Vwf, or von Willebrand factor, is a large adhesive multimeric glycoprotein crucial for hemostasis, regulating the balance between blood clotting and bleeding [3,4]. It acts as a bridge between platelets and the subendothelial matrix after vessel damage [6]. Aberrant regulation of Vwf can lead to a spectrum of diseases, from bleeding disorders like von Willebrand disease (VWD) to thrombotic conditions [4].

In VWD, partial quantitative Vwf deficiency is responsible for the majority of cases. Low Vwf, defined by mild to moderate reductions in plasma Vwf antigen (Vwf:Ag) levels (30-50 IU/dL), still poses clinical challenges in terms of genetic counseling, diagnosis, and management. The number of rare nonsynonymous Vwf variants significantly predicts Vwf:Ag levels, and these variants are associated with VWD type 1 and low Vwf [1,2]. Also, increased Vwf clearance may contribute to the pathobiology of low Vwf [5]. In COVID-19, an increase in Vwf and a decrease in ADAMTS-13 (a Vwf-cleaving protease) create an environment promoting (micro)thrombosis [3]. Plasma Vwf:Ag levels are higher in acute myocardial infarction patients and can predict long-term major adverse cardiopulmonary and cerebrovascular events (MACEs) [6]. However, in children undergoing tonsillectomy, low Vwf levels do not correlate with bleeding [7].

In conclusion, Vwf is essential for maintaining hemostasis. Studies on Vwf, especially through understanding its genetic variants and its role in different disease states such as VWD, COVID-19-related thrombosis, and acute myocardial infarction, contribute to better diagnosis, treatment, and management of these conditions.