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J Thorac Cardiovasc Surg 1995;109:684-693
© 1995 Mosby, Inc.


SURGERY FOR ACQUIRED HEART DISEASE

Pathogenesis of acute ischemic mitral regurgitation in three dimensions

Robert C Gorman, MD (by invitation), James S McCaughan, MD (by invitation), Mark B Ratcliffe, MD (by invitation), Krishanu B Gupta, PhD (by invitation), James T Streicher, MSE (by invitation), Victor A Ferrari, MD (by invitation), Martin G St. John-Sutton, MBBS, FRCP (by invitation), Daniel K Bogen, PhD, MD (by invitation), L. Henry Edmunds, Jr., MD


Philadelphia, Pa

Supported by grant HL 36308 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.

Address for reprints: L. Henry Edmunds, Jr., MD, Department of Surgery, 4 Silverstein, Hospital of the University of Pennsylvania, 3400 Spruce St., Philadelphia, PA, 19104.

Abstract

Changes in the geometric and intravalvular relationships between subunits of the ovine mitral valve were measured before and after acute posterior wall myocardial infarction in three dimensions by means of sonomicrometry array localization. In 13 sheep, nine sonomicrometer transducers were attached around the mitral anulus and to the tip and base of each papillary muscle. Five additional transducers were placed on the epicardium. Snares were placed around three branches of the circumflex coronary artery. One to 2 weeks later, echocardiograms, dimension measurements, and left ventricular pressures were obtained before and after the coronary arteries were occluded. Data were obtained from seven sheep. Coronary occlusion infarcted 32% of the posterior left ventricle and produced 2 to 3+mitral regurgitation by Doppler color flow mapping. Multidimensional scaling of dimension measurements obtained from sonomicrometry transducers produced three-dimensional spatial coordinates of each transducer location throughout the cardiac cycle before and after infarction and onset of mitral regurgitation. After posterior infarction, the mitral anulus enlarges asymmetrically along the posterior anulus, and the tip of the posterior papillary muscle moves 1.5 ± 0.3 mm closer to the posterior commissure at end-systole. The posterior papillary muscle also elongates 1.9 ± 0.3 mm at end-systole. The left ventricle enlarges asymmetrically and ventricular torsion along the long axis changes. The development of postinfarction mitral regurgitation appears to be the consequence of multiple small changes in ventricular shape and contractile deformation and in the spatial relationships of mitral valvular subunits. (J THORAC CARDIOVASC SURG 1995;109:684-93)




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