To investigate the mechanism and time of onset of ventricular dysfunction after mitral valve replacement, 18 patients with pure, severe mitral regurgitation (of whom 10 underwent mitral valve repair and 8 standard mitral valve replacement with papillary muscle excision) were studied by intraoperative two-dimensional echocardiography immediately before and immediately after the operative procedure. No patient sustained a perioperative myocardial infarction or had any residual mitral regurgitation. Although preoperative hemodynamics were similar, postoperatively the patients with valve repair had a lower pulmonary capillary wedge pressure than did the patients with valve replacement (8.6 +/- 1.9 versus 14.4 +/- 7.5 mm Hg, p less than 0.04). Although intraoperative echocardiographic ejection fraction fell significantly after mitral valve replacement (0.64 +/- 0.11 to 0.40 +/- 0.09, p less than 0.0001), it was maintained after valve repair (0.44 +/- 0.20 to 0.49 +/- 0.16, p = NS). Additionally, regional myocardial contractile abnormalities in the anterior and posterior septum were detected immediately after the procedure by intraoperative echocardiography in the patients with valve replacement, but not in those with repair. These postoperative regional contractile abnormalities after papillary muscle resection have not been described previously. Resection of the papillary muscles may disrupt the muscle bundle alignment and induce contractile abnormalities remote from the excised muscle. This study demonstrated that significant global and regional ventricular dysfunction develops immediately after removal of the papillary muscles, whereas myocardial contractility is preserved in patients undergoing mitral valve repair. Therefore, with intraoperative echocardiography to assure minimal residual regurgitation, surgeons should attempt to preserve ventricular function by performing mitral valve reconstruction in patients with mitral regurgitation.
Systolic anterior motion (SAM) of the mitral valve, once considered to be pathognomonic of hypertrophic cardiomyopathy, has been reported in the absence of asymmetric septal hypertrophy. Of the 1,000 open heart operations performed with intraoperative two-dimensional epicardial echocardiography monitoring, four patients developed intraoperative dynamic left ventricular outflow obstruction associated with systolic anterior motion of the mitral valve that was not present preoperatively: three cases of mitral valve annuloplasty with Carpentier ring insertion and one of coronary artery bypass grafting. Though no patient had asymmetric septal hypertrophy or echocardiographic evidence of outflow obstruction by either preoperative cardiac catheterization or echocardiography, intraoperative two-dimensional epicardial echocardiography revealed SAM, and hyperdynamic left ventricles with three of these patients having documented left ventricular outflow tract gradients causing hemodynamic compromise. (Case 4 was hemodynamically stable following mitral valve repair, but had SAM and significant residual mitral regurgitation [MR] requiring reinstitution of cardiopulmonary bypass and re-repair). Measurement of mitral annular dimension demonstrated a normal decrease in size from diastole to systole in control operative subjects but not in the patients who developed outflow obstruction. The pathophysiology, treatment, and role of intraoperative echocardiography of dynamic left ventricular outflow tract obstruction are discussed.
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