We found that Adamts13(-/-) mice developed larger myocardial infarctions than wild-type control mice, whereas treatment of wild-type mice with recombinant human ADAMTS13 (rhADAMTS13) led to smaller infarctions.
A potential pathophysiological role of ADAMTS13 has also been postulated in other diseases i.e. myocardial infarction, atrial fibrillation and diabetic angiopathy.
During the 2-month interval prior to an event, cases (n = 48) had higher levels of the vWF and ADAMTS13 than controls (n = 95; P = .05), but significance was lost after adjusting for the baseline differences in myocardial infarction, unstable angina, and stroke.