ABSTRACT
Investigations of convexo-concave (C/C) valve outlet strut fractures (OSFs) were initially confounded by knowledge that the strut was subject to bending forces in arresting the opening disc. Pulse duplicator studies subsequently showed that closing loads were all born by the inlet strut, along with an understandable focus on the nature of the welds, where most fractures occurred. As observations of explanted valves accumulated, certain features pointed to unusual closing loads that might be contributory factors, but these hypothetical forces could not be verified. Epidemiological extrapolations and case-matched control studies have shown that certain valve and patient characteristics were each associated independently with increased OSF risk, leading to clinically valuable risk stratification, but little additional understanding of why OSFs continued to occur. Detection of the causative, highly transient (< 0.5 ms), outlet-strut-tip impacts due to closing disc over-rotation that have almost ten times the force of disc opening, and the capability of inducing leg-base bending stresses beyond the strut wire's fatigue endurance limit had to await the development of computer-controlled pulse duplicators and strut-leg strain gaging. Exercised young animals easily achieved such strut loading, but most human patients would probably have more difficulty. The actual OSF mechanism is a long-term, valve-patient interaction that requires the concurrence of susceptible valve geometry and sufficient ventricular contractility potential to develop the isovolumic, high dP/dt needed for forceful disc over-rotation. Critical strut tip loading must then occur often enough to fatigue fracture both strut legs within the patient's lifetime with the valve.