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J Thorac Cardiovasc Surg 2003;125:559-569
© 2003 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

Ischemia in three left ventricular regions: Insights into the pathogenesis of acute ischemic mitral regurgitation

From the Department of Cardiovascular and Thoracic Surgery,^a Division of Cardiovascular Medicine,^c and the Department of Biostatistics,^e Stanford University School of Medicine, Stanford; the Department of Surgery,^b Loma Linda University Medical Center, Loma Linda; and the Laboratory of Cardiovascular Physiology and Biophysics,^d Research Institute of the Palo Alto Medical Foundation, Palo Alto, Calif.

Supported by grants HL-29589 and HL-67025 from the National Heart, Lung, and Blood Institute. Drs Timek, Tibayan, Dagum, and Lai are Carl and Leah McConnell Cardiovascular Surgical Research Fellows. Drs Timek, Dagum, and Tibayan were also supported by NHLBI Individual Research Service Awards HL-10452, HL-10000, and HL-67563, respectively. Dr Timek is also a recipient of the Thoracic Surgery Foundation Research Fellowship Award. Dr Lai was supported by a fellowship from the American Heart Association, Western States Affiliate.

Read at the Eighty-second Annual Meeting of The American Association for Thoracic Surgery, Washington, DC, May 5-8, 2002.

Received for publication April 29, 2002. Revisions requested July 8, 2002; revisions received Aug 4, 2002. Accepted for publication Aug 15, 2002. Address for reprints: D. Craig Miller, MD, Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247 (E-mail: dcm{at}stanford.edu).

Background: Acute posterolateral left ventricular ischemia in sheep results in ischemic mitral regurgitation, but the effects of ischemia in other left ventricular regions on ischemic mitral regurgitation is unknown.
Methods: Six adult sheep had radiopaque markers placed on the left ventricle, mitral annulus, and anterior and posterior mitral leaflets at the valve center and near the anterior and posterior commissures. After 6 to 8 days, animals were studied with biplane videofluoroscopy and transesophageal echocardiography before and during sequential balloon occlusion of the left anterior descending, distal left circumflex, and proximal left circumflex coronary arteries. Time of valve closure was defined as the time when the distance between leaflet edge markers reached its minimum plateau, and systolic leaflet edge separation distance was calculated on the basis of left ventricular ejection.
Results: Only proximal left circumflex coronary artery occlusion resulted in ischemic mitral regurgitation, which was central and holosystolic. Delayed valve closure (anterior commissure, 58 ± 29 vs 92 ± 24 ms; valve center, 52 ± 26 vs 92 ± 23 ms; posterior commissure, 60 ± 30 vs 94 ± 14 ms; all P < .05) and increased leaflet edge separation distance during ejection (mean increase, 2.2 ± 1.5 mm, 2.1 ± 1.9 mm, and 2.1 ± 1.5 mm at the anterior commissure, valve center, and posterior commissure, respectively; P < .05 for all) was seen during proximal left circumflex coronary artery occlusion but not during left anterior descending or distal left circumflex coronary artery occlusion. Ischemic mitral regurgitation was associated with a 19% ± 10% increase in mitral annular area, and displacement of both papillary muscle tips away from the septal annulus at end systole.
Conclusions: Acute ischemic mitral regurgitation in sheep occurred only after proximal left circumflex coronary artery occlusion along with delayed valve closure in early systole and increased leaflet edge separation throughout ejection in all 3 leaflet coaptation sites. The degree of left ventricular systolic dysfunction induced did not correlate with ischemic mitral regurgitation, but both altered valvular and subvalvular 3-dimensional geometry were necessary to produce ischemic mitral regurgitation during acute left ventricular ischemia.

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