|Year : 2006 | Volume
| Issue : 2 | Page : 44-54
Device closure of congenital (perimembranous and muscular) and acquired ventricular septal defects using the amplatzer devices: Percutaneous and perventricular techniques
Francisco Garay, Satinder Sandhu, Qi-Ling Cao, Ziyad M Hijazi
The Congenital Heart Center, Departments of Pediatrics and Medicine, University of Chicago Hospitals, Pritzker School of Medicine, Chicago, Illinois
|Date of Web Publication||17-Jun-2010|
Ziyad M Hijazi
Professor of Pediatrics & Medicine Congenital heart Center, University of Chicago 5841 South Maryland Ave., MC4051 Chicago, IL 60637
| Abstract|| |
Ventricular septal defect (VSD) accounts for approximately 20% of all forms of congenital heart disease. The conventional treatment has been the surgical closure of these defects. Percutaneous closure of VSD had been attempted in the past but it was not until the development of Amplatzer Muscular VSD occluder device that the higher closure rates and safety of the procedure made it an attractive alternative to the surgical closure. Amplatzer VSD devices have also been designed to close perimembranous and post infarction muscular VSDs and the results have been encouraging. In addition to the percutaneous conventional approach, an intraoperative (perventricular) technique has been developed to allow safe VSD closure with Amplatzer devices in small infants with poor vascular access avoiding the need of cardiopulmonary bypass or in infants with concomitant cardiac defects requiring surgical repair. In this review the transcatheter VSD closure with Amplatzer VSD occluders will be discussed for each type of VSD and the technical aspects will be detailed.
Keywords: VSDs; congenital heart disease, Amplatzer VSD occlude, catheter closure
|How to cite this article:|
Garay F, Sandhu S, Cao QL, Hijazi ZM. Device closure of congenital (perimembranous and muscular) and acquired ventricular septal defects using the amplatzer devices: Percutaneous and perventricular techniques. Heart Views 2006;7:44-54
|How to cite this URL:|
Garay F, Sandhu S, Cao QL, Hijazi ZM. Device closure of congenital (perimembranous and muscular) and acquired ventricular septal defects using the amplatzer devices: Percutaneous and perventricular techniques. Heart Views [serial online] 2006 [cited 2013 May 20];7:44-54. Available from: http://www.heartviews.org/text.asp?2006/7/2/44/63928
| Introduction|| |
Ventricular septal defect (VSD) is the most common form of congenital heart defect accounting for about 20% of all forms of defects  . According to the classification by Soto  the most common type is the perimembranous one accounting for 80% of all types. Muscular defects account for the 5 to 20% of all the VSD's. Such defects can be single or multiple and can be found anywhere in the muscular septum. The inlet and outlet subsets are more infrequent (5-8%).
Surgical closure of perimembranous VSDs has traditionally been accepted as a highly effective and a low risk procedure. However, it is associated with some morbidity, pain and a sternotomy scar. In addition to this, patients with muscular defects (single or multiple) constitute a group in whom surgical repair is associated with considerable morbidity and mortality, as well as a high incidence of residual defects ,,,, . For these reasons percutaneous VSD closure arises as an attractive alternative to surgery offering high complete closure rates and avoiding the surgical associated morbidity.
Several devices have been used in the past to close VSDs, however only the Amplatzer family of VSD devices (AGA Medical Corporation, Golden Valley, MN) have been specifically designed to occlude these defects. These devices have simple and user-friendly delivery systems, require relatively small delivery sheaths that permit their use in small infants, are available in a range of sizes that allow the operator to close a wide range of defects located in the apical, posterior, anterior or mid-muscular portion of the ventricular septum. Additionally the operator has the ability to reposition or recapture and retrieve the device if misplacement occurs resulting in a low rate of embolization. For all these reasons the Amplatzer VSD occluder devices are considered superior to the formerly used devices  .
The indications for percutaneous closure of congenital VSDs remain and should be the same as for surgical closure. Such indications include: clinical evidence of significant left-to-right shunt with congestive heart failure, poor weight gain, cardiomegaly on chest X ray and or dilated left sided cardiac chambers on echocardiography. Measurement of Qp/Qs is flawed with many errors; therefore, we do not rely solely on this value. Traditionally a value larger than 1.5:1 is considered indicative of significant left-to-right shunt. The main objective of closing these defects is to avoid further development of pulmonary hypertension and to prevent pulmonary vascular disease.
Acquired VSDs are very rare and usually occur in patients post myocardial infarction (0.2%)  . Typically these defects are located in the mid apical region of the ventricular septum. These patients are gravelly ill and their prognosis is bleak, even with surgical repair. Guidelines from the American College of Cardiology (ACC) and American Heart Association (AHA) from 2004 recommend urgent cardiac surgical repair regardless of clinical status  . Finally, a VSD can occur after a traumatic injury to the chest or be the result of a surgical procedure (iatrogenic VSD). Such patients do not tolerate sudden onset of left-to-right shunt and it is indicated to close such defects as they present. The standard treatment for acquired VSDs has been surgical closure, however transcatheter closure has been demonstrated to be a feasible safe alternative approach to correct these defects ,,, .
Transthoracic echocardiography (TTE) is fundamental in the assessment of the location, size and number of defects. It gives important information for planning the interventional approach. The short-axis view near the tips of the mitral valve is important in delineating the location of muscular VSDs. The apical four-chamber view at the level of the atrioventricular valves demonstrates apical, mid and inlet defects. The five-chamber view demonstrates the subaortic and anterior defects, and the long axis view demonstrates the membranous and anterior muscular defects.
In this review the transcatheter closure will be discussed for each type of VSD and technical aspects will be reviewed in particular. Complications that are common for the different procedures will be discussed in the later part of this article.
| Percutaneous Closure of Muscular VSD's|| |
Amin reported the first use and description of the Amplatzer Muscular VSD occluder in a canine model in 1999  . The device [Figure 1] was specifically designed for the muscular septum. It is a self-expandable double-disk device made from a 0.004-0.005 inch nitinol wire mesh with a polyester mesh inside to enhance thrombogenicity. Nitinol is a shape-memory alloy composed of nickel and titanium that is biocompatible and has super elastic properties. The waist of the device is 7 mm long corresponding to the thickness of the muscular septum. The right and left disks are 8 mm larger than this connecting waist. The Amplatzer muscular VSD device is available in sizes ranging from 4 to 16 mm in 2-mm increments. There is a microscrew on one end for attachment to the delivery cable. The device requires a 6-9 Fr sheath for delivery.
For the procedure the femoral vein and artery are accessed routinely. If the VSD is located in mid, posterior or apical septum, the right internal jugular vein is also accessed. The patient is fully heparinized (100 U/kg) to achieve an activated clotting time greater than 200 seconds at the time of the device implantation. Routine right and left heart catheterization is performed to assess hemodynamics (pressures and pulmonary vascular resistance) and to measure the degree of left-to-right shunt. For single muscular VSD, the procedure can be safely performed without transesophageal echocardiography (TEE) guidance, however for multiple defects (Swiss cheese septum) continuous TEE monitoring and guidance is essential. A complete TEE study is performed including standard imaging views. Nearby structures to the VSD are specifically evaluated including papillary muscles, moderator band and the chordae tendinae. AV valves are interrogated at baseline for any regurgitation. Left ventricle angiography in single plane in the hepatoclavicular projection (350 LAO/350 cranial) for mid/apical/posterior defects is performed to define location, size and number of the defect(s). This projection is used to better profile the muscular septum. For anterior defects, the long axial oblique view is preferred. The appropriate device size is chosen to be 1-2 mm larger that the diameter of the defect as measured by color Doppler TEE or angiography (the bigger of the two diameters) at end diastole. Balloon sizing of muscular defects is not necessary.
Next step is in the procedure is to cross the VSD. This is performed using a 4-5 Fr Judkins right coronary catheter advanced from the LV via the defect into the RV. On occasions, the catheter itself may not cross the defect. In such cases, the catheter tip is orientated towards the defect and an angled tip, 0.035" Terumo glide wire is advanced through the defect to the right side. The catheter is then advanced over this wire to the pulmonary artery. The Terumo wire is removed and a 0.035" J-tipped exchange length guide wire is advanced to either branch pulmonary artery. This wire is snared using a goose-neck (ev3, Plymouth, MN) and exteriorized through the right internal jugular vein (mid, posterior or apical muscular defects) or the femoral vein (anterior defects). This provides a stable arteriovenous loop and allows a 6-8 French long Mullins type sheath to be advanced from the jugular or femoral vein and positioned into the LV apex. On occasions some large mid muscular or apical defects can be crossed from the RV side, however care must be exercised not to go through the trabeculae in the right ventricle. In this case, once a catheter is advanced into the LV an exchange length guide wire is advance into the LV apex and a 6-8 French long Mullins type sheath is advanced over this wire and positioned into the body of the LV.
If kinking is noted on the distal part of the delivery sheath when removing the dilator and wire from it, a 0.018" Terumo glide-wire is advanced through the sheath and left inside the sheath during advancement of the device. Once the device reaches the tip of the sheath, this wire is removed. A pigtail catheter is positioned in the LV for angiography to guide device deployment. The LV disk is deployed in the middle of the LV. Then, the entire assembly (cable/sheath) is pulled towards the VSD with further retraction of the sheath to deploy the waist inside the septum. Confirming the position of the device with angiography and TEE is of paramount importance before deploying the RV disk. Once the position is confirmed, the RV disk is deployed by further retraction of the sheath. Again TEE and LV angiography are necessary to confirm the device position prior to its release from the cable. If the position is satisfactory, the device is released by counter-clockwise rotation of the cable using the pin vise. The device orientation commonly changes slightly when it is released from the delivery cable and all the tension on the device is eliminated.
After the release a complete TEE evaluation is performed with additional imaging in multiple views to confirm device placement, to assess residual shunting and any obstruction or regurgitation that may have been induced by the device. Additional defects are then occluded in the same fashion. A last angiogram in the left ventricle is performed 10 minutes after the final device release to assess the result. [Figure 2] and [Figure 3] demonstrate the closure steps of a muscular VSD by TEE and cine fluoroscopy respectively.
Patients receive a dose of an appropriate antibiotic, usually cafazolin (20 mg/kg) during the procedure and two additional doses at eight-hour intervals. The patients are recovered at an appropriate setting and are routinely discharged home the following day. Bacterial endocarditis prophylaxis is recommended for six months or until complete closure is obtained. Patients are instructed to avoid contact sports for one month. Follow up includes TTE with color Doppler, chest radiography and EKG at six months post-closure and yearly thereafter.
Several reports have demonstrated the feasibility and effectiveness of Amplatzer muscular VSD occluder for closure of congenital muscular VSD's ,,,, . The closure rate improves as time from closure to follow-up increases, from 58.7% at one month to 92.3% at 12 months. The remaining residual shunt is usually trivial or small. It has been possible to occlude multiple VSDs with a large device or multiple devices in one or repeated procedures  . Rate for major complications is 10.7% including hypotension, arrhythmias and device embolization. Mortality associated with the procedure is 0-2.7%. It is possible to perform this procedure in patients under 5 kg, however, this is technically very difficult and require an experienced operator. Therefore, in such small patients, it is better to consider the perventricular approach.
| Perventricular Closure of Muscular VSD's|| |
The use of Amplatzer muscular VSD occluder to close muscular VSDs in patients with low weight (< 5 kg), poor vascular access or poor ventricular function, can be performed using the perventricular technique that permits implantation of the device in the hybrid suite, thus avoiding cardiopulmonary bypass with its sequelae ,, .
For this, the chest is opened through a regular median sternotomy, although a subxiphoid minimally invasive incision without full sternotomy has also been reported. Under continuous TEE guidance, the best location for RV puncture is chosen far enough from the septum so as to approach it from a perpendicular angle with the needle and wire. A 5-0 polypropylene purse-string suture is placed at the chosen location and an 18-G needle is introduced into the RV free wall and directed toward the defect to be closed. A 0.035-inch angled Terumo glide wire is passed through the needle and manipulated into the LV cavity through the defect. The needle is then removed keeping the wire in location. A 7F to 10F short (8-13cm) introducer sheath with a dilator is carefully advanced over the wire into the LV cavity. The dilator is removed and the sheath is de-aired. The appropriate device size is chosen to be 1 to 2mm larger than the VSD size as assessed by color Doppler TEE. The device is then screwed to the cable and pulled inside a 6-9 Fr short sheath or loader. We advocate presoaking the device in non-heparinized blood for 10 minutes to allow the tiny fenestrations of the nitinol mesh to thrombose. The device is then advanced inside the short delivery sheath until it is seen by TEE to be close to the tip of the delivery sheath. The LV disk is deployed in mid-LV cavity by gentle retraction of the sheath over the cable. The entire assembly (cable/sheath) is withdrawn gently until the LV disk is against the septum. Further retraction of the sheath over the cable deploys the waist inside the septum. Continuous TEE to confirm the device position is again of paramount importance. Once the position is confirmed, further retraction of the sheath to expand the RV disk is performed. If device position is satisfactory, the device is released by counterclockwise rotation of the cable using the pin vise. A complete TEE study in multiple views is performed to confirm the device placement, assess for residual shunting, and any obstruction or regurgitation induced by the device. If the device is relatively large for a small RV (usually near the apex) and or the RV disk does not expand properly, the device can be recaptured and exchanged for a smaller one or the Amplatzer duct occlud is used instead. On rare occasions, the microscrew of the device may extend through the purse string site, in such cases pledgeted sutures can be used to secure the device in position.
The results with this technique are still limited but encouraging , . The largest published series is a multi-center study that included 13 patients in which only two patients had a mild residual shunt during the follow up and no one had echocardiographic or clinical evidence of significant congestive heart failure, volume overload, or pulmonary hypertension  . Complications during the procedure have not been serious including transitory ventricular arrhythmias induced by the wire and sheath manipulation during the deployment, RV disk malposition and impingement on the tricuspid subvalvar apparatus. No mortality has been reported related to the procedure.
| Percutaneous Closure of Perimembranous/Membranous VSD|| |
The Amplatzer membranous VSD device [Figure 4] has been previously described  . It consists of an asymmetric self-expandable double-disk device made from a 0.003-0.005 nitinol wire mesh with a waist that is 1.5mm long. The aortic end of the left ventricle disk is 0.5mm larger than the waist and the other end is 5.5mm larger than the waist. The right ventricle disk is 2mm larger at both sides. There is a platinum marker positioned in the left ventricle disk. The screw in the device has a flat part that should be aligned on the flat part of the capsule located at the end of the pusher catheter. By doing so, the device almost always exits the delivery sheath in the correct orientation. The device is currently available in sizes ranging from 4-18mm in 2mm increment and a 6 to 9 French delivery sheath is required for the deployment.
The procedure can be performed under general endotracheal anesthesia with continuous TEE guidance or under local anesthesia with either intracardiac echocardiographic (ICE) or TTE guidance. The vascular access is obtained from the femoral vein and artery. The VSD is crossed from the LV side using a 4 or 5 French Judkins right coronary catheter. A 0.035" Terumo glide wire is used to cross the defect and then it is advanced into the pulmonary arteries or superior vena cava. Then the catheter is advanced over the wire into either branch pulmonary artery or superior vena cava; the wire is removed and exchanged by a noodle wire (AGA Medical Corp., Golden Valley, MN), which is advanced to the tip of the catheter. Then the noodle wire is snared using a gooseneck snare catheter and exteriorized out through the femoral vein. This provides a stable arteriovenous loop. Over this wire, the proper size delivery sheath is advanced from the femoral vein all the way until the tip of the sheath reaches the ascending aorta. Slowly the dilator is pulled back to the inferior vena cava-right atrial junction and with the aid of the Judkins catheter positioned in the ascending aorta with the wire inside the tip of the sheath is pushed into the left ventricular apex. It may take some maneuvering to achieve this position. Once the tip of the sheath is in the apex of the LV, the dilator and wire are totally removed. A hand injection angiogram using the delivery sheath will confirm its position and more importantly will delineate the location of the VSD. On rare occasions, more than one fenestration can be documented using this angiogram that were not well seen in the baseline angiogram. The proper-size device is screwed into the delivery cable. The flat part of the microscrew is aligned with the flat part of the capsule located at the end of the pusher catheter. Once the device is loaded, the pin vise is securely tightened to the cable at the end of the hub of the pusher catheter. This is done to prevent the premature disengagement of the two flat parts that will aid in the correct orientation of the LV disk. The left ventricle disk is deployed between the anterior mitral valve leaflet and the left ventricle outflow tract. Echocardiography (TEE/TTE/ICE) is essential to make sure that the mitral valve apparatus is not entangled with the left ventricle disk. The entire assembly is withdrawn back to the septum. This can be seen by echocardiography and confirmed by angiography with a pigtail catheter in the left ventricle. The waist of the device is then deployed. Aligning the left ventricle disk so that the aortic end of the disk is toward the aortic valve is of paramount importance. If the device was properly screwed (flat parts aligned) and the sheath was advanced to the apex of the left ventricle, almost always the flat part of the left ventricle disk is adequately deployed toward the aorta. In addition to this, the platinum marker located in the left ventricle disk should be orientated toward the patient's feet. If so, this indicates proper device position. The right ventricle disk can be deployed after an angiogram to ensure good device position. Echocardiography and repeated angiogram can confirm proper device position prior to disengagement of the two flat parts. For this, the pin vise is loosened and the pusher catheter is withdrawn over the cable. The final step is the release of the device by counter-clockwise rotation of the pin vise. Once the device is released, the cable and the pusher catheter should be brought inside the sheath immediately to prevent any injury from the sharp end of the cable. Repeat echocardiography and an angiogram are performed to assess the final result (closure and residual shunt, assess the function of the tricuspid and aortic valves). As mentioned above, the use of ICE has been reported as an alternative to TEE in guiding the procedure .[Figure 5] and [Figure 6]demonstrate the steps of closure of a perimembranous VSD using TEE and cine fluoroscopy respectively.
Early clinical results with the Amplatzer Membranous VSD occluder have been very encouraging ,,, . Closure rates after the procedure have been reported around 90%, and this number increases during the following months to 98-100% due to thrombosis of the polyester material inside the device and to the endothelialization process. No mortality has been reported related to the procedure. Serious complication rate is low (8.6%) corresponding to occasional cases of complete AV block and aortic insufficiency. The heart block issue (around 2-3%) has been the major reason for the reluctance of interventionalists to use this device. Currently, the manufacturer of the device (AGA Medical Corp.) is in the process of redesigning the device. The redesign entails softening the device by decreasing the thickness of the wire. Obviously, only good clinical trials (registries or randomized trials) will answer the question of safety and effectiveness of device closure of perimembranous VSD.
A perventricular approach to close perimembranous VSD has been reported in an animal model demonstrating that this technique could be possible for small patients with poor vascular access and avoiding CPB effects  . Another report in an animal model demonstrated that the perventricular approach to close perimembranous defects could be possible with a robotically assisted technique, thus avoiding the traditional sternotomy incision  . However this remains preliminary and we will have to wait further clinical application.
| Percutaneous Closure of Post Infarction VSD|| |
The incidence of post myocardial infarction ventricular septal rupture is 0.2%, usually occurring during the first week after the myocardial infarction (MI) and even during the first day  . This group of patients has a poor prognosis and if left untreated the mortality reaches 90%. Even with surgical closure the mortality can be as high as 49%. Isolated case reports and small series of percutaneous device closure of post-MI VSDs have demonstrated that this approach is feasible , .
The Amplatzer post infarction muscular VSD device (AGA Medical) differs slightly from the Amplatzer muscular VSD device. It is available in sizes ranging from 16 to 24mm in 2mm increments. The connecting waist is 10mm long and the RV/LV disks are 5 mm larger than the waist. It requires an 8 to 12 French sheath for delivery. The implantation protocol is the same as that described above for percutaneous closure of congenital muscular VSDs, but the device is selected to be at least 50% larger than the measured diameter of the defect to allow for the predictable continued enlargement of the VSD as times passes from the initial diagnosis.
In the multi-center US experience with 18 patients the 30-day mortality was 28% and long-term mortality was 41%, which compares favorably with the surgical closure mortality  . In this report the persistence of residual shunt was common but usually trivial or small, which is also common in surgically repaired patients. No embolization events occurred. The only approved device for post infarct VSD remains the CardioSEAL device (NMT Medical, Boston, MA). The experience with this device is limited.
| Other Acquired VSDs|| |
Traumatic occurrence of VSDs is observed in a 4.5% of the penetrating cardiac trauma. There exist case reports using Amplatzer muscular VSD occluder and Amplatzer septal occluder (atrial device) to percutaneously close these defects , . There is a report that includes the use of Amplatzer muscular occluder device to percutaneously close a muscular VSD produced after surgical myomyectomy for hypertrophic cardiomyopathy  . An Amplatzer membranous VSD occluder was also used in 2 cases to close a VSD produced after aortic valve replacement  . These isolated case reports support the use of the Amplatzer VSD devices as an effective alternative to surgical closure.
| Complications|| |
Despite the technical differences during closure of muscular or membranous VSDs and the differences in the design of the devices, the procedures share the same spectrum of complications.
Device embolization : this occurrence is rare if the procedure is performed by an experienced operator and under strict echocardiographic guidance (2.7%)  . The devices can migrate to the left or right ventricles and be subsequently embolized to the ascending aorta or pulmonary artery. The device can be snared and retrieved percutaneously, however larger sheaths will be needed. An experienced operator in snaring techniques is required as well the availability of all types and sizes of snaring systems. The presence of a congenital cardiac surgeon in house is essential for VSD device closure program to be initiated at any institution.
Arrhythmias : bradycardia and ventricular arrhythmias can be encountered during the catheter manipulation and the device deployment, particularly in post-infarction patients. They are usually transient but it is essential to have the presence of a congenital cardiac anesthesiologist who can manage all types of rhythm disturbances. Complete AV block after muscular VSD closure has been infrequently observed (1.9%) and is usually transient , . Empirical treatment with high-dose intravenous steroids and high-dose oral anti-inflammatory aspirin has resulted in resolution of the heart block after device closure of perimembranous VSD .
Air embolism: meticulous techniques of catheter and wire exchanges can minimize this complication.
Hemolysis : this is a rare complication usually associated with residual shunt. We have found that pre-soaking the device with the non-heparinized patient's own blood is effective in reducing residual shunt and achieving complete closure. If hemolysis is to occur, medical management is advised by well hydration and alkalinization of the urine. Usually, this will disappear within few days. If hemolysis is severe and the patient requires multiple blood transfusions, we recommend device removal.
Valvular regurgitation : Tricuspid, mitral and aortic valve regurgitation may occur due to impingement of the device or part of it on the tricuspid/mitral subvalvar apparatus or if the device is too close to the aortic valve leaflets. Therefore TEE assessment of the tricuspid/mitral and aortic valves prior to closure and prior to release of the device is extremely important.
Pericardial effusion: this is a very rare complication that may result from catheter irritation or minute wire perforation during the procedure. TTE after 24 hr is essential prior to the discharge of the patient from the hospital. Tamponade is usually due to frank perforation. There have not been reports of delayed pericardial effusion related to Amplatzer VSD device occluder.
In summary, catheter closure of single or multiple muscular VSDs is safe and effective. The device can be deployed percutaneously in the catheterization laboratory or perventricular in the hybrid suite/operating room without the need for cardiopulmonary bypass. The operator needs to be skilled in advanced interventional techniques for successful safe closure of muscular defects. Full echocardiographic skills are also important for successful safe closure. Currently, due to the high risk associated with surgical repair of muscular defects, the device can be offered as an alternative to surgery, however, in the United States, the Amplatzer muscular devices await full United States FDA approval. The results of percutaneous closure of post infarction VSDs have been encouraging, and the device is still under evaluation in the United States. Device closure of perimembranous VSD is still controversial and only good clinical trials with good results will convince skeptics about safety and effectiveness of this technique.
| References|| |
|1.||Rudolph AM. 2001. Ventricular septal defect. In: Rudolph AM. Editor. Congenital diseases of the heart: clinical-physiological considerations, 2nd ed., Armonk, NY: Futura Publishing. P 197-244. |
|2.||Soto B, Becker AE, Moulaert AJ, Lie JT and Anderson RH. Classification of ventricular septal defects. Br Heart J 1980; 43(3):332-343. |
|3.||Wollenek G, Wyse R, Sullivan I, Elliott M, de Leval M, Stark J. Closure of muscular ventricular septal defects through a left ventriculotomy. Eur J Cardiothorac Surg. 1996;10(8):595-598. |
|4.||Stellin G, Padalino M, Milanesi O, Rubino M, Casarotto D, Van Praagh R, Van Praagh S. Surgical closure of apical ventricular septal defects through a right ventricular apical infundibulotomy. Ann Thorac Surg. 2000;69(2):597-601. |
|5.||Kitagawa T, Durham LA 3rd, Mosca RS, Bove EL. Techniques and results in the management of multiple ventricular septal defects. J Thorac Cardiovasc Surg. 1998;115(4):848-56. |
|6.||Seddio F, Reddy VM, McElhinney DB, Tworetzky W, Silverman NH, Hanley FL. Multiple ventricular septal defects: how and when should they be repaired. J Thorac Cardiovasc Surg. 1999;117(1):134-139. |
|7.||Serraf A, Lacour-Gayet F, Bruniaux J, Ouaknine R, Losay J, Petit J, Binet JP, Planche C. Surgical management of isolated multiple ventricular septal defects. Logical approach in 130 cases. J Thorac Cardiovasc Surg. 1992;103(3):437-442. |
|8.||Michel-Behnke I, Le TP, Waldecker B, Akintuerk H, Valeske K, Schranz D. Percutaneous closure of congenital and acquired ventricular septal defects - considerations on selection of the occlusion device. J Interv Cardiol. 2005;18(2):89-99. |
|9.||Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ. Ventricular septal rupture after acute myocardial infarction. N Engl J Med. 2002;347(18):1426-1432. |
|10.||Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction - executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol. 2004;44(3):671-719. |
|11.||Pesenti-Rossi D, Godart F, Dubar A, Rey C. Transcatheter closure of traumatic ventricular septal defect: an alternative to surgery. Chest. 2003;123(6):2144-2145. |
|12.||Fraisse A, Piechaud JF, Avierinos JF, Aubert F, Colavolpe C, Habib G, Bonnet JL. Transcatheter closure of traumatic ventricular septal defect: an alternative to surgical repair. Ann Thorac Surg 2002;74(2):582-584. |
|13.||Chessa M, Carminati M, Cao QL, Butera G, Giusti S, Bini RM, Hijazi ZM. Transcatheter closure of congenital and acquired muscular ventricular septal defects using the Amplatzer device. J Invasive Cardiol. 2002;14(6):322-327. |
|14.||Holzer R, Latson L, Hijazi ZM. Device closure of iatrogenic membranous ventricular septal defects after prosthetic aortic valve replacement using the Amplatzer membranous ventricular septal defect occluder. Catheter Cardiovasc Interv. 2004;62(2):276-280. |
|15.||Amin Z, Gu X, Berry JM, Bass JL, Titus JL, Urness M, Han YM, Amplatz K. New device for closure of muscular ventricular septal defects in a canine model. Circulation. 1999;100(3):320-8. |
|16.||Thanopoulos BD, Karanassios E, Tsaousis G, Papadopoulos GS, Stefanadis C. Catheter closure of congenital/acquired muscular VSDs and perimembranous VSDs using the Amplatzer devices. J Interv Cardiol. 2003;16(5):399-407. |
|17.||Thanopoulos BD, Rigby ML. Outcome of transcatheter closure of muscular ventricular septal defects with the Amplatzer ventricular septal defect occluder. Heart. 2005;91(4):513-516. |
|18.||Holzer R, Balzer D, Cao QL, Lock K and Hijazi ZM. 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. J Am Coll Cardiol 2004; 43:1257-1263. |
|19.||Carminati M, Butera G, Chessa M, Drago M, Negura D, Piazza L. Transcatheter closure of congenital ventricular septal defect with Amplatzer septal occluders. Am J Cardiol. 2005;96(12A):52L-58L. |
|20.||Waight DJ, Bacha EA, Kahana M, Cao QL, Heitschmidt M, Hijazi ZM. Catheter therapy of Swiss cheese ventricular septal defects using the Amplatzer muscular VSD occluder. Catheter Cardiovasc Interv. 2002;55(3):355-361. |
|21.||Amin Z, Gu X, Berry JM, Titus JL, Gidding SS, Rocchini AP. Perventricular closure of ventricular septal defects without cardiopulmonary bypass. Ann Thorac Surg. 1999;68(1):149-153. |
|22.||Bacha EA, Cao QL, Starr JP, Waight D, Ebeid MR, Hijazi ZM. Perventricular device closure of muscular ventricular septal defects on the beating heart: technique and results. J Thorac Cardiovasc Surg. 2003;126(6):1718-1723. |
|23.||Bacha EA, Cao QL, Galantowicz ME, Cheatham JP, Fleishman CE, Weinstein SW, Becker PA, Hill SL, Koenig P, Alboliras E, Abdulla R, Starr JP, Hijazi ZM. Multicenter experience with perventricular device closure of muscular ventricular septal defects. Pediatr Cardiol. 2005;26(2):169-175. |
|24.||Hijazi ZM, Hakim F, Haweleh AA, Madani A, Tarawna W, Hiari A, Cao QL. Catheter closure of perimembranous ventricular septal defects using the new Amplatzer membranous VSD occluder: initial clinical experience. Catheter Cardiovasc Interv. 2002;56(4):508-515. |
|25.||Cao QL, Zabal C, Koenig P, Sandhu S, Hijazi ZM. Initial clinical experience with intracardiac echocardiography in guiding transcatheter closure of perimembranous ventricular septal defects: feasibility and comparison with transesophageal echocardiography. Catheter Cardiovasc Interv. 2005;66(2):258-267. |
|26.||Thanopoulos BD, Tsaousis GS, Karanasios E, Eleftherakis NG, Paphitis C. Transcatheter closure of perimembranous ventricular septal defects with the Amplatzer asymmetric ventricular septal defect occluder: preliminary experience in children. Heart. 2003 Aug;89(8):918-922. |
|27.||Pedra CA, Pedra SR, Esteves CA, Pontes SC Jr, Braga SL, Arrieta SR, Santana MV, Fontes VF, Masura J. Percutaneous closure of perimembranous ventricular septal defects with the Amplatzer device: technical and morphological considerations. Catheter Cardiovasc Interv. 2004;61(3):403-410. |
|28.||Masura J, Gao W, Gavora P, Sun K, Zhou AQ, Jiang S, Ting-Liang L, Wang Y. Percutaneous closure of perimembranous ventricular septal defects with the eccentric Amplatzer device: multicenter follow-up study. Pediatr Cardiol. 2005;26(3):216-219. |
|29.||Fu YC, Bass J, Amin Z, Radtke W, Cheatham JP, Hellenbrand WE, Balzer D, Cao QL, Hijazi ZM. Transcatheter closure of perimembranous ventricular septal defects using the new Amplatzer membranous VSD occluder: results of the U.S. phase I trial. J Am Coll Cardiol. 2006;47(2):319-325. |
|30.||Amin Z, Danford DA, Lof J, Duncan KF, Froemming S. Intraoperative device closure of perimembranous ventricular septal defects without cardiopulmonary bypass: preliminary results with the perventricular technique. J Thorac Cardiovasc Surg. 2004;127(1):234-241. |
|31.||Amin Z, Woo R, Danford DA, Froemming SE, Reddy VM, Lof J, Overman D. Robotically assisted perventricular closure of perimembranous ventricular septal defects: preliminary results in Yucatan pigs. J Thorac Cardiovasc Surg. 2006;131(2):427-432. |
|32.||Goldstein JA, Casserly IP, Balzer DT, Lee R, Lasala JM. Transcatheter closure of recurrent post myocardial infarction ventricular septal defects utilizing the Amplatzer post infarction VSD device: a case series. Catheter Cardiovasc Interv. 2003;59(2):238-243. |
|33.||Szkutnik M, Bialkowski J, Kusa J, Banaszak P, Baranowski J, Gasior M, Chodor P, Zembala M. Post infarction ventricular septal defect closure with Amplatzer occluders. Eur J Cardiothorac Surg. 2003;23(3):323-327. |
|34.||Holzer R, Balzer D, Amin Z, Ruiz CE, Feinstein J, Bass J, Vance M, Cao QL, Hijazi ZM. Transcatheter closure of post infarction ventricular septal defects using the new Amplatzer muscular VSD occluder: Results of a U.S. Registry. Catheter Cardiovasc Interv. 2004;61(2):196-201. |
|35.||Arora R, Trehan V, Thakur AK, Mehta V, Sengupta PP, Nigam M. Transcatheter closure of congenital muscular ventricular septal defect. J Interv Cardiol. 2004;17(2):109-115. |
|36.||Yip WC, Zimmerman F, Hijazi ZM. Heart block and empirical therapy after transcatheter closure of perimembranous ventricular septal defect. Catheter Cardiovasc Interv. 2005;66(3):436-441. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]