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Circulation. 1991;84:2167-2180

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Circulation, Vol 84, 2167-2180, Copyright © 1991 by American Heart Association


ARTICLES

Mechanism of ischemic mitral regurgitation. An experimental evaluation

S Kaul, WD Spotnitz, WP Glasheen and DA Touchstone
Department of Medicine, University of Virginia School of Medicine, Charlottesville 22908.

BACKGROUND. Papillary muscle dysfunction (PMD) has been implicated in the pathogenesis of ischemic mitral regurgitation (MR). We hypothesized that ischemic MR is not caused by PMD and/or dysfunction of the myocardial regions from where the papillary muscles arise but is related to reduction in global left ventricular (LV) function. To test this hypothesis, three groups of dogs were studied. METHODS AND RESULTS. In group 1 dogs (n = 8), varying degrees of regional and global LV dysfunction were produced. In group 2 dogs (n = 7), the circulation to the papillary muscles was isolated from that of the rest of the LV. Dysfunction of one or both papillary muscles was produced without producing global LV dysfunction. Global LV dysfunction was also produced while keeping papillary muscle function intact. The degree of MR (assessed using contrast echocardiography) was correlated in both groups of dogs with thickening of the papillary muscles and regional and global LV function. In the group 3 dogs (n = 6), the spatial distribution of blood flow within each papillary muscle was determined during ischemia by using radiolabeled microspheres. Thickening of the papillary muscles was assessed at three different levels along their lengths and was correlated with average blood flow at these levels. In group 1 dogs, MR was noted only when global LV function was affected and its severity correlated inversely with global LV function (r = - 0.84 with peak positive LV dP/dt and r = -0.95 with global LV thickening, respectively). In comparison, there was poor correlation between MR and anterior and posterior papillary muscle thickening (r = - 0.38 and r = -0.49, respectively). In group 2 dogs, MR did not occur in the presence of either PMD or akinesia of the immediately adjacent LV myocardium. MR occurred only when global LV dysfunction was produced (with the papillary muscle function intact), and its severity correlated inversely with global LV function (r = -0.92 with LV dP/dt and r = -0.86 with global LV thickening, respectively). There was poor correlation between the degree of MR and thickening of the anterior and posterior papillary muscles (r = -0.24 and r = -0.38, respectively). In both groups of dogs, MR was associated with incomplete mitral leaflet closure (IMLC), and the severity of MR correlated linearly with the degree of IMLC (r = 0.98). MR was never associated with mitral valve prolapse. In the group 3 dogs, despite more inhomogeneous flow during ischemia to the anterior compared with the posterior papillary muscle, mean thickening of these muscles was similar (3 +/- 10% and 3 +/- 4%, respectively). Furthermore, there was minimal variability in thickening between different parts of the muscles (3 +/- 2% and 5 +/- 3%, respectively). CONCLUSIONS. It is concluded that PMD and/or dysfunction of the immediately adjacent LV myocardium does not result in MR. MR occurs during ischemia only when global LV function is affected, even when thickening of the papillary muscles and the immediately adjacent LV remains intact. MR in this situation is related to IMLC; the greater the degree of IMLC, the greater the MR. These findings suggest that the mechanism of ischemic MR is not related to PMD. There may also be important therapeutic implications of these findings.


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CirculationHome page
Y. Otsuji, M. D. Handschumacher, E. Schwammenthal, L. Jiang, J.-K. Song, J. L. Guerrero, G. J. Vlahakes, and R. A. Levine
Insights From Three-Dimensional Echocardiography Into the Mechanism of Functional Mitral Regurgitation : Direct In Vivo Demonstration of Altered Leaflet Tethering Geometry
Circulation, September 16, 1997; 96(6): 1999 - 2008.
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CirculationHome page
M. D. Cheitlin, J. S. Alpert, W. F. Armstrong, G. P. Aurigemma, G. A. Beller, F. Z. Bierman, T. W. Davidson, J. L. Davis, P. S. Douglas, L. D. Gillam, et al.
ACC/AHA Guidelines for the Clinical Application of Echocardiography : A Report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Committee on Clinical Application of Echocardiography) Developed in Collaboration With the American Society of Echocardiography
Circulation, March 18, 1997; 95(6): 1686 - 1744.
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Ann. Thorac. Surg.Home page
J. R. Glasson, M. Komeda, G. T. Daughters II, A. F. Bolger, A. MacIsaac, S. N. Oesterle, N. B. Ingels Jr, and D. C. Miller
Three-Dimensional Dynamics of the Canine Mitral Annulus During Ischemic Mitral Regurgitation
Ann. Thorac. Surg., October 1, 1996; 62(4): 1059 - 1067.
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J. Thorac. Cardiovasc. Surg.Home page
J. H. Gorman III, K. B. Gupta, J. T. Streicher, R. C. Gorman, B. M. Jackson, M. B. Ratcliffe, D. K. Bogen, and L. H. Edmunds Jr.
Dynamic Three-Dimensional Imaging of the Mitral Valve and Left Ventricle by Rapid Sonomicrometry Array Localization
J. Thorac. Cardiovasc. Surg., September 1, 1996; 112(3): 712 - 726.
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J. Thorac. Cardiovasc. Surg.Home page
R. C Gorman, J. S McCaughan, M. B Ratcliffe, K. B Gupta, J. T Streicher, V. A Ferrari, M. G St. John-Sutton, D. K Bogen, and L. H. Edmunds Jr.
Pathogenesis of acute ischemic mitral regurgitation in three dimensions
J. Thorac. Cardiovasc. Surg., April 1, 1995; 109(4): 684 - 693.
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CirculationHome page
R. A. Levine, G. J. Vlahakes, X. Lefebvre, J. L. Guerrero, E. G. Cape, A. P. Yoganathan, and A. E. Weyman
Papillary Muscle Displacement Causes Systolic Anterior Motion of the Mitral Valve : Experimental Validation and Insights Into the Mechanism of Subaortic Obstruction
Circulation, February 15, 1995; 91(4): 1189 - 1195.
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