Molecular Creep Induced Fatigue Rupture of Fibrin Clots

This work investigates the mechanisms governing fatigue rupture of fibrin clots under cyclic mechanical loading. Using uniaxial tension, pure shear, and fatigue crack growth experiments, the study quantifies how molecular creep within the fibrin network drives time-dependent failure. Results show that fibrin fibers undergo rate-dependent elongation and molecular unfolding preceding crack propagation, with a measurable fatigue threshold below which failure does not occur. Combining confocal microscopy, rheology, and fracture mechanics, the study links molecular slippage and protofibril unbinding to macroscopic fatigue behavior, providing insights into thrombus stability and embolism risk.