Left ventricular remodeling early after correction of mitral regurgitation: maintenance of stroke volume with decreased systolic indexes

Objective: Mitral valve repair for mitral regurgitation is followed by left ventricle adjustment to new preload and afterload. We evaluated left ventricular geometry and function immediately after mitral valve repair for degenerative prolapse.

Methods: We prospectively studied 25 patients undergoing mitral valve repair; 15 patients undergoing a coronary artery bypass graft served as controls to determine the impact of cardiopulmonary bypass and cardioplegic arrest on left ventricular function. Intraoperative transesophageal echocardiography was conducted after sternotomy before initiation of cardiopulmonary bypass and after termination of cardiopulmonary bypass and protamine infusion. Simultaneous pulmonary catheter data ensured that the images were obtained under similar hemodynamic conditions.

Results: Immediately after mitral valve repair, left ventricular fractional area change decreased significantly from 65% ± 7% to 52% ± 8% (P < .001). Left ventricular end-diastolic area decreased minimally (21.3 ± 5.3 cm(2) vs 19.4 ± 4.5 cm(2); P = .005), whereas left ventricular end-systolic area increased significantly (7.5 ± 2.3 cm(2) vs 9.3 ± 2.5 cm(2); P < .001). Notably, forward stroke volume (thermodilution) remained similar (63 ± 24 mL vs 66 ± 19 mL; P = .5). No significant difference was found in controls between pre- cardiopulmonary bypass and post-cardiopulmonary bypass fractional area change (54% ± 12% vs 57% ± 10%; P = .19), left ventricular end-diastolic area (16.6 ± 6.2 cm(2) vs 15.7 ± 5.0 cm(2); P = .32), and stroke volume (72 ± 29 mL vs 65 ± 19 mL; P = .15); they had a slight decrease in left ventricular end-systolic area (7.9 ± 4.4 cm(2) vs 6.9 ± 3.2 cm(2); P = .03).

Conclusions: Early after correction of mitral regurgitation, left ventricular fractional area change decreases significantly, primarily as the result of a larger end-systolic dimension. This may be a compensatory mechanism to prevent augmentation of forward stroke volume after mitral valve repair.