Stretching to image VWF in shear flow

In this issue of Blood, Bergal et al developed a new method to demonstrate that circulating von Willebrand Factor (VWF) multimers experience less tension and undergo less conformational elongation in shear flow than previously thought.(1) VWF is a blood protein that binds to and activates platelets to initiate hemostatic blood clots, particularly in arterial flow. This process must be precisely regulated, or thrombi would form spontaneously. The primary regulatory mechanism in VWF is mechanical tension; therefore, characterizing VWF tension and elongation in shear flow is critical for understanding the regulation of arterial hemostasis and thrombosis. Indeed, devices such as artificial heart valves and left ventricular assist devices, which introduce higher and different fluid stresses, are associated with the hemostatic and thrombotic dysregulation of VWF in many patients.