Abstract

von Willebrand factor (VWF) is a large glycoprotein involved in the early stages of hemostasis, where it recruits platelets to sites of vessel injury [1]. Plasma VWF is composed of multimers. The biological activity of VWF is related to the size of these multimers, with the larger ones being more hemostatically effective than the smaller forms [2]. VWF multimeric size is modulated by ADAMTS13 (a disintegrin and metalloprotease with thrombospondin motif) [2]. Decreased plasma levels of ADAMTS13 have been reported in patients with myocardial infarction, both acutely [3] and several months after the event [4]. In a recent study on arterial thrombosis at young age, Bongers et al. observed a reduction in plasma levels of ADAMTS13 antigen and activity 1– 3 months after the event in patients with coronary heart disease [5].

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