CLINICAL RESEARCH: CATHETER INTERVENTIONS FOR CONTENITAL DISEASE
Device closure of muscular ventricular septal defects using the Amplatzer muscular ventricular septal defect occluder
Immediate and mid-term results of a U.S. registry
Ralf Holzer, MD*,
David Balzer, MD, FACC ,
Qi-Ling Cao, MD*,
Ken Lock, BS ,
Ziyad M. Hijazi, MD, MPH, FACC*,* Amplatzer Muscular Ventricular Septal Defect Investigators
* Section of Cardiology, Department of Pediatrics, University of Chicago Children's Hospital, Chicago, Illinois, USA
Section of Cardiology, Department of Pediatrics, St. Louis Children's Hospital, St. Louis, Missouri, USA
AGA Medical Corporation, Golden Valley, Minnesota, USA
Manuscript received May 17, 2003;
revised manuscript received September 30, 2003,
accepted October 6, 2003.
* Reprint requests and correspondence: Dr. Ziyad M. Hijazi, Pediatric Cardiology, University of Chicago Children's Hospital, 5841 S. Maryland Avenue, MC 4051, Chicago, Illinois 60637, USA.
zhijazi{at}peds.bsd.uchicago.edu
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Abstract
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OBJECTIVES: We sought to report the results of a U.S. registry of device closure of congenital muscular ventricular septal defects (VSDs) using the new Amplatzer mVSD occluder (AGA Medical Corp., Golden Valley, Minnesota).
BACKGROUND: Muscular VSDs pose a significant surgical challenge with increased morbidity and mortality.
METHODS: Data were prospectively collected from 83 procedures involving 75 patients who underwent an attempt of percutaneous (70 [93.3%] of 75) and/or perventricular (surgical) (6 [8.0%] of 75) device closure of hemodynamically significant muscular VSDs. The patients' median age was 1.4 years (range 0.1 to 54.1 years). Outcome parameters were procedural success, evidence of residual shunts on echocardiography, and occurrence of procedure-related complications. The median follow-up was 211 days (range 1 to 859 days).
RESULTS: The median size of the primary VSD was 7 mm (range 3 to 16 mm) and in 34 of 78 (43.6%) procedures, patients had multiple VSDs (range 2 to 7). The device was implanted successfully in 72 of 83 (86.7%) procedures. In 17 of 83 (20.5%) procedures, multiple devices were implanted (range 2 to 3). Procedure-related major complications occurred in 8 of 75 (10.7%) patients. Device embolization occurred in two patients and cardiac perforation in one patient. There were two (2.7%) procedure-related deaths. The 24-h postprocedural complete closure rate was 47.2% (34 of 72 patients), increasing to 69.6% (32 of 46 patients) at 6 months and 92.3% (24 of 26 patients) at 12 months. Six patients underwent successful closure using the perventricular surgical (beating heart) approach, with complete closure at day 1 in three patients and trivial/small residual shunts in the remainder of the patients.
CONCLUSIONS: The Amplatzer mVSD device (AGA Medical Corp.) offers excellent closure rates and low mortality when used to close congenital muscular VSDs. The device appears to be safe and effective.
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Abbreviations and Acronyms
| | CXR | = chest X-ray | | ECG | = electrocardiogram | | LV | = left ventricle/ventricular | | RV | = right ventricle/ventricular | | TEE | = transesophageal echocardiography | | TTE | = transthoracic echocardiography | | VSD | = ventricular septal defect |
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Surgical closure of muscular ventricular septal defects (VSDs) still poses a significant surgical challenge (1). They are frequently hidden within the coarse right ventricular (RV) trabeculations and, therefore, are difficult to localize through the standard surgical approach via the right atrium. Various different surgical approaches have been proposed; however, overall mortality and the rate of residual VSDs remain higher than with isolated perimembranous VSDs (1–4).
Device closure of VSDs has been used since the late 1980s (5–8). In 1997, Sideris et al. (8) reported their experience using the buttoned device. They were able to successfully implant the device in 18 of 25 (72%) cases. Thirteen of 18 (72%) patients had complete occlusion of the VSD and 2 of 18 (11%) patients required surgical removal of the device (migration/tilting). In 1999, Janorkar et al. (6) reported the use of the Rashkind device (USCI Angiographics, Billerica, Massachusetts) to close muscular VSDs with residual shunts in 5 of 16 (31%) patients and procedure-related deaths in 2 of 16 (12.5%) patients. In 1999, the Amplatzer mVSD occluder (AGA Medical Corp., Golden Valley, Minnesota) was added to the already existing investigational devices for percutaneous closure of VSDs (9). Initial results were promising (10–12).
The objective of this study was to prospectively evaluate the safety and efficacy of the muscular VSD occluder in its clinical use to close congenital muscular VSDs.
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Methods
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Study population.
The study was conducted as a prospective, nonrandomized, interventional registry involving 14 U.S. tertiary referral centers (Appendix). The study was approved by the institutional review board of each center and by the U.S. Food and Drug Administration under a sponsor-initiated Investigational Device Exemption. After the investigators had been selected, qualified, and trained, muscular VSD patients who were eligible for closure were enrolled. A monitor was used to oversee the compliance with the study protocol.
The inclusion criteria for device closure included: 1) the presence of a hemodynamically significant muscular VSD (demonstrated by echocardiography or angiography); and 2) patients with muscular VSD and a history of infective endocarditis.
Left ventricular (LV) enlargement on echocardiography was considered an important finding, but ultimately, the decision as to which VSD was considered hemodynamically significant was left up to the principal investigator at each participating institution. Patients with multiple VSDs/"Swiss cheese" VSDs were included in the study.
Exclusion criteria included patients with a weight below 3 kg, irreversible pulmonary vascular disease (>7 U/m2), sepsis, contraindications to antiplatelet therapy, a perimembranous VSD location, or a distance to the semilunar valves of <4 mm. Patients who previously underwent pulmonary artery banding were included, irrespective of the LV dimensions, either for a perventricular approach at the time of surgical debanding or for transcatheter VSD device closure. Once a patient met the enrolment criteria, he/she or the guardian was fully informed of the available treatment options. The final decision to participate in the study was made by the patient and/or guardian.
Between August 2000 and January 2003, 75 patients were included in the study on an intention-to-treat basis. Two patients had a history of endocarditis.
Data collection.
Data were collected prospectively at the time of the procedure at each participating institution by the responsible Amplatzer investigator and submitted to a central data base at the Research Division of AGA Medical Corp. Collected data included demographic details (date of procedure, age, gender, height, weight), symptoms and signs (congestive heart failure, failure to thrive, recurrent respiratory tract infections, sepsis, heart murmur), electrocardiographic (ECG) details (LV hypertrophy, RV hypertrophy, biventricular hypertrophy, arrhythmias), echocardiographic details (size and number of VSDs, location of VSDs, left atrial/RV/LV enlargement, classification of shunt), procedure details (access route, sheath size, heparin, fluoroscopy time, procedure time, balloon sizing), surgical details (surgical approach, cardiopulmonary bypass, procedure time), and some additional information (medication, aspirin, coagulopathy, pulmonary vascular disease, anaesthesia). The collected data also included follow-up data at 1 day, 1 month, 6 months, 12 months, 24 months, and 36 months after the procedure, regarding echocardiographic findings, ECG details, and the presence of a murmur. For any adverse event occurring at the time of or subsequent to device implantation, information was obtained by the local Amplatzer investigator with regard to the circumstances, treatment, outcome, device, or procedure relation, as well as classification as minor or major. Where data were inconclusive or raised additional questions, the local investigator was directly contacted and asked for clarification. The accuracy of the submitted data was audited for each participating institution using source documents (catheter reports, case notes), which were analyzed by monitors from AGA Medical Corp. during control visits to these institutions. Local experienced pediatric echocardiographers at each participating institution interpreted all echocardiographic data in a nonblinded fashion.
Measured outcome parameters.
The measured outcome parameters were procedural success, as defined by device release in the appropriate position without embolization, complete closure or quantification of a residual shunt, as assessed by color Doppler echocardiography, and the occurrence of procedure- or device-related complications and other adverse events during the follow-up period. Measuring the width of the color jet as it exited through the ventricular septum was used to assess the degree of a residual shunt. It was classified as trivial for a width <1 mm, small for a width between 1 and 2 mm, moderate for a width between 2 and 4 mm, and large for a width  4 mm, in a way similar to the technique used to describe atrial level shunts after device closure (13).
Device.
The Amplatzer mVSD occluder (AGA Medical Corp.) is made of nitinol wire. It is a self-expandable device consisting of two flat disks that are linked via a central connecting waist, the diameter of which determines the size of the device. The two disks are 4 mm larger than the connecting waist. Dacron fabric is incorporated into each disk to enhance thrombosis. Further details have been described in previous reports (10,11). It requires a 6F to 9F sheath for delivery, depending on the size of the device, which is available from 4 to 18 mm.
Closure protocol.
The procedures were performed routinely under general anesthesia. The protocol we used for transcatheter closure of muscular VSDs has been described in details in previous reports (11). Figure 1 demonstrates the different steps of percutaneous device closure. Six patients underwent closure of their defects in the operating room under continuous transesophageal echocardiography (TEE) guidance. Technical details of intraoperative perventricular device closure of VSDs have been reported elsewhere (14). All patients had a chest X-ray (CXR), transthoracic echocardiography (TTE), and ECG within 24 h after the procedure. The follow-up protocol included assessments at 1, 6, 12, and 24 months. All visits included a routine physical examination, as well as CXR (optional at 6 months), ECG (optional at 6 and 12 months), and TTE. Patients were routinely maintained on aspirin or equivalent antiplatelet therapy for the duration of six months after the procedure.
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Figure 1 Cine fluoroscopic images in a seven-month-old female baby with single muscular ventricular septal defect (VSD), demonstrating the steps of percutaneous device closure. (A) Left ventricular (LV) angiogram in the four-chamber view, demonstrating a 6-mm mid-muscular VSD (arrow). (B) Cine fluoroscopic image in the straight frontal projection, demonstrating the guide wire (arrow) across the VSD into the right ventricular (RV) and down the inferior vena cava. The wire was snared from there and exteriorized into the right internal jugular vein. (C) Delivery sheath with an 8-mm Amplatzer device inside (arrow), passing from the right internal jugular vein through the VSD and terminating into the LV. (D) The LV disk is being deployed and pulled against the septum (arrow). (E) Left ventricular angiogram confirms good LV disk position. (F) Cine angiogram after deployment of the connecting waist and RV disk (arrow). (G) Cine fluoroscopic image after the device was released. (H) Final LV angiogram confirming good device position and no residual shunting through the device.
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Statistical analysis.
Basic descriptive statistical reports (mean and median values, variance, standard deviation, and range) were obtained for each parameter, using StatsDirect software (StatsDirect Ltd, Sale, Cheshire, United Kingdom). We used nonparametric tests to compare patient variables, such as weight, number of VSDs, and VSD size, with outcome parameters, such as procedural success (Mann-Whitney U test), residual shunt (Kendal rank correlation), procedure and fluoroscopy time (Kendal rank correlation), and the occurrence of complications (Kendal rank correlation). All tests were performed at alpha = 5%.
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Results
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Seventy-five patients were enrolled in the study and underwent a total of 83 procedures. Thirty-nine of 75 (52.0%) patients were female. The median age of the patients at the time of the procedure was 1.5 years (range 0.1 to 54.1 years). In 26 of 76 (34.2%) procedures, the patient had a history of congestive heart failure and in 22 of 76 (89.9%) procedures, the patient had a history of failure to thrive. Twenty-eight of 75 (37.3%) patients had previous cardiac surgery, such as pulmonary artery banding in 12 patients, an attempt at surgical VSD closure in 11 patients, ligation of a patent ductus arteriosus in four, and coarctation repair in 3 patients.
Either LV, RV, or biventricular hypertrophy was present before the procedure on 53 of 71 (74.6%) ECGs. The presence of multiple VSDs was demonstrated by TTE in 34 of 78 (43.6%) procedures (range 2 to 7 VSDs). The median size of VSD on echocardiography was 7 mm (range 3 to 16 mm). An enlarged LV, RV, or left atrium was present on the echocardiogram in 74 of 83 (89.1%) procedures.
Based on our echocardiographic and angiographic data, the primary VSD was located anterior in 10 of 79 (12.7%) defects, apical in 11 (13.9%), mid-muscular in 26 (32.9%), and posterior in 2 (2.5%). The 30 remaining VSDs (37.9%) were located within combined/multiple septal regions. An elevated pulmonary vascular resistance above 3 U/m2 but below 7 U/m–2 was present in 10 of 80 (12.5%) procedures.
Six patients underwent closure of their defects in the operating room under continuous TEE guidance. The VSD was approached through a RV free wall puncture without cardiopulmonary bypass (14). Cardiopulmonary bypass was used to correct associated lesions after VSD closure in three patients. All procedures were successful (device released) using a single device, and early complete closure at day 1 was achieved in 3 of 6 (50%) patients; the remainder had trivial or small residual leaks. Follow-up data up to 12 months after implantation were available for two patients: one without a residual VSD at 12 months after the procedure and one with still a small residual shunt.
Seventy-seven of 83 (92.8%) procedures were transcatheter attempts of VSD device closure; 74 of 76 (97.4%) of these were performed under general endotracheal anesthesia (Table 1). The procedure was successful (device inserted and released) in 66 of 77 (85.7%). Repeated percutaneous procedures for unsuccessful attempted closure or residual VSDs were required in 7 of 70 (10%) patients. A total of 88 devices were implanted in the 77 transcatheter procedures to close 144 VSDs. The median fluoroscopy time was 54.2 min (range 8.8 to 356 min), and the median total procedure time was 181 min (range 44 to 584 min). Balloon sizing of the defect was optional and was used in 9 of 76 (11.8%) cases. Where data were available in 42 of 75 procedures, the median size of the sheath used for device delivery was 7F (range 5F to 9F). The first disk was deployed in the RV in 5 of 74 (6.7%) procedures and in the LV in 70 of 74 (94.6%) procedures. The device was deployed via the internal jugular vein in 43 of 69 (62.3%) procedures and via the femoral vein in 26 of 69 (37.7%) procedures. During one procedure, the first device deployed was from the RV, and another device was deployed from the LV. The median device size was 8 mm (range 4 to 16 mm). We used two devices in 12 of 66 (18.2%) procedures and three devices in 5 of 66 (7.6%) procedures. The maximum number of devices implanted in any one patient was six over two separate procedures.
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Table 1 Basic Procedural Data of Percutaneous Device Closure of Ventricular Septal Defects Via the Transcatheter Approach (n = 77 Procedures)
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Table 2 summarizes the adverse events of the procedure. A total of 59 adverse events or complications related to the procedure or device occurred in 34 of 75 (45%) patients. Eight of 75 (10.7%) of them had major complications. Two of 75 (2.7%) patients died as a direct result of the procedure. In one patient, a cardiac perforation occurred secondary to the delivery sheath being too close to the free wall, and the device was deployed in the pericardium. This patient underwent emergency surgical repair but sustained severe cerebral damage, and support was finally withdrawn. Another patient sustained a cardiac arrest resulting in cerebral insult secondary to the use of a larger sheath for retrieval of the device, which caused significant blood loss. A third patient died suddenly at home of an unknown cause five months after the last of three transcatheter procedures. This patient had systemic pulmonary artery pressure despite closure of 13 separate ventricular communications (5 devices and 8 coils). On autopsy, the heart appeared to be hypertrophied and enlarged, and all devices and coils were in good position.
Device embolization occurred in 2 of 75 (2.7%) patients, both of which were successfully retrieved. One device was retrieved surgically (the patient was going to have elective tricuspid repair and the Maze procedure for atrial flutter) and one in the catheter laboratory percutaneously. Hypotensive episodes and/or cardiac arrest requiring inotropic support occurred in 9 of 75 (12%) patients. Arrhythmias or conduction abnormalities were encountered in 15 of 75 (20%) of patients, consisting of right bundle branch block (n = 2), second- or third-degree heart block (n = 6), ventricular tachycardia (n = 3), junctional rhythm (n = 3), and episodes of bradycardia (n = 4). Most of these were temporary, but 2 of 75 (2.7%) patients developed permanent right bundle branch block. The described arrhythmias consist of those submitted to the central database as adverse events and likely do not include very transient nonsustained arrhythmias encountered during catheter manipulation. Five of 75 (6.7%) patients required blood transfusion due to significant blood loss. One patient presented with a transient ischemic attack 24 h after the procedure. A brain computed tomographic scan was negative. Two of 75 (2.7%) patients had minor device-related gradients across the LV outflow tract (gradient <15 mm Hg), neither of which required any form of intervention.
A lower weight of the patient at the time of the procedure significantly correlated with an increased risk of procedure- or device-related complications (p = 0.007). Procedure- or device-related complications were encountered in 7 of 13 (53.8%) procedures undertaken in patients weighing <5 kg, comparable to 24 of 63 (38.1%) procedures in patients weighing 5 kg. The median weight of patients who had unsuccessful percutaneous procedures was 6.5 kg, whereas the median weight of patients who had a successful procedure was 9.4 kg. However, this difference was not statistically significant (p = 0.07). There was a statistically significant negative correlation between weight at the time of the procedure and a residual postprocedural shunt (p = 0.03). However, no significant correlation could be established between the number of VSDs and a residual shunt (p = 0.35). The number of VSDs (p = 0.65) and size of the primary VSD (p = 0.11) were not significant risk factors for the occurrence of complications. However, patients with a larger number of VSDs tended to require significantly longer fluoroscopy times (p = 0.002) and procedure times (p = 0.0004). Patients with a lower weight also required significantly longer fluoroscopy times (p = 0.0006).
The median follow-up was 211 days (range 1 to 859 days). After 24 h from the procedure, the VSD was completely closed in 34 of 72 (47.2%) cases. Moderate or large residual shunts were present in 5 of 72 (6.9%) cases. The shunt closure rates (Table 3) improved as the time from closure to follow-up increased. At one month, the complete closure rate was 58.7% (37 of 63); at 6 months, it was 69.6% (32 of 46); and at 12 months, it was 92.3% (24 of 26). No patient had moderate or large residual shunts at 12- or 24-month follow-up. Between hospital discharge and one-year follow-up, the shunts improved from trivial to none in eight patients, from small to none in four patients, and from moderate to none in two patients. One trivial shunt remained unchanged, and in one patient, a trivial shunt that was not previously present was identified.
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Table 3 Follow-Up After Device Closure of Muscular Ventricular Septal Defects: Echocardiographic and Clinical Data
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Discussion
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This series reports the largest cohort of patients with muscular VSDs who underwent device closure. The success rates (complete closure or any residual shunt  2 mm) have been very good (100% at 12 months and 2 years), although the interpretation of these results has to be regarded with some caution, as only 38% completed the one-year follow-up. In contrast, the rate of reoperation for residual VSDs after surgical closure has been reported to be as high as 5% to 10% (1,4,15).
The early mortality (30 days) in our population was 2.7%, which compares well to the results after surgical correction of muscular VSDs, which has been reported to be as high as 7% to 17% (1,4). However, in 1998, Kitagawa et al. (15) reported 0% mortality in 33 patients with multiple muscular VSDs.
Closing VSDs using the Amplatzer mVSD device (AGA Medical Corp.) is a fairly new technique, and as such, each operator will have a learning curve in using this device. With increasing experience, ventricular perforations, such as the one leading to death in one of our patients, may potentially be preventable in the future.
Other complications encountered were short-lived and resolved without residual morbidity in most of the patients. The rate of permanent conduction disturbances of 2.6% is below the incidence after surgical closure of VSDs (16). However, current data on the incidence of conduction disturbances solely after the closure of muscular VSDs is not available, and therefore comparisons are difficult to make. In two patients, a mild gradient across the LV outflow tract developed. This could be avoided in future cases by allowing a larger distance to the semilunar valves or by using the Amplatzer membranous VSD device (AGA Medical Corp.) for anterior muscular VSDs with only a minimal muscular rim to the aortic valve.
Various other devices have been used in the past to close VSDs. In the introduction, we referred to reported rates of residual shunting of 28% using the Sideris device and 31% using the Rashkind device. Compared with these previously used devices and the CardioSEAL device (NMT Medical, Boston, Massachusetts), the Amplatzer mVSD occluder (AGA Medical Corp.) has the following advantages: a small delivery system and excellent control by the operator, with the ability to recapture the device before release.
The indications for using the Amplatzer mVSD device (AGA Medical Corp.) are not limited by patient size or VSD size, although the chances of procedural success are reduced. Some larger and multiple VSDs were successfully closed using larger devices up to 16 mm, as well as by the ability to use multiple devices (17). In our series, we were able to percutaneously close VSDs in children as small as 3.2 kg. However, the decision for device closure in a child weighing <5 kg should be made very carefully. The increased risk of residual shunts and procedure-related complications requires a very experienced operator and a firm indication for this approach. Weight, although not statistically significant, was lower in the group with primarily unsuccessful procedures. This is an important consideration, as other factors of poor procedural success (number of VSDs, size of VSDs, location of VSDs) were not evident from our data.
In addition to the obvious advantages (no scar, less pain and discomfort, no cardiopulmonary bypass), the percutaneous approach has additional advantages, including a shorter hospital stay, whereas surgical VSD closure usually involves a hospital stay of no <4 days. Procedural costs may well be below the standard surgical approach. However, this would need to be more formally addressed in a prospective cost analysis study.
Our data demonstrate that perventricular device closure is feasible. In particular, the subgroup of patients who underwent pulmonary artery banding for large muscular VSDs may benefit from such an approach of combining pulmonary artery debanding with perventricular device closure of VSDs. However, the number of involved patients is insufficient to draw any strong conclusions.
Study limitations.
Our study has some limitations. Patients were not randomized between surgical and percutaneous closure, and as such, a comparison between the two approaches may be biased. Our follow-up data are incomplete, and long-term conclusions cannot be made at this stage. In addition, restrictive muscular VSDs with only mild LV volume loading would be conservatively managed by many institutions, thereby trying to avoid any invasive procedure. Also, interventional closure is not a simple technique. The challenge of advancing a wire through the VSD into a position where snaring is feasible, as well as the difficulties in advancing a sheath through the VSD without kinking or causing damage to adjacent structures, should not be underestimated. The procedure requires considerable technical operator skills, which may only be obtained and maintained in larger institutions. The technical challenge of this procedure is reflected in the relatively long procedure and fluoroscopy times.
Conclusions.
Our study has demonstrated excellent closure rates and low mortality using the Amplatzer mVSD device (AGA Medical Corp.) to close congenital muscular VSDs. The device appears to be safe and effective. The incidence of permanent morbidity after this procedure is low. However, patient selection (weight, VSD size and location) and an experienced operator are very important for procedural success. Device closure using the Amplatzer mVSD device (AGA Medical Corp.) should be considered an important alternative to the surgical approach in treating congenital muscular VSDs.
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APPENDIX
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For a complete list of the Amplatzer mVSD device investigators, please see the April 7, 2004, issue of JACC at www.cardiosource.com/jacc.html.
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Acknowledgments
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The authors thank Ms. Mary Heitschmidt, RN, from the University of Chicago, for her help during data collection.
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Footnotes
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Drs. Hijazi and Balzer are consultants for AGA Medical Corp., and Mr. Lock is an employee, who runs the clinical trials, of AGA Medical Corp., which manufactures the device.
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Abstract
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