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J Thorac Cardiovasc Surg 1994;107:416-0423
© 1994 Mosby, Inc.
Surgery for Acquired Heart Disease |
Charleston, S.C.
Supported in part by National Institutes of Health NHLBI R01 HL38185grant (Blase A. Carabello) and medical research funds from the Veterans Administration, Washington, D.C. (Blase A. Carabello, Michael R. Zile, George Cooper IV).
Received for publication Sept. 16, 1992. Accepted for publication July 12, 1993. Address for reprints: Blase A. Carabello, MD, Cardiology Division, Medical University of South Carolina, 816 Clinical Science Building, 171 Ashley Ave., Charleston, SC 29425.
Abstract
Severe mitral regurgitation (regurgitant fraction 0.75 ± 0.02) was created in eight dogs by our closed-chest chordal rupture technique. After 3 months of chronic mitral regurgitation all indices of contractile function were depressed. Mitral valve repair was then attempted. Postoperative regurgitant fraction was reduced compared with the preoperative value in all eight dogs. Concomitantly, forward cardiac output increased in all dogs and pulmonary capillary wedge pressure fell in all dogs. However, in some dogs, significant regurgitation persisted despite repair. Postoperative regurgitant fraction ranged from 0% to 60%. Postoperative residual regurgitant fraction was related significantly to postoperative cardiac output (r = 0.99), pulmonary capillary wedge pressure (r = 0.77), ejection fraction (r = 0.75), and two indices of contractile functionthe mass-corrected end-systolic stress volume relationship (r = 0.87) and end-systolic stiffness (r = 0.93). In general, these parameters returned to their normal values before mitral regurgitation when postoperative regurgitant fraction was less than 30%. Myocytes isolated from the ventricles at the end of study also demonstrated normal contractile function when regurgitant fraction was less than 30%. (J THORAC CARDIOVASC SURG 1994;107:416-23)
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