Gundry S R, Coughlin T R, Goldberg N H, Hankins J R, Mackenzie C F, Flowers J, Moorman R, McLaughlin J S
Department of Surgery, University of Maryland School of Medicine, Baltimore 21201.
Ann Thorac Surg. 1988 Sep;46(3):278-82. doi: 10.1016/s0003-4975(10)65925-5.
Survival after repair of postinfarction ventricular septal defects remains poor, often due to extensive loss of contractile muscle in the septum or left ventricle. We evaluated whether a contractile flap of right ventricular muscle could be used to repair a similar ventricular septal defect to augment left ventricular performance in 7 fully instrumented mongrel dogs (weight, 23 to 28 kg). By using hypothermic bypass and cold fibrillatory arrest, a trapezoidal right ventricle flap was fashioned from the free wall of the mid to lower right ventricle, basing its widest portion anteriorly on the septum and left ventricle. A large, 2-cm-diameter core of septum was excised beneath this flap to simulate a postinfarct ventricular septal defect. The right ventricular flap was then invaginated through the defect and sewn to the left ventricular side of the septum with pledgeted sutures taken full thickness through the flap and septum in a "vest-over-pants" fashion. Contraction of the right ventricular flap was confirmed visually and by postbypass multiple gated acquisition scans. The right ventricular defect was closed with fascia lata. All dogs were weaned from bypass without inotropes. Precardiac and postcardiac outputs of 2.5 +/- 0.5 versus 2.3 +/- 0.4 L/min and left ventricular end-diastolic pressures of 4 +/- 2 versus 4 +/- 3 mm Hg were identical. No shunts were detected by oxygen saturation. Autopsies confirmed the integrity of the repair. We conclude that septal defects can be repaired by using contractile right ventricular muscle, thus preserving left ventricular function. This technique offers promise for repair of postinfarction ventricular septal defects by using autologous, already conditioned to contract, cardiac muscle, but its application in humans must await long-term testing.
心肌梗死后室间隔缺损修补术后的生存率仍然很低，这通常是由于室间隔或左心室的收缩性肌肉大量丧失所致。我们评估了右心室肌肉的收缩瓣是否可用于修复类似的室间隔缺损，以增强7只完全植入监测装置的杂种犬（体重23至28千克）的左心室功能。通过使用低温体外循环和冷颤停搏，从右心室中下部的游离壁制作一个梯形右心室瓣，其最宽部分向前基于室间隔和左心室。在该瓣下方切除一个直径2厘米的大的室间隔核心，以模拟心肌梗死后的室间隔缺损。然后将右心室瓣通过缺损内翻，并以“背心套裤子”的方式用带垫片的缝线全层穿过瓣和室间隔，缝至室间隔的左心室侧。通过视觉观察和体外循环后多次门控采集扫描确认右心室瓣的收缩。用阔筋膜关闭右心室缺损。所有犬均在不使用血管活性药物的情况下脱离体外循环。心脏前和心脏后的输出量分别为2.5±0.5对2.3±0.4升/分钟，左心室舒张末期压力分别为4±2对4±3毫米汞柱，两者相同。通过血氧饱和度未检测到分流。尸检证实了修补的完整性。我们得出结论，室间隔缺损可以通过使用收缩性右心室肌肉进行修复，从而保留左心室功能。这项技术为使用自体的、已经适应收缩的心肌修复心肌梗死后的室间隔缺损提供了希望，但其在人类中的应用必须等待长期测试。
