Ann Thorac Surg 1999;67:758-759
© 1999 The Society of Thoracic Surgeons
a Division of Cardiovascular-Thoracic Surgery, Childrens Memorial Hospital, 2300 Childrens Plaza, M/C Box 22, Chicago, IL 60614, USA
Doctor Hisatomi and colleagues have addressed a very focused question, Is direct closure dangerous for treatment of doubly committed subarterial ventricular septal defect? They operated on 21 patients with conal ventricular septal defects, all of whom underwent direct closure of the ventricular septal defect with pledgeted sutures. Exposure was through the pulmonary artery, with the sutures tied at the base of the pulmonary valve. Indications for operation were aortic valve prolapse or aortic valve regurgitation, or both. There were no residual ventricular septal defects, and all patients had either reduction or nonprogression of their aortic insufficiency. They concluded that direct suture closure is safe and reliable for patients with doubly committed subarterial ventricular septal defects. The technique was particularly effective in younger patients (< 10 years of age), in that subgroup most children had no postoperative aortic regurgitation.
The approach to the patient with a doubly committed subarterial (conal, supracristal) ventricular septal defect has evolved considerably in the past decade. Many of the features of the authors current review I strongly agree with, including (1) aortic valve prolapse is an indication for operative intervention in these patients, (2) early ventricular septal defect closure results in preservation of the aortic valve; and (3) excellent results can be obtained by approaching the conal ventricular septal defect through the pulmonary artery.
Since initially reviewing the manuscript I have had the opportunity in 1 patient to directly close a conal ventricular septal defect as described by the authors, and the technique worked well. However, I also had a recent experience with a patient with a larger conal ventricular septal defect in whom the direct closure technique was not successful. That patient had prolapse of both the right and the noncoronary cusps through the ventricular septal defect. In keeping with the report by Dr Hisatomi and colleagues, I proceeded with direct closure. This approach resulted in severe aortic valve insufficiency (by intraoperative transesophageal echocardiography), which was corrected by removing the direct closure sutures and then using a patch for the ventricular septal defect closure. This child left the hospital with only trivial aortic valve insufficiency. It is my opinion that a patient with prolapse of more than just the right coronary cusp or with a large ventricular septal defect is not necessarily a candidate for direct suture closure.
In our review of conal ventricular septal defects, we stated that 
We would agree with Spencer and colleagues that it is very important to repair the defect with a patch because there is a danger of pulling the valve down to the septum and making the aortic valve insufficiency worse. Indeed we believe that the patch helps support the aortic valve, preventing prolapse and progressive aortic insufficiency.
It was Spencer and associates  who stated in their review that "direct suture produces a downward displacement of the annulus and destruction of commissural support, precise patch closure preserves annular level and commissural support." Of note, in our review of 36 children, all of whom underwent repair with a patch, there were no residual ventricular septal defects, and mild aortic valve insufficiency became trivial in many and has remained at the trivial level at follow-up . No patient with mild or even moderate aortic insufficiency had progression of the aortic valve insufficiency, and this lack of progression has continued during long-term follow-up.
The authors have successfully answered the question they posed. The question they have not answered is, Which is betterpatch or direct suture closure? What is needed to answer that question is a randomized, prospective study of patch versus direct closure of doubly committed subarterial ventricular septal defect. In point of fact such a study would be extremely difficult to perform because of the many clinically significant variables. I believe that the contribution of the present report is its demonstration that direct closure of small conal ventricular septal defects is safe and reliable in reducing mild aortic insufficiency. Whether that approach is actually better than patch closure remains to be demonstrated. I think it is important to recognize that the authors technique may not be applicable for the patient with a large ventricular septal defect or with prolapse of more than one cusp of the aortic valve. Just as important as the results of direct closure is the affirmation by the authors that these patients should undergo repair early in life; that aortic valve prolapse alone is an indication for operation; and that the conal ventricular septal defect may be successfully approached through the pulmonary artery.
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