The underlying mechanism can likely be attributed to (a combination of) three causes: (1) changes in the (conformation of) VWF itself (e.g. VWD type 2B [13]), (2) changes in endothelial secretion (e.g. malaria [20], diabetes [17]), processing or clearance of VWF (e.g. TTP [13], HELLP [14]) or (3) increased shear stress (e.g. mild aortic stenosis [32], first STEMI [18]). Here, VWF is linked to aortic stenosis.