for clot formation during primary hemostasis. ADAMTS-13 = A disintegrin and metalloproteinase with thrombospondin motifs 13. The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur ) Copyright © 2018 The Society of Thoracic Surgeons Terms and Conditions

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