DISTORTIONS OF THE MITRAL-VALVE IN ACUTE ISCHEMIC MITRAL REGURGITATION

Background. In the absence of papillary muscle rupture, the precise de formations that cause acute postinfarction mitral valve regurgitation are not understood and impair reparative efforts. Methods. In 6 Dorset t hybrid sheep, sonomicrometry transducers were placed around the mitr al annulus (n = 6) and at the tips and bases of both papillary muscles (n = 4). Later, specific circumflex coronary arteries were occluded t o infarct approximately 32% of the posterior left ventricle and produc e acute 2 to 3+ mitral regurgitation. Before and after infarction, dis tance measurements between sonomicrometry transducers produced three-d imensional coordinates of each transducer every 5 ms. Results. After i nfarction, the annulus dilated asymmetrically orthogonal to the line o f leaflet coaptation, but the annular area increased only 9.2% +/- 6.3 % (p = 0.02). At end-systole, posterior papillary muscle length increa sed 2.3 +/- 0.9 mm (p = 0.005); the posterior papillary muscle tip mov ed closer to the annular plane and centroid, and the anterior papillar y muscle tip moved away.Conclusions. Small deformations in mitral valv ular spatial geometry after large posterior infarctions are sufficient to produce moderate to severe mitral regurgitation. The most importan t changes are asymmetric annular dilatation, prolapse of leaflet tissu e tethered by the posterior papillary muscle, and restriction of leafl et tissue attached to the anterior papillary muscle. (C) 1997 by The S ociety of Thoracic Surgeons.