ArticleCardiovascular research2016
The role of ADAMTS13 in acute myocardial infarction: cause or consequence?
Article in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Perioperative Profiling of a Disintegrin and Metalloprotease with Thrombospondin Type 1 Motif, Member 13 (ADAMTS13) Activity in Cardiac Surgery: Kinetics and Mechanistic Insights.Journal of clinical medicine · 2025Article
- No-reflow after stroke reperfusion therapy: An emerging phenomenon to be explored.CNS neuroscience & therapeutics · 2024Review
- Transcriptome analysis reveals ADAMTS15 is a potential inflammation-related gene in remote ischemic postconditioning.Frontiers in cardiovascular medicine · 2023Article
- ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease.Advances in pharmacology (San Diego, Calif.) · 2022Article
- COVID-19 Sepsis: Pathogenesis and Endothelial Molecular Mechanisms Based on "Two-Path Unifying Theory" of Hemostasis and Endotheliopathy-Associated Vascular Microthrombotic Disease, and Proposed Therapeutic Approach with Antimicrothrombotic Therapy.Vascular health and risk management · 2021Review
- A Disintegrin and Metalloproteinase (ADAM) and ADAM with thrombospondin motifs (ADAMTS) family in vascular biology and disease.Biochemical pharmacology · 2019Review
- Noninvasive Evaluation of No-Reflow Phenomenon.Circulation. Cardiovascular imaging · 2018Article
- Molecular Imaging of VWF (von Willebrand Factor) and Platelet Adhesion in Postischemic Impaired Microvascular Reflow.Circulation. Cardiovascular imaging · 2018Article
- Epigenetics and Immunometabolism in Diabetes and Aging.Antioxidants & redox signaling · 2018Review
- ADAMTS-13 and von Willebrand factor: a dynamic duo.Journal of thrombosis and haemostasis : JTH · 2018Review
- Recombinant ADAMTS 13 in thrombotic thrombocytopenic purpura.Oncoscience · 2017Article
- The role of infiltrating immune cells in dysfunctional adipose tissue.Cardiovascular research · 2017Review
- Increased Von Willebrand factor, decreased ADAMTS13 and thrombocytopenia in melioidosis.PLoS neglected tropical diseases · 2017Article
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsADAMTS13, a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13, is a metalloprotease that cleaves von Willebrand factor (VWF). There is considerable evidence that VWF levels increase and ADAMTS13 levels decrease in ST-elevation myocardial infarction (STEMI) patients. It is unclear whether this contributes to no reflow, infarct size, and intramyocardial haemorrhage (IMH). We aimed to determine the role of ADAMTS13 in STEMI patients and to investigate the benefits of recombinant ADAMTS13 (rADAMTS13) in a porcine model of myocardial ischaemia-reperfusion. METHODS AND
resultsIn 49 consecutive percutaneous coronary intervention (PCI)-treated STEMI patients, blood samples were collected directly after through 7 days following PCI. Cardiac magnetic resonance was performed 4-6 days after PCI to determine infarct size and IMH. In 23 Yorkshire swine, the circumflex coronary artery was occluded for 75 min. rADAMTS13 or vehicle was administered intracoronary following reperfusion. Myocardial injury and infarct characteristics were assessed using cardiac enzymes, ECG, and histopathology. In patients with IMH, VWF activity and VWF antigen were significantly elevated directly after PCI and for all subsequent measurements, and ADAMTS13 activity significantly decreased at 4 and 7 days following PCI, in comparison with patients without IMH. VWF activity and ADAMTS13 activity were not related to infarct size. In rADAMTS13-treated animals, no differences in infarct size, IMH, or formation of microthrombi were witnessed compared with controls.
conclusionsNo correlation was found between VWF/ADAMTS13 and infarct size in patients. However, patients suffering from IMH had significantly higher VWF activity and lower ADAMTS13 activity. Intracoronary administration of rADAMTS13 did not decrease infarct size or IMH in a porcine model of myocardial ischaemia-reperfusion. These data dispute the imbalance in ADAMTS13 and VWF as the cause of no reflow.
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