Occlusive thrombosis in arteries

Thrombus formation in major arteries is life threatening. In this review article, we discuss how an arterial thrombus can form under pathologically high shear stresses, with bonding rates estimated to be the fastest K o n values in biochemistry. During occlusive thrombosis in arteries, the growth rate of the thrombus explodes to capture a billion platelets in about 10 min. Close to 100% of all platelets passing the thrombus are captured by long von Willebrand factor (vWF) strands that quickly form tethered nets. The nets grow in patches where shear stress is high, and the local concentration of vWF is elevated due to α-granule release by previously captured platelets. This rapidly formed thrombus has few red blood cells and so has a white appearance and is much stronger and more porous than clots formed through coagulation. Understanding and modeling the biophysics of this event can predict totally new approaches to prevent and treat heart attacks and strokes.Thrombus formation in major arteries is life threatening. In this review article, we discuss how an arterial thrombus can form under pathologically high shear stresses, with bonding rates estimated to be the fastest K o n values in biochemistry. During occlusive thrombosis in arteries, the growth rate of the thrombus explodes to capture a billion platelets in about 10 min. Close to 100% of all platelets passing the thrombus are captured by long von Willebrand factor (vWF) strands that quickly form tethered nets. The nets grow in patches where shear stress is high, and the local concentration of vWF is elevated due to α-granule release by previously captured platelets. This rapidly formed thrombus has few red blood cells and so has a white appearance and is much stronger and more porous than clots formed through coagulation. Understanding and modeling the biophysics of this event can predict totally new approaches to prevent and treat heart attacks and strokes.