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J Thorac Cardiovasc Surg 2007;133:912-918
© 2007 The American Association for Thoracic Surgery
Surgery for Congenital Heart Disease |
a Department of Cardiology, Childrens HospitalBoston, Boston, Mass
b Department of Cardiovascular Surgery, Childrens HospitalBoston, Boston, Mass
c Department of Pediatrics, Harvard Medical School, Boston, Mass.
Received for publication August 7, 2006; revisions received September 15, 2006; accepted for publication September 28, 2006. * Address for reprints: Jeffery Meadows, MD, Department of Cardiology, Childrens HospitalBoston, 300 Longwood Ave, Boston, MA 02115. (Email: Jeffrey.Meadows{at}cardiochboston.org).
Objective: Creation or enlargement of a ventricular septal defect is indicated in rare clinical situations. In the setting of double-outlet right ventricle requiring single-ventricle palliation, left ventricular outflow tract obstruction caused by progressive restriction at the ventricular septal defect poses an uncommon but recognized dilemma. In this situation surgical ventricular septal defect enlargement may be desirable but risks damage to the atrioventricular valve or conduction system. We report the results of a novel technique for transcatheter creation or enlargement of ventricular septal defects as an alternative to reoperation when decompression of an isolated ventricle is indicated.
Methods: Eight patients had undergone transcatheter ventricular septal defect enlargement or creation, and 3 of these patients had undergone 4 prior surgical attempts at left ventricular decompression. Ventricular aneurysms had developed in 3 patients before intervention.
Results: Five patients underwent ventricular septal defect creation, and 3 patients underwent enlargement of existing ventricular septal defects. Initial intervention resulted in a decreased ventricular septal defect pressure gradient from 76.9 mm Hg to 20.3 mm Hg (P = .004). There was no procedural mortality or sustained heart block. Two patients had moderate-to-severe atrioventricular valve regurgitation, and 1 required surgical repair. At last follow-up, all ventricular septal defects remained patent, with recurrent obstruction in the majority of cases caused by muscular hypertrophy beyond the stent margins. In 1 patient a ventricular aneurysm has regressed in size. Repeat intervention reduced recurrent obstruction, but recurrence was the rule.
Conclusions: When reoperation is considered high risk, transcatheter creation and enlargement of ventricular septal defects is possible with excellent short-term results. Recurrent obstruction is common but responds to repeated intervention. Further studies are required to establish clinical benefit.
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