CORONARY ARTERY DISEASE Mitral valve prolapse in short - term experimental coronary occlusion : a possible mechanism of ischemic mitral regurgitation

Experimental coronary occlusions were carried out in 12 closed-chest dogs to investigate the functional anatomic characteristics of the mitral valve complex during acute myocardial ischemia. Two-dimensional echocardiography was used to assess left ventricular function, the mitral valve complex, and left atrial size. Presence of mitral regurgitation was assessed by left ventricular contrast echocardiography. Thirty-seven coronary occlusions of up to 10 min in duration were carried out in proximal or distal locations in the left anterior descending and the left circumflex coronary arteries. Mitral regurgitation, which was mild in severity as judged by a small rise in pulmonary artery wedge pressures, was observed in 15 of 37 brief coronary occlusion experiments. Mitral valve prolapse was noted in all 15 experiments, as well as in four additional studies in which mitral regurgitation was not seen. The development of experimental mitral valve prolapse was explained by measurements that demonstrated a relative displacement of the papillary muscle tips toward the mitral orifice. We conclude that mitral valve prolapse is a common sequela of short-term coronary occlusion and is often associated with mild mitral regurgitation. Relative displacement of ischemic papillary muscles toward the mitral orifice appears to be a likely mechanism of acute ischemic mitral valve prolapse. Circulation 68, No. 1, 183-189, 1983. THE CLINICAL MANIFESTATIONS of papillary muscle dysfunction were first described by Burch et al.' in 1963. They proposed two major pathophysiologic mechanisms by which ischemic dysfunction may lead to mitral regurgitation and speculated that failure of an ischemic or fibrotic papillary muscle to shorten during ventricular contraction would cause mitral valve leaflet prolapse. Another hypothesis emphasized incomplete valve leaflet coaptation that resulted from abnormal spatial relationships between papillary muscle and mitral cusps caused by an aneurysmal left ventricle and displaced papillary muscle accompanying From the Division of Cardiology, Department of Medicine, CedarsSinai Medical Center, the Wadsworth Veterans Administration Medical Center, and UCLA School of Medicine, Los Angeles. Supported in part by grants HL 14644-09 and HL 17651-07 from the National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda; the American Heart Association, Greater Los Angeles Affiliate, Group Investigatorship Award; the Ahmanson Foundation; the W. M. Keck Foundation; and the Mitchell Family Foundation. Dr. Tei is a Senior Investigator of the American Heart Association, Greater Los Angeles Affiliate. Address for correspondence: Pravin M. Shah, M.D., Cardiology (691/11 1E), Wadsworth Veterans Administration Medical Center, Wilshire & Sawtelle Blvds., Los Angeles, CA 90073. Received Jan. 14, 1983; revision accepted March 17, 1983. Vol. 68, No. 1, July 1983 regional myocardial infarction. Divergent conclusions were derived from limited studies of isolated papillary muscle infarction in mongrel dogs that demonstrated no significant mitral regurgitation2'; other studies showed that papillary muscle dysfunction, acting in concert with abnormal left ventricular wall dynamics or dilatation, could indeed produce mitral regurgitation.54 In a review of the functional anatomic characteristics of mitral regurgitation, Perloff and Roberts9 observed that if papillary muscle dysfunction is present, then the chordae tendinae slacken as the ventricular apex moves toward the mitral anulus in systole, causing valve leaflets to prolapse under ventricular pressure into the left atrium. Steelman et al.10 described midsystolic clicks, which may suggest mitral prolapse in the clinical syndrome of papillary muscle dysfunction. The relationship between mitral regurgitation and short-term myocardial ischemia has not been extensively studied with two-dimensional echocardiography, even though this noninvasive method is suitable for comprehensive assessment of regional wall motions and ventricular function and for systematic de183 by gest on July 5, 2017 http://ciajournals.org/ D ow nladed from