Epidemiological extrapolations and case-matched control studies have shown that certain valve and patient characteristics were each independently associated with increased risk of outlet strut fracture (OSF), leading to clinically valuable risk stratification, but little additional understanding of why OSFs occur. Detection of the causative, highly transient (<0.5 ms), outlet-strut-tip impacts, due to closing disc over-rotations that are capable of causing leg-base bending stresses beyond the fatigue endurance limit of the strut wire, had to await the development of computer-controlled pulse duplicators and strut-leg strain gaging. The OSF mechanism involves a long-term, valve-patient interaction, requiring concurrence of susceptible valve geometry and sufficient ventricular contractility potential to develop the isovolumic, high dP/dt needed for forceful disc over-rotation. Critical tip loading must then occur often enough to cause fatigue fractures of both strut legs within the patient's lifetime with the valve.