{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T09:30:44Z","timestamp":1790501444838,"version":"4.1.0"},"reference-count":64,"publisher":"MDPI AG","issue":"9","license":[{"start":{"date-parts":[[2021,9,15]],"date-time":"2021-09-15T00:00:00Z","timestamp":1631664000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JCDD"],"abstract":"<jats:p>von Willebrand factor (VWF) is an adhesive protein involved in primary hemostasis and facilitates platelet adhesion to sites of vascular injury, thereby promoting thrombus formation. VWF exists in plasma as multimers of increasing size, with the largest (high molecular weight; HMW) expressing the greatest functional activity. A deficiency of VWF is associated with a bleeding disorder called von Willebrand disease (VWD), whereas an excess of VWF, in particular the HMW forms, is associated with thrombosis. ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin type 1 motif-13), also known as VWF-cleaving protease, functions to moderate the activity of VWF by cleaving multimers of VWF and limiting the expression of the largest multimers of VWF. A deficiency of ADAMTS13 is therefore associated with an excess of (HMW forms of) VWF, and thus thrombosis. Indeed, any disturbance of the VWF\/ADAMTS13 ratio or \u2018axis\u2019 may be associated with pathophysiological processes, including prothrombotic tendency. However, both thrombosis or bleeding may be associated with such disturbances, depending on the presenting events. This review evaluates the relationship of VWF and ADAMTS13 with cardiac disease, including cardiac failure, and associated pathophysiology.<\/jats:p>","DOI":"10.3390\/jcdd8090115","type":"journal-article","created":{"date-parts":[[2021,9,15]],"date-time":"2021-09-15T12:00:44Z","timestamp":1631707244000},"page":"115","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["The Intriguing Relationships of von Willebrand Factor, ADAMTS13 and Cardiac Disease"],"prefix":"10.3390","volume":"8","author":[{"given":"Benjamin","family":"Reardon","sequence":"first","affiliation":[{"name":"Institute of Clinical Pathology and Medical Research (ICPMR), Westmead Hospital, Westmead, NSW 2145, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leonardo","family":"Pasalic","sequence":"additional","affiliation":[{"name":"Institute of Clinical Pathology and Medical Research (ICPMR), Westmead Hospital, Westmead, NSW 2145, Australia"},{"name":"NSW Health Pathology, Westmead, NSW 2145, Australia"},{"name":"Westmead Clinical School, University of Sydney, Westmead, NSW 2145, Australia"},{"name":"Sydney Centres for Thrombosis and Haemostasis, Westmead Hospital, Westmead, NSW 2145, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2103-1661","authenticated-orcid":false,"given":"Emmanuel J.","family":"Favaloro","sequence":"additional","affiliation":[{"name":"Institute of Clinical Pathology and Medical Research (ICPMR), Westmead Hospital, Westmead, NSW 2145, Australia"},{"name":"NSW Health Pathology, Westmead, NSW 2145, Australia"},{"name":"Sydney Centres for Thrombosis and Haemostasis, Westmead Hospital, Westmead, NSW 2145, Australia"},{"name":"School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, NSW 2650, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2021,9,15]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"A6","DOI":"10.1016\/0735-1097(93)90455-A","article-title":"The epidemiology of heart failure: The Framingham Study","volume":"22","author":"Ho","year":"1993","journal-title":"J. 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