Abstract: Atrial septal defect (ASD) is one of the most common congenital heart defects, accounting for 7%-10% of all congenital heart disease (CHD) in children and 30%-33% of defects diagnosed in adults with CHD. This review highlights the evolution of transcatheter ASD closure, indications, follow-up, outcomes, and complications with a focus on the erosion issue with certain devices.
J INVASIVE CARDIOL 2013;25(5):257-264
Key words: atrial septal defect, transcatheter ASD closure
Atrial septal defect (ASD) is one of the most common congenital heart defects, accounting for 7%-10% of all congenital heart disease (CHD) in children and 30%-33% of defects diagnosed in adults with CHD. If left untreated, there is significant risk of atrial arrhythmias and late morbidity; therefore, closure of hemodynamically significant defects (right ventricle volume overload as evidenced by transthoracic echocardiography or Qp:Qs >1:5:1) is advised in childhood.1 Historically, surgery has been the gold standard; however, the initial description of transcatheter closure by King and Mills in 19762 laid the groundwork for the development of refined and clinically acceptable transcatheter alternatives to surgery. This initial work by King and Mills was truly revolutionary, and 25-year follow-up data on the 5 patients who underwent transcatheter closure were reported in 2003 with 4 of these patients alive and well.3 Unfortunately, following this huge step, work on transcatheter closure of ASD lay fallow for a number of years until 1983, when Rashkind reported successful delivery of a single foam-covered six-ribbed device with hooks at the ends of three of these ribs.4 Modifications of this basic design led to the development of the Clamshell device, a double-hinged paired umbrella with four arms that folded on themselves.5 Clinical studies with this device were halted due to concerns regarding device fracture and residual shunting.6-8
In 1993, Das et al reported on a new device called the Angel Wing, which was the first self-centering device and had two Dacron-covered square disks and nitinol frames with midpoint torsion spring eyelets.9 One of the authors of this paper (ZMH) implanted the first Angel Wing device in June 7, 1995;10 however, because of the relative stiffness of the frame and the design of the attachment mechanism, it was not easy to retrieve by catheter and due to 2 cases of device erosion, the device was redesigned and named the Guardian Angel. However, that device was never used in humans. The real breakthrough with transcatheter ASD closure came with the development of the Amplatzer septal occluder in the mid 1990s (Figure 1).
This device design consists of a nitinol wire mesh that is tightly woven into two disks with a connecting waist between the two disks corresponding to the approximate thickness of the interatrial septum. The first clinical report was published in 1997.11 United States Food and Drug Administration (FDA) approval followed in 2001. Although many other devices have been reported, the other mainstream device in clinical use today in the United States is the Helex septal occluder (Figure 2). This device consists of a single nitinol wire covered by an ultrathin membrane of expanded polytetrafluoroethylene. In its occlusive configuration, the device forms two round flexible discs that straddle the septum.
Anatomy of the Atrial Septum
The atrial septum is formed by the septum primum, which originates from the atrial roof and septum secundum. Formation of the septum occurs through several stages. The septum primum grows as a crescenteric flap, leaving an opening between the left and right atria called the ostium primum. With growth of the septum primum, the ostium primum narrows and a second opening (ostium secundum) is formed. As the septum secundum grows anteriorly to meet the septum primum posteriorly, it leaves a small opening called the foramen ovale (FO), providing a continuous pathway for shunting of blood across the pulmonary vascular bed in fetal life. Thus, the foramen ovale is not a true deficiency in the atrial septum. Following birth, and decrease in pulmonary vascular resistance, the hooded morphology of the septum primum collapses over the foramen ovale to provide functional closure. The muscular rims of the foramen ovale are known as the limbus and form the raised margin around the FO. Autopsy studies have showed that FO is circular to elliptical in shape and represents a part of the anterosuperior portion of the atrial septum, with a mean diameter of 4.9 mm and mean length of 8 mm.12 Ostium secundum ASD is the most common form of atrial defect, and mostly relates to deficiency in the septum primum or rarely the septum secundum. Indeed, the vast majority of these defects reflect complete absence, deficiency, or multiple fenestrations of the septum primum. In the absence of the valve of the fossa ovalis, the ASD is usually elliptical in shape and located centrally; however, ASD position, shape, and size vary widely and defects may extend toward the vena cavae, right pulmonary veins, coronary sinus, or atrioventricular valves. The relationship to these structures remains important when considering device closure.13,14 Due to the anatomical limitations, effective transcatheter closure of sinus venous, coronary sinus, or ostium primum defects is not considered viable.
Indications for Closure
The indications for closure of an ASD in the pediatric population are outlined in Table 1. Under usual circumstances, flow through an ASD occurs from left to right, but to a variable degree depending on the size of the ASD, the ventricular compliance, and the pulmonary vascular resistance (PVR). Excessive flow through the defect will eventually lead to right atrial and ventricular volume overload. If the shunt is large and results in significant right heart volume loading, the patient may experience symptoms of shortness of breath, reduced exercise tolerance, or palpitations in the second or third decade of life.15 5%-10% of patients who have large ASDs with right heart volume overload evident by echocardiography will develop late complications, such as reduced exercise tolerance, atrial arrhythmia, or elevated PVR.15 Intervention in older patients has also been shown to be advantageous, with Konstantinides and colleagues demonstrating significant improvement in the survival rate in symptomatic patients older than 40 years undergoing surgical ASD closure compared to those treated medically.16
Transcatheter ASD closure is deemed feasible if the balloon-stretched diameter of the defect is less than 35 mm and the defect has sufficient rims (>5 mm) of surrounding atrial tissues. However, transcatheter closure has been routinely performed in defects with deficient rims, particularly of the anterosuperior atrial septum. Attempted closure in patients with 2 or more deficient rims is not advised and device embolization is thought to be higher in patients with significantly deficient posterior and inferior rims. Weight restrictions have lessened over time and multiple reports have demonstrated safe and effective closure in patients weighing less than 15 kg.17
The American Heart Association recommendations for closure in adults reflect those for children as well as documented orthodeoxia-platypnea, and ASD with left-to-right shunt and PVR less than two-thirds of the systemic vascular resistance.1,18
Contraindications for ASD device closure include elevated PVR in excess of 7 Wood units (indexed), although closure in patients with secundum ASD and pulmonary arterial hypertension can be successfully performed in selected subjects and is associated with good outcomes.19 Other contraindications include acute or recent sepsis, or contraindications for antiplatelet therapy.
Prior to defect closure, it is crucial to identify the number of defects, defect size, location, morphology, and the surrounding atrial septal tissue to determine whether the defect is amenable to transcatheter closure or not. Baseline assessment of cardiac structures that may be affected by the procedure should also be carried out. Echocardiography remains the noninvasive gold standard imaging tool for detecting an interatrial communication. Three-dimensional transthoracic and transesophageal and intracardiac echocardiography have also been used.
Although transcatheter closure of small-to-moderate sized defects with good rims is frequently straightforward, it should be performed only in laboratories and by experienced operators equipped to deal with complications and unexpected challenges of the procedure, and surgical back-up should be available.Conscious sedation may be used if intracardiac echocardiography (ICE) is used to guide closure; however, general anesthesia is preferred when TEE is used or with younger patients as they may not be cooperative.
Access is obtained usually in the right femoral vein. If ICE is used, an additional sheath is needed in the left or right femoral vein depending on the patient’s weight. If the weight is >35 kg, we access the femoral vein in the right using two separate punctures a few millimeters from each other; however, if the weight is <35 kg, we access the contralateral vein. The main advantages of ICE over TEE during this procedure include avoidance of anesthesia, better view of the left atrium and the posteriorinferior rim of the septum, and need for fewer personnel, because the interventional cardiologist will be able to perform the interventional procedure independently with the need for an anesthesiologist or echocardiographer. The foremost disadvantage is the additional cost of the imaging catheter.20 Intravenous heparin should be given to keep an activated clotting time >200 seconds throughout the procedure as the risk of thrombus in the left atrium will predispose the patient to stroke.21
A thorough hemodynamic evaluation should be carried out before device deployment and special attention should be given to the pulmonary artery pressures, PVR, Qp:Qs, left atrial pressure, and the left ventricular end-diastolic pressure. Right upper pulmonary venous angiography may be performed, since it profiles the atrial septum and the defect size and may serve as a roadmap during device deployment. This view is obtained with 35° left anterior oblique and 35° cranial angulation. Intraprocedural echocardiography is used to assess the size of the defect and the septal rims in multiple planes, with confirmation of pulmonary venous drainage (particularly right-sided) to the left atrium and the degree of atrioventricular valve regurgitation. Balloon sizing of the defect is recommended in all ASD device closure cases; however, some operators may choose not to balloon-size based on the size and location of the defect. Once the defect is crossed and a catheter advanced into the left upper pulmonary vein, a stiff exchange-length guidewire is positioned in that vein. Following this, an appropriate-sized sizing balloon (St Jude Medical or NuMED, Inc) is advanced across the defect. The balloon is inflated under echocardiography guidance until no residual shunt through the defect is seen (stop-flow technique).
At this stage, the diameter of the balloon is measured by cine recording and echocardiography. In the case of the Amplatzer devices, a device approximately no more than 2 mm greater than the stop-flow diameter is usually chosen. The Helex device is usually not recommended for defects greater than 18 mm in diameter and a device:balloon size ratio of 2:1 is chosen for best results. The delivery sheath is then advanced over the wire and once the tip of the dilator crosses the defect, the dilator is held and the sheath advanced over the dilator into the left upper pulmonary vein. The wire and the dilator are then slowly withdrawn and the sheath held below the level of the heart to allow back-bleed to eliminate any possibility of air embolism. The device is then loaded and advanced to the tip of the sheath (Figures 3-6).
The delivery sheath is pulled out of the pulmonary vein into the left atrium, and at this point the delivery cable is fixed firmly while retracting the sheath over the cable and deploying the left atrial disc in the left atrium. Then, the entire assembly (sheath/cable) is withdrawn toward the septum. Once the left disc is within a few millimeters of the septum, the connecting waist is deployed partially in the left atrium with continuous traction toward the defect. The purpose is to “stent” the defect with the waist. Then, with continuous traction toward the right atrium, the right atrial disc is deployed in the right atrium. Once the entire disc is deployed, the delivery cable is then pushed toward the septum to approximate the two discs of the device to each other.
The mechanism for deployment of the Helex device is outlined in Figures 3 and 4. Echocardiography and cine fluoroscopy should be used to document and monitor all stages of device deployment with full assessment prior to device release.
Various strategies have been described to promote stability of the device in the setting of a deficient anterosuperior rim, including use of the Hausdorf sheath, the pulmonary vein deployment technique, use of the dilator to maintain the left atrial disc on the left atrial aspect of the septum during deployment, and use of a balloon across the defect to maintain the device in a stable position.22-24 Recently, the manufacturer of the Amplatzer device (St Jude Medical) introduced a new delivery system (TorqView FX) that has an inner softer cable that does not produce much tension on the device. Once the right atrial disc is deployed, the stiffer cable is retracted and the softer inside cable is pushed; this allows better alignment of two discs with the atrial septum.
Within 24 hours of device implantation, an echocardiogram should be done on all patients to evaluate the device position and any residual shunt and to look for any potential complications (device erosion, embolization, etc). Twelve-lead electrocardiogram should also be performed, since rare cases of heart block have been reported with large devices.25 Hill and colleagues reported an increased incidence of atrial arrhythmias and conduction abnormalities early after device closure.26 Postprocedure follow-up visits for all patients should be done at 6 months, 1 year, and then every 1-2 years thereafter. At each visit, physical exam, electrocardiogram, and echocardiography should be performed. If complete closure is documented at the 6-month follow-up visit, aspirin and SBE prophylaxis may be discontinued. It has been well documented that right ventricular size will improve rapidly in the first month; however, long-standing right ventricular dilation may improve more slowly and may not normalize completely.27
In 2002, a trial comparing surgical closure and transcatheter closure with the Amplatzer septal occluder demonstrated comparable closure rates.28 However, complication rates in the surgical group were significantly higher than the device closure group (24% vs 7%, respectively), and the length of the procedure and the hospital stay were shorter in the patients who underwent transcatheter closure.
Furthermore, in 2007 a multicenter pivotal study compared transcatheter ASD closure with the Helex device to surgical closure.29 There was no significant difference in the efficacy and safety between the two groups; however, the length of sedation and the hospital stay were longer in the surgically treated group.
Patel et al studied 113 patients >40 years old and demonstrated that ASD closure using the Amplatzer septal occluder in these patients was safe and effective with minimal complications.28 They reported a remarkable decrease in symptoms, which included fatigue, dyspnea, exercise intolerance, and palpitations, as well as decrease in the right ventricle size.30 In another study, percutaneous ASD closure was found to result in early and remarkable cardiac geometric improvements that nearly reverted the right-to-left volumetric imbalance completely. Most of this remodeling occurs within a few weeks after ASD closure. Even in patients >60 years old, transcatheter ASD closure is safe and effective, and right ventricle remodeling is still reported.31
The most common complications are outlined in Table 2. Complications that relate to the procedure and the device are rare. The following complications may occur during transcatheter ASD closure: device migration; device malposition; cardiac erosion/perforation leading to tamponade and death; atrioventricular block; bacterial endocarditis; and the complications encountered from cardiac catheterization, including air embolism, infection, and hematomas. The Helex device has not been associated with device erosion; however, there have been numerous cases of wire-frame fracture, with a quoted incidence between 5% and 7%, particularly with the larger (35 mm) device. Although these fractures typically cause no clinical sequelae, rare cases of damage to the mitral valve have been reported.29 Device embolization is the most commonly encountered complication, which may relate to inadequate rims, improper sizing, or placement of the device.32 Arrhythmia is the second most common complication and it tends to be more common in adult patients.32 In the majority of cases, this complication improves with time. Device erosion into the aortic root or the roof of the left or right atrium is one of the most serious complications; however, it is rare with an approximate incidence of 0.1% in the United States.33
In a recent presentation at the April 2012 Pediatric Interventional Cardiac Symposium (PICS), data review from multiple databases suggested an incidence of erosion to be 0.07%-0.11% in the United States and 0.04%-0.17% worldwide.34 All erosion cases except two had either a deficient anterior superior rim or were oversized.35 Device erosion symptoms typically include chest pain, dizziness, shortness of breath, hemodynamic collapse, or sudden death, but patients can also be totally asymptomatic.35 Pericardial effusion/tamponade, hemopericardium, and aortic to atrial fistula have been associated with erosion of the device after closure. Furthermore, the mortality rate due to device erosion is very rare, ranging from 0.004%-0.015% for the worldwide experience and from 0.008%-0.016% in the United States. Such rare rates compare very well with those of surgical repair of ASD. The Amplatzer device is not the only device that has been linked to erosion, but other devices with two flat discs have also been linked (Starflex; CardioSeal).32 Most erosions occurred at the roof of the atria, near the aortic root, and in most cases symptoms developed within 72 hours after the procedure. A small number have been reported from 8 months to 6 years after closure.34 Some of the factors that may increase the risk of the erosion are deficient aortic rim with or without deficient superior rim and the use of an over-sized device. The United States FDA held a panel meeting in May 2012 to examine the issue of device erosions. The final recommendations of the FDA Circulatory Device System are still pending at the time of this writing.
ASD Closure Devices
Many devices have been developed, with only two devices receiving FDA approval in the United States. These are the Amplatzer septal occluder and the Helex septal occluder.
1. The Amplatzer septal occluder. The Amplatzer septal occluder is one of two closure devices being used in the United States manufactured by St Jude Medical. It is a self-centering device that consists of two circular retaining discs made of nitinol wire mesh and linked together by a short connecting waist. While the waist centers the device in the defect and occludes it, the retaining discs provide stability on opposite sides of the defect. The size is determined by the size of the waist and ranges from 4-40 mm; however, the 40 mm device is not approved in the United States. It is delivered by a long sheath available in different sizes.
2. The Gore Helex septal occluder. The Gore Helex is the second device approved for use in the United States and is manufactured by WL Gore & Associates. No cases of migration or erosion have been reported for this device. The occluder is composed of an expanded polytetrafluoroethylene material with hydrophilic coating, which is supported by a nitinol frame. The occluder has a double disc shape that bridges the defect. A 2:1 ratio between the device size and the defect size “balloon-stretched diameter” should be used for optimal results, and the device diameter should not exceed 90% of the measured septal length. The septal tissue margins should be sufficient in size and integrity to prevent device embolization, and residual leaks are more common when the defect size is measured to be more than 18 mm.
In one large study, 87% of 342 patients had the Helex device implanted successfully. There were significant adverse events (mostly device removal for different reasons) in 5.8%.36 Overall composite success was seen in 91.5%. Significant residual shunt and frame fracture were reported; however, no device erosion or cardiac perforation have been reported thus far with the Helex. A newer modification of this device, the Gore septal occluder (GSO) just received United States FDA approval for initiation of an IDE clinical trial. It is also comprised of a nitinol wire frame covered with expanded polytetrafluoroethylene (ePTFE). The wire frame is formed from five wires shaped into the right and left atrial discs, the eyelets, and the lock loop. The five-wire design provides conformability, allowing each individual wire within a right or left atrial disc to conform to the heart anatomy. The ePTFE includes a hydrophilic surface treatment to facilitate echocardiographic imaging of the occluder and surrounding tissue during implantation. Figure 7 depicts this new device.
3. The Occlutech Figulla Flex II device. The Occlutech Figulla Flex II (Occlutech gmbH) is a self-expanding nitinol wire mesh, very similar to the Amplatzer device in shape, but with a different design that eliminates the left atrial microscrew.This is fully recapturable and repositionable, and allows 50% reduction of meshwork material on the left atrial side with greater flexibility compared with Amplatzer device. Furthermore, the delivery cable mechanism is different and allows pivoting of the device, which facilitates positioning across the septum, an advantageous feature especially in large defects. Figures 8 and 9 depict the device and its delivery cable.
4. Transcatheter Patch device. The Transcatheter Patch utilizes a balloon-mounted, porous, polyurethane patch in combination with a defect bridging system for device apposition and immobilization until patch integration into adjacent tissue occurs. This device is flexible, biodegrades in situ and eventually will be replaced with native tissue. It is manufactured by Custom Medical Devices.
5. Cardioseal/Starflex. The Cardioseal/Starflex family of devices consists of two square patches of polyster fabric hand-sewn to a stainless-steel skeleton. Usually, it is used to close defects <16 mm. The manufacturer of these devices (Nitinol Medical Technologies) ceased to exist due to financial problems and the technology was sold to WL Gore & Associates.
6. Bioabsorbable devices (Biostar, Biotrek). Biostar and Biotrek are unique in using bioabsorbable materials to optimize the biological response of the defect closure and reduce the burden of prosthetic material that remains in the heart once the closure is achieved. The Biostar has an engineered porcine intestinal collagen layer scaffold, while the Biotrek uses the synthetic polymer poly-4-hydroxybutyrate. The manufacturer of these two devices is the same as the CardioSeal and ceased to exist.
7. Cardia devices. There are multiple generations of Cardia occluders (manufactured by Cardia Inc). Overall, the device has a double umbrella, with a frame of four arms. These devices have evolved and improved remarkably over the last 1-2 decades. There is a plan for a clinical trial in the United States.
8. Solysafe septal occluder. The Solysafe septal occluder consists of a self-centering device with two foldable polyester patches attached to eight metal wires made of phynox, which has been used in surgical implants for years. The course of the wires and the device’s patch enable the device to self-center in defects of variable diameters, with a maximum diameter given by the distance between the wires. With five device sizes, defects with stretched diameter up to 30 mm can be effectively closed. Gielen et al37 reported a very high incidence of device fracture in their most recent study. The incidence of device fracture was 82.3% after 5 years of implantation. The device was also associated with erosions and was therefore discontinued by the manufacturer (Swissimplant AG).
9. PFM device (ASD-R). Manufactured by PFM gmbH, the PFM is a double-disc device made of nitinol wire, which is woven tightly in a single piece without welding or hubs on either side, which may reduce the risk of clot on the disc. A self-centering waist is achieved by reverse configuration of the left atrial disc.
Despite the recent concern about device erosions associated with some devices, albeit very rare, transcatheter ASD closure has continued to be a very safe procedure with comparable results to surgical closure, and long-term follow up studies have shown that the overall outcomes remain excellent. Device closure of the appropriate defect is an attractive alternative option to open surgical techniques. The United States FDA Circulatory Device System recommendations regarding device erosions are still pending and perhaps will shape the future of ASD device closure in the United States.
- Feltes TF, Bacha E, Beekman RH 3rd, et al. Indications for cardiac catheterization and intervention in pediatric cardiac disease: a scientific statement from the American Heart Association. American Heart Association Congenital Cardiac Defects Committee of the Council on Cardiovascular Disease in the Young; Council on Clinical Cardiology; Council on Cardiovascular Radiology and Intervention. Circulation. 2011;123(22):2607-2652.
- King TD, Thompson SL, Steiner C, Mills NL. Secundum atrial septal defect. Nonoperative closure during cardiac catheterization. JAMA. 1976;7;235(23):2506-2509.
- Mills NL, King TD. Late follow-up of nonoperative closure of secundum atrial septal defects using the King-Mills double-umbrella device. Am J Cardiol. 2003;92(3):353-355.
- Rashkind WJ. Transcatheter treatment of congenital heart disease. Circulation. 1983;67(4):711-716.
- Rome JJ, Keane JF, Perry SB, Spevak PJ, Lock JE. Double-umbrella closure of atrial defects. Initial clinical applications. Circulation. 1990;82(3):751-758.
- Bridges ND, Hellenbrand W, Latson L, Filiano J, Newburger JW, Lock JE. Transcatheter closure of patent foramen ovale after presumed paradoxical embolism. Circulation. 1992;86(6):1902-1908.
- Justo RN, Nykanen DG, Boutin C, McCrindle BW, Freedom RM, Benson LN. Clinical impact of transcatheter closure of secundum atrial septal defects with the double umbrella device. Am J Cardiol. 1996;77(10):889-892.
- Koike K, Echigo S, Kumate M 3rd, el al. Transcatheter closure of atrial septal defect with a prototype clamshell septal umbrella: one year follow-up. J Cardiol. 1994;24(1):53-60.
- Das GS, Voss G, Jarvis G, Wyche K, Gunther R, Wilson RF. Experimental atrial septal defect closure with a new, transcatheter, self-centering device. Circulation. 1993;88(4 Pt 1):1754-1764.
- King TD, Mills NL. Historical perspectives on ASD device closure. In: Hijazi ZM, Feldman T, Al-Qbandi MA, Sievert H, eds. Transcatheter Closure of ASDs and PFOs, A Comprehensive Assessment. Minneapolis, MN: Cardiotext Publishing; 2010:37-64.
- Masura J, Gavora P, Formanek A, Hijazi ZM. Transcatheter closure of secundum atrial septal defects using the new self-centering amplatzer septal occluder: initial human experience. Cathet Cardiovasc Diagn. 1997;42(4):388-393.
- Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc. 1984;59(1):17-20.
- Edwards W. Cardiac anatomy and examination of cardiac specimen. In: Allen HD, Driscoll DJ, Shaddy RE, Feltes TF, eds. Atrial Septum. Moss and Adams Heart Disease in Infants, Children and Adolescent: Including the Fetus and Young Adult. 7th ed. Philadelphia, PA: Wolters Kluwer; 2007:10-11.
- Porter CJ, Edwards W. Atrial septal defects. Anatomy, embryology, and pathology. In: Allen HD, Driscoll DJ, Shaddy RE, Feltes TF, eds. Moss and Adams Heart Disease in Infants, Children, and Adolescent: Including the Fetus and Young Adult. 7th ed. Philadelphia, PA: Wolters Kluwer; 2007:632-645.
- Steele PM, Fuster V, Cohen M, Ritter DG, McGoon DC. Isolated atrial septal defect with pulmonary vascular obstructive disease — long-term follow-up and prediction of outcome after surgical correction. Circulation. 1987;76(5):1037-1042.
- Konstantinides S, Geibel A, Olschewski M, et al. A comparison of surgical and medical therapy for atrial septal defect in adults. N Engl J Med. 1995;333(8):469-473.
- Diab KA, Cao QL, Baca EA, Hijazi ZM. Device closure of atrial septal defects with the Amplatzer septal occluder: safety and outcome in infants, J Thorac Cardiovasc Surg. 2007;134(4):960-966.
- Warnes CA, Williams RG, Bashore TM, et al. ACC/AHA 2008 Guidelines for the Management of Adults with Congenital Heart Disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to develop guidelines on the management of adults with congenital heart disease). Circulation. 2008;118(23):e714-e833.
- Balint OH, Samman A, Haberer K, et al. Outcomes in patients with pulmonary hypertension undergoing percutaneous atrial septal defect closure. Heart. 2008;94(9):1189-1193.
- Abdullah Al-Qbandi MH, Cao Q, Hijazi ZM. Imaging to guide ASD and PFO closure: intracardiac echocardiography. In: Hijazi ZM, Feldman T, Abdullah Al-Qbandi MH, Sievert H, eds. Transcatheter Closure of ASDs and PFOs. A Comprehensive Assessment. Minneapolis, MN: Cardiotext Publishing; 2010:111-124.
- Egan M, Holzer RJ. How to close simple ASDs. In: Hijazi ZM, Feldman T, Abdullah Al-Qbandi MH, Sievert H, eds. Transcatheter Closure of ASDs and PFOs. A Comprehensive Assessment. Minneapolis, MN: Cardiotext Publishing; 2010:167-176.
- Varma C, Benson LN, Silversides C, et al. Outcomes and alternative techniques for device closure of large secundum atrial septal defect. Catheter Cardiovasc Interv. 2004;61(1):131-139.
- Wahab HA, Bairam AR, Cao QL, Hijazi ZM. Novel technique to prevent prolapse of the Amplatzer septal occluder through large atrial septal defect. Catheter Cardiovasc Interv. 2003;60(4):543-545.
- Dalvi BV, Pinto RJ, Gupta A. New technique for device closure of large atrial septal defects. Catheter Cardiovasc Interv. 2005;64(1):102-107.
- Al-Anani SJ, Weber H, Hijazi ZM. Atrioventricular block after transcatheter ASD closure using the Amplatzer septal occluder: risk factors and recommendations. Catheter Cardiovasc Interv. 2010;75(5):767-772.
- Hill SL, Berul CI, Patel HT, et al. Early ECG abnormalities associated with transcatheter closure of atrial septal defects using the Amplatzer septal occluder. J Interv Card Electrophysiol. 2000;4(3):469-474.
- Veldtman GR, Razack V, Siu S, et al. Right ventricular form and function after percutaneous atrial septal defect device closure. J Am Coll Cardiol. 2001;37(8):2108-2113.
- Du ZD, Hijazi ZM, Kleinman CS, Silverman NH, Larntz K. Comparison between transcatheter and surgical closure of secundum atrial septal defects in children and adults: results of a multicenter non randomized trial. J Am Coll Cardiol. 2002;39(11):1836-1844.
- Jones TK, Latson LA, Zahn E, et al. Results of the U.S. multicenter pivotal study of the Helex septal occluder for percutaneous closure of secundum atrial septal defects. J Am Coll Cardiol. 2007;49(22):2215-2221.
- Patel A, Lopez K, Banerjee A, Joseph A, Cao QL, Hijazi ZM. Transcatheter closure of atrial septal defects in adults >40 years of age: immediate and follow-up results. J Interv Cardiol. 2007;20(1):82-88.
- Elshershari H, Cao QL, Hijazi ZM. Transcatheter device closure of atrial septal defects in patients older than 60 years of age: immediate and follow-up results. J Invasive Cardiol. 2008;20(4):173-176.
- Chessa M, Carminati M, Butera G, et al. Early and late complications associated with transcatheter occlusion of secundum atrial septal defect. J Am Coll Cardiol. 2002;39(6):1061-1065.
- Amin Z, Hijazi ZM, Bass JL, Cheatham JP, Hellenbrand WE, Kleinman CS. Erosion of Amplatzer septal occluder device after closure of secundum atrial septal defects: review of registry of complications and recommendations to minimize future risk. Cathet Cardiovasc Interv. 2004;63(4):496-502.
- Diab K, Kenny D, Hijazi ZM. Erosions, erosions and erosions! device closure of atrial septal defects: how safe is safe?. Cathet Cardiovasc Interv. 2012;80(2):168-174.
- Divekar A, Gaamangwe T, Shaikh N, Raabe M, Ducas J. Cardiac perforation after device closure of atrial septal defects with the Amplatzer septal occluder. J Am Coll Cardiol. 2005;45(8):1213-1218.
- Latson LA, Jones TK, Jacobson J, et al. Analysis of factors related to successful transcatheter closure of secundum atrial septal defects using the HELEX septal occluder. Am Heart J. 2006;151(5):1129.e7-1129.e11.
- Gielen S, Riede F, Schuler G, Dahnert I. Wire fractures in Solysafe septal occluders: a single center experience. Catheter Cardiovasc Interv. 2012;79(7):1161-1168.
- Chan KC, Godman MJ, Walsh K, Wilson N, Redington A, Gibbs JL. Transcatheter closure of atrial septal defect and interatrial communications with a new self expanding nitinol double disc device (Amplatzer septal occluder): multicentre UK experience. Heart. 1999;82(3):300-306.
- Waight DJ, Koenig PR, Cao QL, Hijazi ZM. Transcatheter closure of secundum atrial septal defects using the Amplatzer septal occluder: clinical experience and technical considerations. Current Interv Cardiol Rep. 2000;2(1):70-77.
- Chessa M, Carminati M, Butera G, et al. Early and late complications associated with transcatheter occlusion of secundum atrial septal defect. J Am Coll Cardiol. 2002;39(6):1061-1065.
- Spies C, Timmermanns I, Schräder R. Transcatheter closure of secundum atrial septal defects in adults with the Amplatzer septal occluder: intermediate and long-term results. Clin Res Cardiol. 2007;96(6):340-346.
From the Rush Center for Congenital & Structural Heart Disease, Departments of Medicine and Pediatrics, Rush University Medical Center, Chicago, Illinois.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein. Conflict of Interest: Dr Hijazi is a consultant for Occlutech.
Manuscript submitted December 26, 2012, provisional acceptance given January 28, 2013, final version accepted February 7, 2013.
Address for correspondence: Ziyad M. Hijazi MD, MPH, Rush Center for Congenital & Structural Heart Disease, Jones 770, 1653 W. Congress Parkway, Chicago, IL 60612. Email: Zhijazi@rush.edu