scholarly journals Experimental measurement and numerical modelling of dye washout for investigation of blood residence time in ventricular assist devices

2018 ◽  
Vol 41 (4) ◽  
pp. 201-212 ◽  
Author(s):  
Alessandra Molteni ◽  
Zubair PH Masri ◽  
Kenny WQ Low ◽  
Haitham N Yousef ◽  
Johann Sienz ◽  
...  
Keyword(s):  
Residence Time ◽  
Fluid Dynamic ◽  
Ventricular Assist Devices ◽  
Heartmate Ii ◽  
Ventricular Assist ◽  
Acquired Von Willebrand Syndrome ◽  
Assist Devices ◽  
Total Residence Time ◽  
End Stage ◽  
Von Willebrand

Ventricular assist devices have become the standard therapy for end-stage heart failure. However, their use is still associated with severe adverse events related to the damage done to the blood by fluid dynamic stresses. This damage relates to both the stress magnitude and the length of time the blood is exposed to that stress. We created a dye washout technique which combines experimental and numerical approaches to measure the washout times of ventricular assist devices. The technique was used to investigate washout characteristics of three commercially available and clinically used ventricular assist devices: the CentriMag, HVAD and HeartMate II. The time taken to reach 5% dye concentration at the outlet (T05) was used as an indicator of the total residence time. At a typical level of cardiac support, 5 L/min and 100 mmHg, T05 was 0.93, 0.28 and 0.16 s for CentriMag, HVAD and HeartMate II, respectively, and increased to 5.06, 1.64 and 0.96 s for reduced cardiac support of 1 L/min. Regional variations in washout characteristics are described in this article. While the volume of the flow domain plays a large role in the differences in T05 between the ventricular assist devices, after standardising for ventricular assist device volume, the secondary flow path was found to increase T05 by 35%. The results explain quantitatively, for the first time, why the CentriMag, which exerts low shear stress magnitude, has still been found to cause acquired von Willebrand Syndrome in patients.

Platelet secretion defects and acquired von Willebrand syndrome in patients with Ventricular Assist Devices

2019 ◽  
Author(s):  
Ulrich Geisen ◽  
Kerstin Brehm ◽  
Georg Trummer ◽  
Michael Berchtold-Herz ◽  
Claudia Heilmann ◽  
...  
Keyword(s):  
Ventricular Assist Devices ◽  
Ventricular Assist ◽  
Acquired Von Willebrand Syndrome ◽  
Assist Devices ◽  
Von Willebrand ◽  
Platelet Secretion

scholarly journals Acquired von Willebrand syndrome associated with left ventricular assist device

Blood ◽  
2016 ◽  
Vol 127 (25) ◽  
pp. 3133-3141 ◽  
Author(s):  
Angelo Nascimbene ◽  
Sriram Neelamegham ◽  
O. H. Frazier ◽  
Joel L. Moake ◽  
Jing-fei Dong
Keyword(s):  
Left Ventricular ◽  
Ventricular Assist Devices ◽  
Left Ventricular Assist Devices ◽  
Ventricular Assist ◽  
Acquired Von Willebrand Syndrome ◽  
Left Ventricular Assist ◽  
End Stage ◽  
Von Willebrand ◽  
Internal Rotor ◽  
Willebrand Factor

Abstract Left ventricular assist devices (LVAD) provide cardiac support for patients with end-stage heart disease as either bridge or destination therapy, and have significantly improved the survival of these patients. Whereas earlier models were designed to mimic the human heart by producing a pulsatile flow in parallel with the patient’s heart, newer devices, which are smaller and more durable, provide continuous blood flow along an axial path using an internal rotor in the blood. However, device-related hemostatic complications remain common and have negatively affected patients’ recovery and quality of life. In most patients, the von Willebrand factor (VWF) rapidly loses large multimers and binds poorly to platelets and subendothelial collagen upon LVAD implantation, leading to the term acquired von Willebrand syndrome (AVWS). These changes in VWF structure and adhesive activity recover quickly upon LVAD explantation and are not observed in patients with heart transplant. The VWF defects are believed to be caused by excessive cleavage of large VWF multimers by the metalloprotease ADAMTS-13 in an LVAD-driven circulation. However, evidence that this mechanism could be the primary cause for the loss of large VWF multimers and LVAD-associated bleeding remains circumstantial. This review discusses changes in VWF reactivity found in patients on LVAD support. It specifically focuses on impacts of LVAD-related mechanical stress on VWF structural stability and adhesive reactivity in exploring multiple causes of AVWS and LVAD-associated hemostatic complications.

scholarly journals Bleeding in critical care associated with left ventricular assist devices: pathophysiology, symptoms, and management

Hematology ◽  
2019 ◽  
Vol 2019 (1) ◽  
pp. 88-96
Author(s):  
F. W. G. Leebeek ◽  
R. Muslem
Keyword(s):  
Critical Care ◽  
Left Ventricular ◽  
Ventricular Assist Devices ◽  
Bleeding Complications ◽  
Left Ventricular Assist Devices ◽  
Ventricular Assist ◽  
Assist Devices ◽  
Left Ventricular Assist ◽  
End Stage ◽  
Von Willebrand

Abstract Chronic heart failure (HF) is a growing health problem, and it is associated with high morbidity and mortality. Left ventricular assist devices (LVADs) are nowadays an important treatment option for patients with end-stage HF not only as a bridging tool to heart transplantation but also, as a permanent therapy for end-stage HF (destination therapy). The use of LVAD is associated with a high risk for bleeding complications and thromboembolic events, including pump thrombosis and ischemic stroke. Bleeding is the most frequent complication, occurring in 30% to 60% of patients, both early and late after LVAD implantation. Although the design of LVADs has improved over time, bleeding complications are still the most common complication and occur very frequently. The introduction of an LVAD results in an altered hemostatic balance as a consequence of blood-pump interactions, changes in hemodynamics, acquired coagulation abnormalities, and the strict need for long-term anticoagulant treatment with oral anticoagulants and antiplatelet therapy. LVAD patients may experience an acquired coagulopathy, including platelet dysfunction and impaired von Willebrand factor activity, resulting in acquired von Willebrand syndrome. In this educational manuscript, the epidemiology, etiology, and pathophysiology of bleeding in patients with LVAD will be discussed. Because hematologist are frequently consulted in cases of bleeding problems in these individuals in a critical care setting, the observed type of bleeding complications and management strategies to treat bleeding are also reviewed.

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