Avtor/Urednik		Poglajen, Gregor; Harlander, Matevž; Geršak, Borut
Naslov		Ex vivo study of altered mitral apparatus geometry in functional mitral regurgitation
Tip		članek
Vir		Heart Surg Forum
Vol. in št.		Letnik 13, št. 3
Leto izdaje		2010
Obseg		str. E172-6
Jezik		eng
Abstrakt		Background: Functional mitral regurgitation (FMR) in patients with ischemic or nonischemic cardiomyopathy has been related to several overlapping factors. In vivo, these factors are very difficult to study independently of dynamic processes, such as ventricular wall motion or annular contraction. We developed an ex vivo left ventricular model that allows independent variations of annular size, papillary muscle (PM) position, and transvalvular pressure. We tested the hypothesis that FMR is a consequence of an altered balance of the tethering and coapting forces acting on leaflets. Methods: Measurements were made on 4 excised porcine valves under physiological pressures and flows. Testing was done by systematically varying annular size and PM position. We evaluated 3 annulus sizes (normal, 15% dilation, and 25% symmetric dilation) by sequentially displacing PMs in lateral, posterolateral, and apicoposterolateral positions. Results: Our results show that annular dilation is a major determinant of mitral regurgitation. Displacement of PMs also affects the regurgitant flow, but to a much lesser degree. Apical and posterolateral PM displacement increases regurgitant flow to a higher degree than isolated lateral or posterolateral displacement. Increased transvalvular pressure decreases regurgitant flow for any given geometric configuration of the mitral valve (MV). Conclusion: Clinically observed pathologic configurations of the MV can be accurately reproduced ex vivo by altering the tethering and coapting forces acting on mitral leaflets. Our results support the mechanism of mitral regurgitation in which increased tethering forces and decreased coapting forces acting on the leaflets create the regurgitant orifice.
Deskriptorji		MITRAL VALVE INSUFFICIENCY CARDIOMYOPATHY, CONGESTIVE HEART VENTRICLE PRESSURE DISEASE MODELS, ANIMAL MODELS, CARDIOVASCULAR