OBJECTIVE: The development of a novel surgical tool or technique for mitral valve repair can be hampered by cost, complexity, and time associated with performing animal trials. A dynamically pressurized model was developed to control pressure and flowrate profiles in intact porcine hearts in order to quantify mitral regurgitation and evaluate the quality of mitral valve repair. METHODS: A pulse duplication system was designed to replicate physiological conditions in explanted hearts. To test the capabilities of this system in measuring varying degrees of mitral regurgitation, the output of eight porcine hearts was measured for two different pressure waveforms before and after induced mitral valve failure. Four hearts were further repaired and tested. Measurements were compared with echocardiographic images. RESULTS: For all trials, cardiac output decreased as left ventricular pressure was increased. After induction of mitral valve insufficiencies, cardiac output decreased, with a peak regurgitant fraction of 71.8%. Echocardiography clearly showed increases in regurgitant severity from post-valve failure and with increased pressure. CONCLUSIONS: The dynamic heart model consistently and reliably quantifies mitral regurgitation across a range of severities. Advantages include low experimental cost and time associated with each trial, while still allowing for surgical evaluations in an intact heart.
OBJECTIVE: The development of a novel surgical tool or technique for mitral valve repair can be hampered by cost, complexity, and time associated with performing animal trials. A dynamically pressurized model was developed to control pressure and flowrate profiles in intact porcine hearts in order to quantify mitral regurgitation and evaluate the quality of mitral valve repair. METHODS: A pulse duplication system was designed to replicate physiological conditions in explanted hearts. To test the capabilities of this system in measuring varying degrees of mitral regurgitation, the output of eight porcine hearts was measured for two different pressure waveforms before and after induced mitral valve failure. Four hearts were further repaired and tested. Measurements were compared with echocardiographic images. RESULTS: For all trials, cardiac output decreased as left ventricular pressure was increased. After induction of mitral valve insufficiencies, cardiac output decreased, with a peak regurgitant fraction of 71.8%. Echocardiography clearly showed increases in regurgitant severity from post-valve failure and with increased pressure. CONCLUSIONS: The dynamic heart model consistently and reliably quantifies mitral regurgitation across a range of severities. Advantages include low experimental cost and time associated with each trial, while still allowing for surgical evaluations in an intact heart.
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