|Year : 2003 | Volume
| Issue : 2 | Page : 3
Transcatheter Closure of Perimembranous and Muscular Ventricular Septal Defects in Children with the Amplatzer Occluder: Experience in Qatar
Assad Al-Hroob1, A Eltohami1, SM Gendi1, Y El Yemeni2, MT Nuhman1, Z Hijazi3
1 Section of Pediatric Cardiology, Department of Cardiology and Cardiovascular Surgery, Hamad Medical Corporation, Doha, Qatar
2 Section of Pediatric Intensive Care Unit, Department of Pediatrics, Hamad Medical Corporation, Doha, Qatar
3 Department of Pediatric Cardiology, University of Chicago, IL, USA
|Date of Web Publication||22-Jun-2010|
Consultant Pediatric Cardiologist, Section of Pediatric Cardiology, Department of Cardiology and Cardiovascular Surgery, Hamad Medical Corporation, P.O. Box 3050, Doha
| Abstract|| |
Transcatheter Amplatzer device closure has been used to close muscular ventricular septal defects with satisfactory results. A new asymmetric Amplatzer perimembranous ventricular septal occluder has been specially designed for closure of perimembranous ventricular septal defects.
We report our initial experience with ventricular septal defect (VSD) device closure from January 1, 2003 to August 31, 2003 using the new Amplatzer perimembranous and muscular ventricular septal occluders. During the eight-month period, we closed 13 VSDs percutaneously, 10 perimembranous and 3 muscular. The mean age was 9 years (range 3-17 yrs), mean weight of 33 kg (range from 10.6-69 kg). The mean VSD size by TEE was 9.7 mm (range 6-12 mm); Qp: Qs was a mean of 1.44:1 (range of 1.1:1 to 2.2: 1). The mean device size was 10.0 mm (6-14 mm). Immediate and complete closure was achieved in 11 patients (92%). One patient with a muscular defect had a residual shunt and multiple other smaller defects. In another patient, the device was retrieved because of device related aortic insufficiency (AI). Complications included LBBB in one patient; two patients developed tricuspid regurgitation (TR), one mild and the other moderate; two patients developed trivial AI, and one with pre-closure AI, improved after closure. On follow up, the LVEDD improved from a mean of 4.4 cm (3.4-5.9) to a mean of 4.0 cm (3.2-5.5cm) at three months.
We conclude that transcatheter occlusion of perimembranous and muscular VSDs is safe, feasible and effective; however, this excellent immediate result and short term follow up need to be confirmed by large scale intervention trials and long term follow up.
|How to cite this article:|
Al-Hroob A, Eltohami A, Gendi S M, El Yemeni Y, Nuhman M T, Hijazi Z. Transcatheter Closure of Perimembranous and Muscular Ventricular Septal Defects in Children with the Amplatzer Occluder: Experience in Qatar. Heart Views 2003;4:3
|How to cite this URL:|
Al-Hroob A, Eltohami A, Gendi S M, El Yemeni Y, Nuhman M T, Hijazi Z. Transcatheter Closure of Perimembranous and Muscular Ventricular Septal Defects in Children with the Amplatzer Occluder: Experience in Qatar. Heart Views [serial online] 2003 [cited 2013 May 21];4:3. Available from: http://www.heartviews.org/text.asp?2003/4/2/3/64454
| Introduction|| |
Surgical closure of muscular and perimembranous VSD has a low mortality and morbidity and has been the standard treatment for patients with pulmonary flow overload and heart failure. There have been several trials to close muscular VSDs with different kinds of devices as an alternative to surgery to avoid associated mortality and morbidity and scar with relatively good results ,,
Recently, transcatheter closure of muscular VSD has been performed successfully using the Amplatzer muscular VSD occluder with excellent results ,, .
Perimembranous VSD closure trials with different devices and coils have not been very successful because of high rates of residual shunt, and most of the devices are not user friendly.
A new Amplatzer device specifically designed to close perimembranous defects was developed recently. This device was made to prevent aortic insufficiency (AI), which is one of the major concerns in perimembranous VSD closure, as the defect is very close to the aortic valve.
We reportour initial experience in closing both muscular and perimembranous VSDs with the new Amplatzer septal occluder.
| Materials and Methods|| |
VSD Amplatzer occluder (AGA, Golden Valley MN) is a self-expanding and self-centering mesh. It is well rounded for muscular defects and specially designed for membranous defects in a way to avoid any compromise to the aortic valve.
The left ventricular (LV) disk is asymmetrical with a 1 mm superior rim designed to avoid the aortic valve and 5 mm inferior rim (with platinum marker) to clasp the muscular septum. The device is retrievable and redeployable [Figure 1]. A detailed description of the device and the implantation procedure was reported previously , ,[Figure 2].
Available diameters range from 4-18 mm in 2 mm increments. Delivery sheath is available in 6 Fr (for 4 mm), 7 Fr (for 6 mm), 8 Fr (for 8-12 mm) and 9 Fr (for 14-18 mm).
The parents of all patients gave written informed consent to VSD Amplatzer device closure. Patients were given Heparin 100 u/kg IV. All procedures were performed under general anesthesia. Closure was guided by single plane angiography and transesophageal echocardiography (TEE) except one patient where we used only trans- thoracic echocardiography, because the appropriate TEE probe was not available.
Standard right and left heart cardiac catheterization were performed; VSD size and separation from aortic valve were confirmed and compared with the TEE and/or TTE.
The VSD size was determined by both TTE and TEE using 2D and color Doppler on long and short axis to obtain the largest diameter. A device size, 1-2 mm larger than the defect diameter, was selected to close the defect. LVEDD was measured by TTE and TEE.
The VSD was crossed from the left ventricle. A floppy exchange guide wire was then snared from the pulmonary artery or SVC (in muscular defects) and withdrawn from the femoral vein. The delivery sheath and dilator were advanced from the femoral vein across the VSD into the ascending aorta and placed in the left ventricle by a special maneuver , . The device was advanced to the tip of the sheath. The left ventricle disk was deployed under fluoroscopic and TEE guidance. In the perimembranous VSD, the inferior direction of the platinum disk mark was confirmed. Good position and absence of residual shunt and AI were confirmed by echocardiography and left ventriculography. Then the right ventricular disk was deployed, again positioned and absence of residual shunt, tricuspid, mitral, and aortic regurgitation were confirmed before release by unscrewing the microscrew. Finally, left ventriculogram and aortogram were performed after the release of the device.
All patients received three doses of cefazoline, one at the beginning of the procedure and two doses at 8 hour-intervals. All patients were maintained on aspirin, 100 mg daily for 6 months. The patients were observed for 24 hours and all were discharged the day after the procedure.
CXR, ECG, and echocardiogram were performed 24 hours after placement and at 1, 3, 6, and 12 months after the procedure to look for any residual shunt, AI, TR and LVEDD. Holter monitoring was performed at 1 month and another 12 months post closure. Endocarditis prophylaxis was recommended for 6 months for all patients, whenever necessary.
| Patients|| |
13 patients with clinical or echocardiographic evidence of a significant left to right shunt secondary to muscular or perimembranous VSD were selected. Those with perimembranous VSD had at least 1-2 mm of tissue inferior to the aortic valve and all had aneurysmal tissue partially covering the defect.
| Results|| |
Thirteen patients underwent attempted closure, 11 membranous and 3 muscular defects. The demographic data and statistical analysis are summarized in [Table 1]. A ventricular septal aneurysm was present in all patients and the distance from the aortic valve to the rim of the VSD was at least 1 mm. Complete closure was achieved in 11 patients (92%), confirmed by TEE and LV angiography [Figure 2]. In one patient who had a 6 mm residual VSD at the upper margin of a surgical patch of a previous surgical repair of atrioventricular canal and another device placed at another institution, the device was retrieved because of device related AI and mild narrowing of the left ventricular outflow tract without obstruction. Although there was adequate aortic rim, the device was not oriented well to stay away from the aortic cusps.
[Additional file 1]
One patient with a muscular VSD was found to have a residual shunt around the device and from other tiny muscular defects. There was mild tricuspid regurgitation in one patient and moderate in another after device implantation. There was a patient with pre-closure aortic prolapse, AI and TR, whose TR remained the same and the AI improved. In another patient, the AI resolved when we changed the size of the device to one of the same size as the defect. In one patient, the sheath was difficult to place in the left ventricular apex so the left ventricular disc was opened in the ascending aorta before it was gently pulled down against the defect.
All patients were discharged on the day after procedure. The median follow-up period was 4 months with a maximum of 8, months and all patients have reported for follow-up. Upon follow up, all patients showed significant decrease in LVEDD, and regression was observed on the second day and progressed gradually.
| Discussion|| |
Recently, the Amplatzer occluder has been successfully used to close muscular ventricular defects. Lately, a specially designed Amplatzer ventricular septal occluder has also been reported as an acceptable device to close membranous/ perimembranous defects ,,, . The device fits all the criteria for successful implantation in such defects, mainly to avoid contact with the aortic and tricuspid valves. Its delivery system is relatively small, retrievable, and user friendly.
In our experience, we were able to achieve promising successful results similar to the few published reports. Complete occlusion was achieved in 92 % of our cases. The one case which had a residual shunt was muscular and there were associated other tiny VSDs. Two patients developed trivial aortic regurgitation, which we believe to be secondary to the catheters used and sheath manipulations, rather than device related. In fact, one patient with pre-VSD closure AI improved after closure, which encourages us to consider closing defects associated with aortic valve prolapse, especially if the prolapse and regurgitation are mild. In one patient who developed AI, the device was easily retrieved. The easy retrievability is an important advantage of this device, especially in patients where the subaortic area is deformed by previous surgery such as in one of our patient. In such patients, the orientation is not as straightforward as in unoperated VSDs.
One patient with a perimembranous VSD, which measured 6.7 mm developed mild aortic regurgitation immediately after placement of an 8mm device. The AI resolved completely by using a 6 mm device; the 8 mm device size was noticed to exert minimum pressure on the non-coronary aortic cusp, which usually happens when the patient has a lot of aneurysmal tissue partially closing the defect. This may indicate that patients who have a lot of aneurysmal tissue may not need a device exactly matching the VSD size.
Only one patient developed LBBB, and the patient is still being followed. Bass et al  reported one patient with temporary LBBB which resolved within a month after closure. One patient developed mild TR and in another it was mild to moderate, probably secondary to rupture of one of the TV chordae tendineae. We suspected the rupture while snaring the wire from the pulmonary artery when we noticed an abnormal curve .
Different ages and weights as low as 3 years and 11 kg respectively were closed without difficulties. This is within the range of age and weight at which surgical repair is usually performed. In all patients, the aortic rim was 2 mm with a maximum of 3 mm for membranous VSDs, thus excluding the possibility of the VSD being high muscular.
All patients received the usual dose of heparin 100u/kg; activated clotting time (ACT) was kept above 200, with careful flushing and handling of the long sheath to prevent any thromboembolic incidents.
Our fluoroscopy time was relatively high, but the trend is going down as our learning curve is improving.
Our initial experience with the new Amplatzer muscular and membranous occluder device is similar to the few previous reports which indicate that transcatheter occlusion of perimembranous and muscular VSDs is safe, feasible and effective; however, the excellent immediate and short term results need to be confirmed by long term follow-up of large scale trials.
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[Figure 1], [Figure 2]