Abstract

The surgical replacement of diseased heart valves is based on the premise that the prosthesis chosen to replace a stenotic or insufficient valve will have a beneficial impact on the patient’s heart function, taking into account the risks of surgery and the recognized complications of prosthetic heart valves. It is well established that mitral valve replacement (MVR) is associated with higher short- and long-term mortality than mitral valve repair.1,2 Although the exact mechanism for this discrepancy is unknown, it increases the importance of repairing valves whenever possible and, when MVR is necessary, intervening to prevent prosthesis- and/or patient-related factors that may lead to less favorable postoperative outcomes. Article p 1417 A growing literature has identified aortic valve patient-prosthesis mismatch (PPM) after aortic valve replacement. Studies have suggested that aortic PPM may be accompanied by lower rates and absolute degree of regression of left ventricular hypertrophy. Some authors have linked incomplete regression of left ventricular hypertrophy to more postoperative cardiac events and worse long-term survival.3–7 This linkage is controversial, however; other authors suggest that PPM is of less importance after aortic valve replacement and indeed that valve size may not matter.8 Many fewer data are available regarding PPM after MVR. In this issue of Circulation , Magne et al9 investigate the impact of PPM on survival after MVR. The authors hypothesize that the effective orifice area (EOA) of prosthetic valves is often small relative to the patient’s size, thus causing a mismatch between valve EOA and flow across the valve. As a result, seemingly normally functioning mitral prostheses often have relatively high transvalvular gradients. These gradients mimic those found in patients with mitral stenosis. In addition to delaying the regression of left atrial and pulmonary artery hypertension, these high gradients and the resulting high left atrial pressures …

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