Transcatheter device closure of ventricular septal defects: Immediate results and intermediate-term follow-up

Background Transcatheter closure is an accepted mode of treatment in selected cases of congenital heart disease. Lately, this technology has been applied to closure of ventricular septal defect (VSD). Methods and Results We performed percutaneous transcatheter closure of VSD in 30 patients. The location of VSD was perimembranous in 28 patients and muscular trabecular in 2. Two (7%) patients also had left ventricular–right atrial communication. There were 17 male subjects and 13 female subjects, with an age range of 5.5 to 33 years (mean ± SD, 12.9 ± 5.7; median 12.2). The diameter of VSD ranged from 3 to 8 mm (mean ± SD 4.7 ± 1.3; median 4.5). In 5 (17%) patients, the pulmonary to systemic blood flow (Qp/Qs) was ≥2.1 (range 2.0 to 2.6). The defect was at least 6 or 8 mm from the aortic valve in patients in whom a 12- or 17-mm Rashkind double umbrella device was deployed, respectively. In 1 patient, the defect was closed with a detachable stainless steel coil, size 8 mm, with 4 loops (8 × 4). The devices were successfully deployed in 87% of patients. In 6 (20%) patients, the procedure had to be repeated primarily because of the use of undersized umbrella deices. Unsuccessful deployment of the device occurred in 4 (13%) patients. In one of these procedures, the coil embolized to the left pulmonary artery, and it was successfully retrieved. A minimal residual shunt seen as a thin streak on transthoracic color flow mapping persisted in 8 (30%) patients, which remained unchanged over a follow-up period of 5 to 28 (17.1 ± 6.4) months. Both patients with left ventricular/right atrial communication showed complete abolition of the shunt. No patient developed new-onset aortic or tricuspid regurgitation or intravascular hemolysis. At follow-up, no patient had developed infective endocarditis, bundle branch block, or late valvular insufficiency. Conclusions Transcatheter closure is safe and efficacious in selected cases of perimembranous and muscular VSD. (Am Heart J 1999;138:339-44.)