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Transatrial Repair of Postinfarction Posterior Ventricular Septal Defect John A. Rousou, M.D., Richard M. Engelman, M.D., Robert H. greyer, M.D., Peter Whittredge, M.D., and Reed Schnider, M.D. ABSTRACT Repair of a postinfarction posterior ventricu- lar septal defect generally has been performed by ven- triculotomy in the infarct zone. This approach carries a significant mortality and morbidity from hemorrhage, ex- tending infarction, or further compromise of ventricular function secondary to suture placement. A successful transatrial repair of a postinfarction posterior ventricular septal defect is presented. The simplicity of this operation and the patient’s rapid recovery contrasted remarkably with the transventricular approach used in previous patients. Repair of postinfarction posterior ventricular septal de- fect (VSD) generally has been performed by incision in the infarct zone, as proposed by Daggett and colleagues [l]. Although excellent results have been achieved with this technique in some centers, the procedure is associ- ated with a high mortality and morbidity in most sur- geons’ hands [2-41. In this report we describe the second successful trans- atrial repair of an acquired VSD performed at our institu- tion. The first transatrial repair was performed for a traumatic septal rupture caused by closed-chest resusci- tation [5]. To our knowledge, the present successful re- pair is the first reported for posterior VSD secondary to septal necrosis after a large inferoposterior myocardial infarction. The patient‘s rapid postoperative recovery and lack of complications are attributed to the transatrial approach and prompted this case report. A 57-year-old man with recent onset of unstable an- gma was admitted with a large inferoposterior myo- cardial infarction. He was stable until six days after myo- cardial infarct, when a pansystolic murmur at the left sternal border, pulmonary edema, and rapidly dete- riorating renal function developed. Severe tachycardia and oliguria subsequently developed, requiring large doses of diuretics and inotropic support. His blood urea nitrogen rose rapidly to 50 mg/dl with a creatinine level of 2.0 mg/dl. The diagnosis of VSD was made by demon- strating a 4:l left-to-right shunt. An intraaortic balloon pump was inserted, and cardiac catheterization was per- formed on an emergency basis. The study demonstrated From the Baystate Medical Center, Springfield, MA Accepted for publication July 15, 1986. Address reprint requests to Dr. Rousou, Baystate Medical Center, 759 Chestnut St, Springfield, MA 01199. 50% left main stenosis, 100% occlusion of the right coro- nary artery near its origin, and 85% circumflex stenosis. Pulmonary artery pressures were 60130 mm Hg. A large VSD was confirmed by ventriculogram, which also re- vealed compromised left ventricular function (ejection fraction, 40%). At operation a large inferoposterior and right ventric- ular myocardial infarct was confirmed. A double coro- nary bypass was performed using saphenous vein grafts into the left anterior descending and circumflex marginal coronary arteries. Because of the extent of myocardium at risk, an attempt at transatrial repair of the VSD was undertaken. Exposure was obtained by opening the right atrium and retracting the tricuspid valve. The VSD was identified by injecting saline through a left ventricu- lar vent placed through the right superior pulmonary vein. The VSD measured approximately 2 cm in diame- ter and had an irregular necrotic border. The defect was closed (Figure) using a Dacron patch (Meadox Medical, Oakland, NJ) and pledgeted, interrupted mattress su- tures of 0-Tevdek (Deknatel, Floral Park, NY). After the completion of the repair, a Kay [6] tricuspid annulo- plasty was performed. Crystalloid cardioplegic arrest was used for the entire procedure, which required 115 minutes of ischemia. Oxygen saturation measurements obtained after the completion of the repair both in the operating room and, serially, in the intensive care unit showed elimination of the left-to-right shunt. Hemodynamic function improved postoperatively, al- lowing for the removal of the intraaortic balloon within 24 hours. Renal function returned to normal within the next several days. He was discharged eight days after operation with a Grade 2/6 soft systolic murmur at the left sternal border, but without evidence of a shunt by Doppler study or any element of congestive heart fail- ure. He was seen three months postoperatively, at which time he was on maintenance therapy of digoxin and furosemide (Lasix) without congestive heart failure or disability (American Heart Association Class 11). Comment The transatrial repair of postinfarction VSDs has not gained popularity because of three potential problems using this technique. First, the trabeculations of the right ventricle could make the exact identification and expo- sure of the VSD difficult. Second, the placement of a patch on the right side of the septum is not optimal because of the left-to-right pressure gradient during sys- tole. Third, placement of sutures from the right side through the tricuspid valve may interfere with chordae 665 Ann Thorac Surg 43665-666, June 1987
