PubMed1988
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.