John L. Bass

Erosion of Amplatzer septal occluder device after closure of secundum atrial septal defects: Review of registry of complications and recommendations to minimize future risk

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.Catheter Cardiovasc Interv 2004;63:496–502.

Catheter closure of moderate- to large-sized patent ductus arteriosus using the new amplatzer duct occluder : Immediate and short-term results

OBJECTIVES The aim of this study was to assess the immediate and short-term results of anterograde catheter closure of a moderate- to large-sized patent ductus arteriosus (PDA) using the new self-expandable, respositionable Amplatzer duct occluder (ADO) device. BACKGROUND Transcatheter closure of a PDA using devices or coils is technically challenging and may be accompanied by a 38% incidence of residual shunts. METHODS Twenty-four patients (6 male, 18 female) underwent attempted transcatheter closure of a PDA using the ADO at a median age of 3.8 years (range 0.4 to 48) and a median weight of 15.5 kg (range 6 to 70). The mean PDA diameter at its narrowest segment was 3.7+/-1.5 mm. A 6F long sheath was used for delivery of the ADO. Follow-up evaluation was performed with color flow mapping of the main pulmonary artery within 24 h and at 1 and 3 months after closure. RESULTS Twenty three of the 24 patients had successful device placement. Angiography showed that 7 patients had complete immediate closure, 14 had a trace shunt (foaming through the device with no jet), and 2 had a small residual shunt (with a jet). Within 24 h, color Doppler revealed complete closure in all patients. The unsuccessful attempt was during an initial trial with a prototype that has been modified. The median fluoroscopy time was 13.5 min (range 6.3 to 47). All patients were discharged home the next day. There were no complications. Of the 23 patients, 21 completed the 1-month follow-up, all (95% confidence interval [CI] 86% to 100%) with complete closure, and 18 of 23 patients completed the 3-month follow-up, also all (95% CI 83% to 100%) with complete closure. CONCLUSIONS 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.

Balloon dilation angioplasty of aortic coarctations in infants and children.

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.

Balloon dilation angioplasty of hypoplastic and stenotic pulmonary arteries.

Balloon dilation angioplasty (BDA) was attempted in seven children with either stenosis or hypoplasia (a narrowing greater than 1 cm long extending past the lung hilum) of both right and left pulmonary arteries (PAs). In two of these seven, the procedure could not be performed because of technical difficulties. In each of the remaining five children (1½–16 years old), the right ventricular (RV) pressure was greater than ⅔ left ventricular pressure, main PA pressure was greater than 60 mm Hg, and previous operative attempts to relieve RVoutflow obstruction, including the branch PA obstruction, were unsuccessful. BDA was performed in only one PA in each patient, and was considered successful if the pressure gradient decreased, angiographic diameter increased and the percentage of blood flow directed to the dilated lung increased. BDA was successful in all five children: RV pressure fell from 104 + 42 to 80 ± 30 mm Hg (p < 0.05), the gradient across the obstruction fell from 61 ± 51 to 32 22 mm Hg (p < 0.05), the diameter of the narrowed segment increased from 3.7 ± 1.2 to 6.8 ± 1.1 mm, p = 0.02), and the percentage of blood flow (as determined by quantitative lung scan) to the dilated lung increased from 41 16% to 52 ± 22% (p < 0.05). No morbidity was observed in any patient. Follow-up angiograms (2–12 months) in three of five patients indicate persistence of the anatomic improvement. While BDA did not restore right-heart pressures and anatomy to normal, it provided significant hemodynamic relief to a group of patients in whom traditional operative management has usually been unsuccessful. Final determination of the role of BDA in such patients must await the results of further studies.

Transcatheter closure of postinfarction ventricular septal defects using the new Amplatzer muscular VSD occluder: Results of a U.S. Registry.

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. Catheter Cardiovasc Interv 2004;61:196–201.

Initial human experience with the Amplatzer perimembranous ventricular septal occluder device

Transcatheter closure of perimembranous ventricular septal defects with coils or devices designed to close other lesions may be complicated by embolization or aortic insufficiency. A new asymmetric Amplatzer perimembranous ventricular septal occluder and delivery system was specifically designed for perimembranous defects. This report describes the first use of this device in 27 patients. Implantation was successful in 25 (93%), with 1 removed for device‐related aortic insufficiency and inability to position the delivery sheath in another. Device orientation was excellent when the device was initially advanced through a standard delivery sheath positioned in the left ventricular apex. Twenty‐three had complete occlusion within 1 week (92%), with a tiny (< 2 mm) residual shunt in the other two. In the 25 subjects with the device left in place, device‐related aortic or tricuspid insufficiency, arrhythmias, and embolization were not observed. These excellent acute results need to be confirmed by long‐term follow‐up. Cathet Cardiovasc Intervent 2003;58:238–245.

Balloon angioplasty-branch pulmonary artery stenosis: Results from the Valvuloplasty and Angioplasty of Congenital Anomalies Registry

Balloon angioplasty for branch pulmonary artery stenosis was reported from 27 institutions to the Valvuloplasty and Angioplasty of Congenital Anomalies Registry. One hundred eighty-two procedures were performed in 156 patients ranging in age from 0.2 to 46.2 years (mean 7.7). Short-term angiographic appearance, hemodynamic results and immediate complications were recorded. Vessel dimension at the site of stenosis increased from 4.5 +/- 2.0 (mean +/- standard deviation) to 6.8 +/- 3.0 mm (p less than 0.001) with greater increases in vessel dimension at the site of stenosis if the balloon diameter was greater than 3 X the original dimension of the stenosis. There was no significant benefit related to age or prior surgical intervention. The mean peak systolic pressure gradient was reduced from 49 +/- 25 to 37 +/- 26 mm Hg (p less than 0.001) and pressure proximal to the stenosis decreased from 69 +/- 25 to 63 +/- 24 mm Hg (p less than 0.001). Complications occurred in 21 patients and included vessel rupture and death in 2 patients, vessel perforation or rupture with survival in 3, cardiac arrest and death in 1, paradoxical embolism and death in 1 and low output and death in 1. Balloon angioplasty for branch pulmonary artery stenosis increases vessel dimension at the site of stenosis, reduces systolic pressure gradient and to a minor degree, reduces proximal pressure. Long-term outcome and potential complications are as yet uncertain.

Intraoperative closure of muscular ventricular septal defect in a canine model and application of the technique in a baby

Isolated muscular ventricular septal defects (VSDs) account for 10% of VSDs. Among these, inlet and midmuscular VSDs are relatively easy to approach surgically, but apical and anterior muscular VSDs can be difficult to visualize during the operation. 2 Intraoperative closure of muscular VSDs with a device during cardiopulmonary bypass (CPB) has been described with good results. The current report describes the use of a new transcatheter device to close muscular VSDs intraoperatively without using CPB in three dogs and later in an 8-month-old girl. Animal studies. The Amplatz VSD device (AGA Medical Corporation, Golden Valley, Minn.) is a modified version of the Amplatz septal occlusion device. It is made of fine nitinol wires that are woven into two discs with a connecting waist. The discs are filled with polyester to enhance thrombogenicity. The device is custom built to correspond to the size of the VSD and thickness of the ventricular septum. It has a screw mechanism on one side for connection to the delivery cable. The device is withdrawn into a loader before introduction into the delivery sheath. All animals received humane care in compliance with the “Guide for the Care and Use of Laboratory Animals” (NIH Publication No. 86-23, revised 1985). The study protocol was approved by institutional animal care committee of the University of Minnesota. To determine the feasibility of intraoperatively closing muscular VSDs, we created an anterior or apical VSD in three dogs with the help of a punch device. The diameter of the punch device was 10 mm. With the animal under general endotracheal anesthesia and aseptic technique, the chest was entered by median sternotomy. The pericardium was opened. Two stay stitches were applied on the right ventricular free wall. A purse-string suture was placed on the left atrial appendage. The index finger of the left hand was inserted in the left atrium and advanced in the left ventricle. A right ventriculotomy was performed and the punch device inserted through the incision in the right ventricle. With a burring action, the septum was traversed until the punch device touched the index finger in the left ventricle. The punch was locked and removed, and the right ventriculotomy was closed with 5-0 running Prolene suture (Ethicon, Inc., Somerville, N.J.). The size of the defect was measured by epicardial echocardiography. In one dog two VSDs were created. An Amplatz VSD device that corresponded to the size of the VSD was screwed onto the delivery cable and withdrawn with the delivery sheath immersed in saline solution to avoid entrapment of air bubbles. The sheath was pushed through the right ventricular free wall. With the aid of epicardial echocardiographic guidance the sheath was aimed toward the muscular VSD. Once the sheath was across the VSD, the left disc was deployed in the left ventricle. The sheath was withdrawn and the right disc deployed in the right ventricle. The device was disconnected from the cable by counterclockwise rotation of the cable. Residual shunt was checked with the help of epicardial echocardiography. Results. A total of four VSDs were created in three dogs. The smallest measured 7 mm and the largest 11 mm. Three muscular VSDs were closed during the operation and the fourth one in the catheterization laboratory. The first dog died 2 hours after the operation because of ventricular fibrillation. Dissection of the heart revealed the device in good position. The second dog was put to death after 3 months. Examination of the heart revealed the device in the optimal location with complete endothelialization. The third dog (with two devices) is still alive. Six months’ follow-up echocardiogram and angiogram revealed no shunt. Muscular VSDs in an 8-month-old baby. The operation was done on the basis of compassionate need. Informed consent and approval of the Institutional Review Board of the University of Minnesota, Minneapolis, were obtained before placement of the device. Baby A was born with multiple muscular VSDs (anterior and apical muscular) and coarctation of aorta. She underwent repair of aortic coarctation and pulmonary artery banding on the fourth day of life. At the age of 8 months she had debanding with closure of large muscular VSDs. Postoperatively a significant residual shunt was identified, but the VSD could not be located during CPB. From the Departments of Cardiology and Cardiovascular Surgery, University of Minnesota, Minneapolis, Minn., and Department of Cardiology, Children’s Memorial Medical Center, Northwestern University Medical School, Chicago, Ill.

New device for closure of muscular ventricular septal defects in a canine model

BACKGROUND Repair of muscular ventricular septal defects (MVSDs) has always been challenging to the surgeon. Long-term morbidity and mortality are significantly increased if the defects are closed via left ventriculotomy or if they are associated with other complex congenital anomalies. The purpose of this study was to close MVSDs with the Amplatz ventricular septal defect device. This device is constructed from 0.004-in nitinol wire mesh filled with polyester fibers. It is retrievable, repositionable, self-centering, and of low profile. METHODS AND RESULTS MVSDs were created with the help of a sharp punch in 10 dogs. The location of the defects was anterior muscular (n=3), midmuscular (n=3), apical (n=3), and inlet muscular (n=1). The diameter of the defects ranged from 6 to 14 mm. All defects were closed in the catheterization laboratory. The device was placed with the help of transesophageal echocardiography and fluoroscopy. A 7F sheath was used to deploy the device from the right ventricular side in 8 and the left ventricular side in 2 dogs. Placement was successful in all animals. The complete closure rate was 30% (3/10) immediately after placement and 100% at 1-week follow-up. Pathological examination of the heart revealed complete endothelialization of the device in dogs killed after 3 months. CONCLUSIONS The Amplatz ventricular septal defect device appears highly efficacious in closing MVSDs. The advantages include a small delivery sheath, complete retrievability before release, and the fact that it is self-centering and self-expanding, thereby making it an attractive option in smaller children.

Transvenous angioplasty of experimental branch pulmonary artery stenosis in newborn lambs.

A dilatable form of bilateral branch pulmonary artery stenosis was created in 27 newborn lambs. Nine lambs were long-term survivors and were dilated with modified Gruntzig balloon dilation catheters. They were allowed to recover for 6-9 weeks, during which time there was no significant change in the mean systolic gradients across the narrowed sites. Thirteen arteries underwent dilation. Dilation was associated with a decrease in the systolic gradient in all cases (from 34.9 mm Hg to 8.1 mm Hg) and an increase in the diameter of the narrowed site (from 4.6 to 7.6 mm) as estimated by angiography. Flows and flow distribution were measured in four lambs before and after unilateral dilation using 15-p radiolabeled microspheres; in each case, the fraction of total flow to the dilated lung rose after dilation (19.2 to 45.4%), as did the total flow to the dilated lung (30.0 to 69.2 ml/kg-min). Four lambs were catheterized every 2-4 weeks for an average of 16 weeks after dilation; the average gradient in these lambs remained below 10 mm Hg despite considerable growth (from 9.6 to 25.9 kg). Gross pathologic examination showed an intact vascular adventitia in all cases; there were multiple linear tears in the intima in recently (less than 7 days) dilated cases, but complete intimal healing had occurred by 2 months after dilation. No significant morbidity could be attributed to the dilation procedure. These results indicate that clinical trials are warranted.