Evidence map›Paper›PMID 27143258›Full record

ReviewBlood2016

Acquired von Willebrand syndrome associated with left ventricular assist device.

Angelo Nascimbene, Sriram Neelamegham, O H Frazier, Joel L Moake, Jing-Fei Dong

Abstract readReview
In one paragraph

Review in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

83 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Review
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  7. Article
  8. Fibrosis 4 Index Predicts Haemocompatibility-Related Adverse Events in Patients Using Left Ventricular Assist Devices.European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery · 2025
    Article
  9. Left Ventricular Assist Device in the Management of Heart Failure: A Single-Center Experience.The International journal of angiology : official publication of the International College of Angiology, Inc · 2025
    Article
  10. Article
  11. Review
  12. Article
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  19. Article
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23 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Angelo NascimbeneCenter for Advanced Heart Failure, Health Science Center at Houston, University of Texas, Houston, TX;
Sriram NeelameghamDepartment of Chemical and Biological Engineering, University at Buffalo, the State University of New York, Buffalo, NY;
O H FrazierTexas Heart Institute, Baylor College of Medicine, Houston, TX;
Joel L MoakeTexas Heart Institute, Baylor College of Medicine, Houston, TX; J.W. Cox Laboratory for Biomedical Engineering, Rice University, Houston, TX;
Jing-Fei DongBloodWorks Northwest Research Institute, Seattle, WA; and Division of Hematology, Department of Medicine, School of Medicine, University of Washington, Seattle, WA.

Funding

Ultra-Large VWF and Thrombotic MicroangiopathyR01HL071895 · NHLBI · BLOODWORKS · PI DONG, JING-FEI · 2003 to 2012
$3.4M
VON WILLEBRAND FACTOR STRUCTURE-FUNCTION UNDE FLUID FLOWR01HL077258 · NHLBI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI NEELAMEGHAM, SRIRAM · 2006 to 2015
$3.0M
VWF Activity: Molecular Biology, Ethnic Diversity and Disease AssociationsR01HL125957 · NHLBI · BLOODWORKS · PI DONG, JING-FEI, YU, FULI · 2015 to 2018
$2.5M
NHLBI NIH HHS R01 HL071895NHLBI NIH HHS R01 HL077258NHLBI NIH HHS R01 HL125957
6 · The paper itself

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.

Indexed as

Heart-Assist DevicesHeart FailureHeart TransplantationHemostasisHumansThrombosisVentricular Dysfunction, Leftvon Willebrand Diseasesvon Willebrand Factorvon Willebrand Factor

Identifiers

PMID27143258
PMCPMC4920020

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.