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Ann Thorac Surg 1996;62:1059-1067
© 1996 The Society of Thoracic Surgeons
Department of Cardiovascular and Thoracic Surgery and Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford; and Cardiac Surgery and Cardiology Sections, Department of Veterans Affairs Medical Center, and Department of Cardiovascular Physiology and Biophysics, Research Institute of the Palo Alto Medical Foundation, Palo Alto, California
Background. It has been suggested that ischemic mitral regurgitation results, at least in part, from generalized end-systolic mitral annulus (MA) dilatation, but the role of the MA is incompletely understood and the segmental dynamics of the MA during left ventricular ischemia have not been described.
Methods. We used radiopaque markers and simultaneous biplane videofluoroscopy to measure three-dimensional in vivo lengths of eight MA segments in 7 sedated dogs before and after induction of ischemic MR (produced by circumflex coronary artery balloon occlusion and verified by Doppler echocardiography). As viewed from the left atrium, the MA segment between markers 1 and 2 (S12) was defined as starting at the posteromedial commissure, and remaining segments were numbered sequentially clockwise around the MA (ie, the posterior MA encompassed S12, S23, S34, S45; the anterior MA included S56, S67, S78, S81). Marker images obtained 7 to 12 days after implantation were used to construct x, y, and z coordinates of each marker at end-diastole and end-systole.
Results. During regional (posterolateral walls) left ventricular ischemia, the end-systolic MA area increased (4.9 ± 0.8 cm2 [control] versus 5.9 ± 0.6 cm2; p = 0.005). End-systolic MA segment lengths were as follows (control, ischemia [mm, mean ± standard deviation]): S12 = 9 ± 2, 10 ± 3; S23 = 10 ± 2, 12 ± 3; S34 = 13 ± 1, 15 ± 1; S45 = 8 ± 2, 9 ± 2; S56 = 11 ± 2, 11 ± 2; S67 = 12 ± 2, 12 ± 2; S78 = 10 ± 3, 11 ± 2; and S81 = 11 ± 1, 12 ± 1. Values for S12, S23, S34, and S81 were significant (p
0.05 for control versus ischemia by paired t test).
Conclusions. During ischemic mitral regurgitation, the MA enlarged at end-systole, but in an asymmetric manner; most posterior annular segments lengthened, whereas most anterior annular segment lengths did not change. These data suggest that alterations in regional MA mechanics may be important in the pathogenesis of ischemic mitral regurgitation. Further three-dimensional studies of MA dynamics and shape should be conducted so that new knowledge may result in improved mitral valve surgical techniques.
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