According to its definition, prosthesis-patient mismatch is present when the cardiac output of the patient is too large for the opening of a prosthetic valve. This causes symptoms similar to native... Show moreAccording to its definition, prosthesis-patient mismatch is present when the cardiac output of the patient is too large for the opening of a prosthetic valve. This causes symptoms similar to native aortic stenosis, which can lead to heart failure and mortality. To classify patients with PPM, a cut-off value of indexed effective orifice area is used in clinical practice.This thesis evaluates the underlying assumptions of using indexed effective orifice area as a parameter of valve performance. As these assumptions are inaccurate, the current definition of prosthesis-patient mismatch is unsuitable to diagnose patients with too small prosthetic valves after aortic valve replacement. Show less
Background Prosthesis-patient mismatch (PPM), routinely used to characterize the degree of hemodynamic obstruction caused by a prosthetic heart valve, is associated with adverse patient outcomes... Show moreBackground Prosthesis-patient mismatch (PPM), routinely used to characterize the degree of hemodynamic obstruction caused by a prosthetic heart valve, is associated with adverse patient outcomes after aortic valve replacement (AVR). In the common definition of PPM, the opening area of the valve is related to the patients' cardiac output, by indexing effective orifice area (EOA) with body surface area (BSA). The aim of this study is to assess the implications of using BSA as a proxy for cardiac output. Methods 744 patients with normal LV function underwent echocardiographic assessment after surgical AVR. To validate the use of BSA as a proxy for cardiac output, the relation between these variables was analyzed. The effects of BSA on the classification of PPM (EOAi < 0.85 cm(2)/m(2)) and the presence of hemodynamic obstruction (mean gradient >= 20 mmHg and/or Doppler velocity index < 0.35) were estimated. Results There was a weak correlation between BSA and cardiac output (r: 0.29, 95% CI: 0.22;0.35), and cardiac output was not proportional to BSA (Cardiac output = 1.5 x BSA +1.9). As a result, the increased risk of patients with a large BSA to be labelled with PPM (OR: 5.2, 95% CI: 2.5,11 per m(2) BSA), was not reflected by a significantly higher risk of hemodynamic obstruction (OR: 1.5, 95% CI: 0.5,4.9 per m(2) BSA). Conclusions The current definition of PPM results in a systematic overestimation of hemodynamic obstruction in patients with a larger BSA, and we recommend cautious use in this subgroup. Show less
