Nonsurgical closure of congenital and acquired ventricular septal defects (VSD) has become increasingly acceptable with the availability of various occlusion systems that allow percutaneous treatment of muscular and membranous defects. This study describes a series of 12 patients (0.2–74‐years‐old) who underwent defect closure with six different occlusion systems. Device selection according to anatomy and outcome is highlighted. Seven VSDs were located in the membranous part of the septum, five in the mid‐muscular septum. Complex heart lesions were present in five postmyocardial infarction VSD in one and residual postsurgical defects in three patients. The size of the VSD ranged from 2.6 to 10 mm. The applied devices were: Amplatzer muscular VSD occluder (n = 4), Amplatzer septal occluder (n = 2), Amplatzer duct occluder (n = 1), Amplatzer membranous VSD occluder (n = 2), Nit‐Occlud coil (n = 2), and Cook PDA coil (n = 1). The devices were implanted successfully in nine patients. There was complete VSD closure in eight patients within the first 24 hours. In one patient, a trivial residual shunt disappeared at 6 months follow‐up. Because of device instability, two occluders were removed during catheterization. In two other cases, tricuspid valve tissue was entrapped in the occluder and had to be removed surgically, one of them during the consecutive Rastelli operation. Neither significant arrhythmia, nor thromboembolism or hemolysis occurred in out patients during follow‐up. Transcatheter closure of VSD is an attractive alternative to surgery. In complex congenital heart disease, surgical‐interventional hybrid therapy may improve morbidity and total outcome. The recently developed Amplatzer VSD devices allow closure of muscular and membranous VSDs. Implantation and short‐term follow‐up are superior to the formerly used devices. Long‐term effects have to be evaluated in further studies.
The incidence of doubly committed lesions is high in our experience, frequently associated with AoVR and other associated malformation. Early detection is crucial to prevent further progression of the disease. Patch closure remains the gold standard in management, not least since it allows simultaneous repair of associated intracardiac defects.
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