Goldman M E, Mora F, Guarino T, Fuster V, Mindich B P
J Am Coll Cardiol. 1987 Sep;10(3):568-75. doi: 10.1016/s0735-1097(87)80199-7.
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.
为研究二尖瓣置换术后心室功能障碍的机制和发病时间，对18例单纯重度二尖瓣反流患者（其中10例行二尖瓣修复术，8例行标准二尖瓣置换术并切除乳头肌）在手术操作前及操作后立即进行术中二维超声心动图检查。所有患者均未发生围手术期心肌梗死，也无残余二尖瓣反流。尽管术前血流动力学相似，但术后二尖瓣修复患者的肺毛细血管楔压低于二尖瓣置换患者（8.6±1.9对14.4±7.5mmHg，p<0.04）。尽管二尖瓣置换术后术中超声心动图测得的射血分数显著下降（0.64±0.11至0.40±0.09，p<0.0001），但二尖瓣修复术后射血分数得以维持（0.44±0.20至0.49±0.16，p=无显著性差异）。此外，二尖瓣置换患者术后立即通过术中超声心动图检测到前间隔和后间隔区域心肌收缩异常，而二尖瓣修复患者未出现这种情况。乳头肌切除术后的这些术后区域收缩异常此前尚未见报道。乳头肌切除可能会破坏肌束排列，并诱发远离切除肌肉部位的收缩异常。本研究表明，切除乳头肌后立即出现显著的全心和局部心室功能障碍，而二尖瓣修复患者的心肌收缩力得以保留。因此，在术中超声心动图确保残余反流最小的情况下，外科医生应尝试通过对二尖瓣反流患者进行二尖瓣重建来保留心室功能。
