The von Willebrand factor (VWF) is a multifunctional, large glycoprotein with important functions in primary haemostasis. In patients with aortic valve stenosis, elevated shear stress leads to a structural change of VWF multimers, which allows proteolytic cleavage by the plasma protease ADAMTS13. Consequently, the multimers decrease in size and lose their important role in maintaining optimal haemostasis. A VWF deficiency therefore leads to elevated bleeding tendencies [
1]. The assumption that high shear stress is a cause of aVWS, suggests that other cardiovascular disorders with elevated shear forces from a left ventricular assist device and a broad range of congenital and acquired cardiac defects can also possibly lead to augmented bleeding complications [
4]. Intravascular haemolysis has been described in patients with prosthetic and dysfunctional native aortic valves and it has been suggested that the severity of intravascular haemolysis is associated with the transvalvular flow velocity [
5]. In our patient, intravascular haemolysis was unlikely to be the main cause of the anaemia since total bilirubin and the absolute reticulocyte count on admission were within reference range (3 μmol/l, reference range <21 μmol/l and 87.8 10
9/l, reference range 25.0–105 10
9/l, respectively) and lactate dehydrogenase measured before elective transcatheter aortic valve implantation was not elevated (205 U/l, reference range <214 U/l).