MITRAL-VALVE REPLACEMENT WITH AND WITHOUT CHORDAL PRESERVATION IN PATIENTS WITH CHRONIC MITRAL REGURGITATION - MECHANISMS FOR DIFFERENCES IN POSTOPERATIVE EJECTION PERFORMANCE

Background. Standard mitral valve replacement (MVR) in patients with chronic mitral regurgitation consistently results in a decrease in postoperative left ventricular (LV) ejection performance. This fall in ejection performance has been attributed, at least in part, to unfavorable loading conditions imposed by the elimination of the low-impedance pathway for LV emptying into the left atrium. In contrast to standard MVR in which the chordae tendineae are severed, however, MVR with chordal preservation (MVR-CP) does not usually decrease LV ejection performance despite similar removal of the low-impedance pathway. The purpose of the present study was to define the mechanisms responsible for this discordance in postoperative ejection performance between MVR with and without chordal preservation. Methods and Results. Echocardiography and sphygmomanometer blood pressures were obtained in 15 patients with pure chronic mitral regurgitation before and 7-10 days after mitral valve surgery. These measurements were used to calculate ventricular volume, wall stress, and ejection fraction. Seven patients underwent MVR with chordal transection (MVR-CT), and eight patients underwent MVR-CP. MVR-CT resulted in no postoperative change in LV end-diastolic volume, a significant increase in LV end-systolic volume, a significant increase in end-systolic stress, from 89+/-9 to 111+/-12 g/cm2 (p<0.05), and a significant decrease in ejection fraction, from 0.60+/-0.02 to 36+/-0.02 (p<0.05). In contrast, patients who underwent MVR-CP had a significant decrease in LV end-diastolic and end-systolic volumes. End-systolic wall stress actually fell from 95+/-6 to 66+/-6 g/cm2 (p<0.05), and ejection fraction was unchanged (0.63+/-0.01 before and 0.61+/-0.02 after mitral valve surgery) instead of reduced. Conclusions. MVR-CT resulted in a decrease in ejection performance caused in part by an increase in end-systolic stress, which in turn increased end-systolic volume. Conversely, MVR-CP resulted in a smaller LV size, allowing a reduced end-systolic stress and preservation of ejection performance despite closure of the low-impedance left atrial ejection pathway.