The objectives of this study were to identify possible risk factors that may lead to erosion of the Amplatzer septal occluder (ASO) and recommend ways to minimize future risk. There have been rare occurrences of adverse events with development of pericardial effusion after ASO placement. Identification of high-risk cases, early recognition, and prompt intervention may minimize the future risks of adverse events. In all patients who developed hemodynamic compromise after ASO placement, echocardiograms (pre-, intra-, and postprocedure), atrial septal defect (ASD) size (nonstretched, stretched), size of the device used, cineangiograms, and operative records were reviewed by a panel selected by AGA Medical Corporation. The findings were compared to the premarket approval data obtained from FDA-approved clinical trials that were conducted in the United States, before the device was approved. A total of 28 cases (14 in United States) of adverse events were reported to AGA Medical. All erosions occurred at the dome of the atria, near the aortic root. Deficient aortic rim was seen in 89% and the defect described as high ASD, suggesting deficient superior rim. The device to unstretched ASD ratio was significantly larger in the adverse event group when compared to the FDA trial group. The incidence of device erosion in the United States was 0.1%. The risk of device erosion with ASO is low and complications can be decreased by identifying high-risk patients and following them closely. Patients with deficient aortic rim and/or superior rim may be at higher risk for device erosion. Oversized ASO may increase the risk of erosion. The defect should not be overstretched during balloon sizing. Patients with small pericardial effusion at 24 hr should have closer follow-up.

Anterograde transcatheter closure using the new ADO is an effective therapy for patients with a PDA diameter up to 6 mm. Further clinical trials are underway.

Transcatheter closure of a PmVSD is technically feasible and seems safe enough in children over 8 kg in weight to warrant continuation of clinical trials to assess the long-term safety and efficacy.

The objective of this study was to assess the immediate and mid-term results of transcatheter closure of postinfarct muscular ventricular septal defects (VSDs) using the new Amplatzer postinfarct muscular VSD device (PIMVSD). Ventricular septal rupture occurs in 0.2% of myocardial infarcts and remains associated with very high morbidity and mortality. Data were prospectively collected for 18 patients who underwent attempted device closure of postinfarction VSDs between 2000 and 2003. Five patients underwent the closure in the acute phase (within 6 days from the infarct); the remaining patients underwent closure on day 14-95 after the diagnosis of the infarct. Outcome parameters included procedural success, evidence of residual shunts on echocardiography, and occurrence of procedure-related complications. The procedure was successful in deploying a device across the VSD in 16 of 18 patients. The 30-day mortality was 28%. Eleven patients are still alive and have been followed up for a median of 332 days. Two patients required a second procedure to close a residual VSD. At the most recent outpatient follow-up, the VSD was completely closed in two patients, six patients had a trivial or small residual shunt, and two patients had a moderate residual shunt. We conclude that percutaneous device closure of postinfarction VSDs using the Amplatzer PIMVSD occluder appears to be safe and effective. Further trials are required to assess long-term efficacy and compare the results with those of surgical closure.

Balloon dilation angioplasty (BDA) was attempted nine times in eight infants and children with aortic coarctation. In three infants (all with associated ventricular septal defect or atrioventricular canal and marked hemodynamic instability) dilation was attempted at a site of aortic narrowing that had not been operated on previously. Although the coarctation gradient fell 40% or more over the short term in two of the three, there was no angiographic or late gradient evidence of improvement. All three underwent subsequent coarctation surgery. Five dilations were performed in four infants and children who had previously undergone coarctation surgery (end-to-end anastomosis, attempted jump graft, and subclavian flap) and had residual gradients. Dilation was successful in all five cases, resulting in an increase in the diameter at the coarctation site (4.7 +/- 2.6 to 7.7 +/- 4.0 mm, p less than .05) and a decrease in the gradient measured 24 hr after dilation (42.0 +/- 15.5 to 11.8 +/- 11.2 mm Hg, p less than .05). In one child with a long area of hypoplasia of the thoracic aorta and similar lesions of the brachiocephalic vessels, a preliminary attempt to dilate a severely narrowed subclavian artery was unsuccessful. Postdilation angiography demonstrated evidence of intimal tears in three of five successful dilations. Follow-up (1 to 6 months) has demonstrated continued gradient relief in four of five children. BDA is frequently, but not always, a successful treatment for human aortic coarctation. The chief determinant of success appears to be the nature of the lesion; short-term changes in coarctation gradient are unreliable indicators of success of failure. Although BDA was not associated with mortality or significant morbidity in this group of patients, its role in the management of children with coarctation is yet to be determined.