Evidence map›Paper›PMID 30867356›Full record

ReviewJournal of atherosclerosis and thrombosis2019

Acquired von Willebrand Syndrome Associated with Cardiovascular Diseases.

Hisanori Horiuchi, Tsuyoshi Doman, Koichi Kokame, Yoshikatsu Saiki, Masanori Matsumoto

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of atherosclerosis and thrombosis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
11.6field-weighted citation impact, top 1% of its field
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

49 citing papers in PubMed, 123 citations in OpenAlex.

  1. Review
  2. Heyde syndrome secondary to hypertrophic obstructive cardiomyopathy: a case report.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2026
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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 at 3 institutions in 1 country.

Hisanori HoriuchiDepartment of Molecular and Cellular Biology, Institute of Development, Aging and Cancer, Tohoku University.
Tsuyoshi DomanDepartment of Molecular and Cellular Biology, Institute of Development, Aging and Cancer, Tohoku University.
Koichi KokameDepartment of Molecular Pathogenesis, National Cerebral and Cardiovascular Center.
Yoshikatsu SaikiDivision of Cardiovascular Surgery, Tohoku University Graduate School of Medicine.
Masanori MatsumotoDepartment of Blood Transfusion Medicine, Nara Medical University.
Tohoku University · JPNara Medical University · JPNational Cerebral and Cardiovascular Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The blood glycoprotein von Willebrand factor (VWF) plays an important role in hemostasis and thrombosis.VWF is produced and secreted as large multimers by endothelial cells and megakaryocytes. It is then cleaved in a sheer-stress dependent manner by a specific protease, ADAMTS13, into multimers consisting of 2-80 subunits. Among VWF multimers, high molecular weight (HMW) multimers play important roles in platelet aggregation. Therefore, their loss induces a hemostatic disorder known as von Willebrand disease (VWD) type 2A. Various cardiovascular diseases, such as aortic stenosis, hypertrophic obstructive cardiomyopathy (HOCM), and several congenital structural diseases, as well as mechanical circulatory support systems, generate excessive high shear stress in the bloodstream. These cause excessive cleavage of VWF multimers resulting in a loss of HMW multimers, known as acquired von Willebrand syndrome (AVWS), a hemostatic disorder similar to VWD type 2A. Bleeding often occurs in the gastrointestinal tract since a fragile angiodysplasia develops associated with these diseases. Radical treatment for AVWS is to remove the pathological high shear causing AVWS.

Indexed as

AnimalsCardiovascular DiseasesHumansPrognosisvon Willebrand Diseasesvon Willebrand Factorvon Willebrand FactorAcquired von Willebrand’s syndromeAortic stenosisECMOHeyde’s syndromeLeft ventricular assist devicevon Willebrand factor

Identifiers

PMID30867356
PMCPMC6456452
OpenAlexW2921098278

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.