ArticleJournal of thrombosis and haemostasis : JTH2022
ADAMTS13 inhibition to treat acquired von Willebrand syndrome during mechanical circulatory support device implantation.
Article in Journal of thrombosis and haemostasis : JTH, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Historical, current and future treatments for von Willebrand disease.Haematologica · 2026Review
- Critical hematological parameters in bleeding during extracorporeal membrane oxygenation support.Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs · 2025Review
- Anticoagulation in venovenous extracorporeal membrane oxygenation.Frontiers in medicine · 2025Review
- Preservation of von Willebrand Factor Activity With the ModulHeart Device.JACC. Basic to translational science · 2024Article
- Cattle-FRETS71, a novel fluorogenic substrate with broad applicability for characterizing ADAMTS13 properties and function.Journal of thrombosis and haemostasis : JTH · 2023Article
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Authors and funding
18 authors at 8 institutions in 5 countries.
Funding
Abstract
backgroundAcquired von Willebrand syndrome (aVWS) is common in patients with mechanical circulatory support (MCS) devices. In these patients, the high shear stress in the device leads to increased shear-induced proteolysis of von Willebrand factor (VWF) by A Disintegrin And Metalloprotease with Thrombospondin type 1 repeats, number 13 (ADAMTS13). As a result, the high molecular weight (HMW) VWF multimers are lost, leading to a decreased VWF function and impaired hemostasis that could explain the bleeding complications that are frequently observed in these patients. To counteract this abnormal VWF degradation by ADAMTS13, we developed a novel targeted therapy, using an anti-ADAMTS13 monoclonal antibody (mAb) that inhibits the shear-induced proteolysis of VWF by ADAMTS13.
methodsHuman or bovine blood was circulated through in vitro MCS device systems with either inhibitory anti-ADAMTS13 mAb 3H9 or 17C7 (20 μg/ml) or control anti-ADAMTS13 mAb 5C11 or phosphate buffered saline (PBS). VWF multimers and function (collagen binding activity) were determined at different time points. Next, Impella pumps were implanted in calves and the calves were injected with PBS and subsequently treated with mAb 17C7. VWF, ADAMTS13, and blood parameters were determined.
resultsWe demonstrated that blocking ADAMTS13 could prevent the loss of HMW VWF multimers in in vitro MCS device systems. Importantly, our antibody could reverse aVWS in a preclinical Impella-induced aVWS calf model.
conclusionHence, inhibition of ADAMTS13 could become a novel therapeutic strategy to manage aVWS in MCS device patients.
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