Pediatr Cardiol (2015) 36:106–110 DOI 10.1007/s00246-014-0971-x
ORIGINAL ARTICLE
Retrograde Closure of Perimembranous Ventricular Septal Defect Using Muscular Ventricular Septal Occluder: A Single-Center Experience of a Novel Technique Kalyanasundaram Muthusamy
Received: 18 February 2014 / Accepted: 16 July 2014 / Published online: 20 August 2014 Ó Springer Science+Business Media New York 2014
Abstract We herein report the advantages of retrograde ventricular septal defect (VSD) closure using a muscular VSD device for perimembranous VSDs. Perimembranous VSDs are conventionally closed by an antegrade technique (arteriovenous looping technique) using a patent ductus arteriosus or asymmetric perimembranous VSD device. However, we used a symmetrical muscular VSD device in all cases described in this report. Use of the antegrade technique for the first few patients with VSD resulted in prolonged procedural and fluoroscopic times and frequent slippage of the device into the right ventricle. Subsequent use of the retrograde technique shortened the procedural time and allowed for easier closure of the perimembranous VSD. We performed retrograde closure of perimembranous VSDs using a symmetrical muscular VSD device in 130 patients. We obtained a high rate of successful deployment (88.5 %) and a low rate of complications (6.0 %). We also achieved shorter procedural and fluoroscopic times than those associated with the antegrade technique. Keywords Ventricular septal defect Amplatzer muscular VSD device Cera Lifetech muscular VSD device Antegrade technique Retrograde technique Arteriovenous looping
Introduction Transcatheter closure of atrial septal defects, patent ductus arteriosus (PDA), and ventricular septal defects (VSDs) has been regularly performed since the introduction of the K. Muthusamy (&) G. Kuppuswamy Naidu Memorial Hospital, Coimbatore, India e-mail: [email protected]
123
Amplatzer septal occluder (AGA Medical Corporation, Plymouth, MN) in 1996 [1, 3]. However, few design modifications have been performed for atrial septal defect and PDA devices. Attempts were made to change the design of PDA devices to better facilitate their use in small and lowweight children, but with limited success. VSD device closure was initially performed with great enthusiasm, but the number of such procedures later substantially decreased because of complex deployment procedures and a high incidence of complete heart block [10, 13]. The exact cause of complete heart block after VSD device closure remains unclear. Potential causes of complete heart block include a high clamping force due to a short waist length and high radial tension due to the effect of the use of a high-profile perimembranous VSD device on the conducting system. Another possible cause of conducting system injury is catheter manipulation during use of the arteriovenous (AV) looping technique (antegrade technique). Therefore, we modified our approach by using a device with a longer waist length and lower radial force that is deployed via a retrograde technique.
Materials and Methods VSD device closure was performed in 153 patients (74 male and 79 female patients) from February 2009 to January 2014. Of these 153 patients, 139 had perimembranous VSDs, 7 had muscular VSDs, and 7 had subpulmonic VSDs. The patients’ ages ranged from 7 months to 20 years [12], and their weights ranged from 3.7 to 62.0 kg. The indications for VSD closure were recurrent respiratory tract infections, heart failure, poor weight gain, exertional dyspnea, cardiomegaly as shown on chest radiographs, left ventricular hypertrophy as shown by
Pediatr Cardiol (2015) 36:106–110
electrocardiography, left heart enlargement as shown by echocardiography, and no aortic cusp prolapse as shown by echocardiography. The patients’ cardiac output was evaluated using the Qp/Qs ratio, which ranged from 1.3 to 4.0. 1 day prior to the procedure, all patients were given a loading dose of dual antiplatelet therapy (aspirin, 5 mg/kg with a maximum of 600 mg; clopidogrel, 3 mg/kg with a maximum of 300 mg). The first four patients successfully underwent the AV looping technique. Two of these four patients had muscular VSDs, and other two had perimembranous VSDs. We used a PDA device in one of the patients with a perimembranous VSD, and the deployment was successfully performed using the antegrade technique. However, the device became embolized when the pigtail was removed from the left ventricle following the completion of left ventricular angiogram to check the residual shunt. The embolized device was retrieved with a snare, and the VSD was closed with a muscular VSD device using a retrograde technique. We thereafter used muscular VSD devices in all patients, and the deployment was performed through the retrograde technique. We initially used Cook’s Mullein sheath for device deployment, but later switched to an Amplatzer delivery system (AGA Medical Corporation, Plymouth, MN) because of repeated kinking in the unbraided Cook’s sheath. Devices used in our cases were the Lifetech PDA device (no. 1) (Lifetech Scientific (Shenzhen) Co., Ltd., Shenzhen, China), Lifetech muscular VSD device (no. 88) (Lifetech Scientific (Shenzhen) Co., Ltd. Shenzhen, China), Amplatzer muscular device (no. 9) (AGA Medical Corporation, Plymouth, MN), and
107
Fig. 2 Patient in Fig. 1. A 10-mm Lifetech muscular ventricular septal defect device was deployed, and an angiogram showed no residual shunt
Fig. 3 Patient in Fig. 1. Immediately after release of device
Fig. 1 10-month-old male patient, 5.9 kg. A left ventricular angiogram in the left anterior oblique cranial 50/30 view showed an 8-mm perimembranous ventricular septal defect
Amplatzer ADO-II device (no. 32) (AGA Medical Corporation, Plymouth, MN). Left ventricular angiography was performed in the left anterior oblique cranial 50/30-degree plane with a 5-French pigtail catheter (Figs. 1, 4). The size of the device chosen was 0–2 mm greater than the actual size of the VSD. The device was upsized or downsized if any residual leakage was present or the device was oversized. An angiographic evaluation was performed using a Berman catheter from the right ventricular side in the left anterior oblique cranial 50/30-degree plane, and the levophase was used to check the device position and identify any residual
123
108
Fig. 4 13-month-old female patient, 7.3 kg. A left ventricular angiogram in the left anterior oblique cranial 50/30 view showed an 8-mm perimembranous ventricular septal defect
Pediatr Cardiol (2015) 36:106–110
Fig. 6 Patient in Fig. 4. Immediately after release of device
the day after the procedure and at the 1-month follow-up visit.
Results
Fig. 5 Patient in Fig. 4. A 10-mm Lifetech ventricular septal defect device was deployed, and an angiogram obtained showed no residual shunt
leakage (Figs. 2, 5). Transthoracic echocardiography was used during and after deployment of the device to check the position of the device and identify any residual leakage, right ventricular outflow tract obstruction, or significant aortic or tricuspid regurgitation. The electrocardiographic and hemodynamic parameters of the patients were checked before releasing the device (Figs. 3, 6). After 2–3 h of observation in the postcatheterization ward, the patients were moved to a hospital room. All patients were discharged the next day. Electrocardiography was performed
123
All patients who underwent successful device deployment exhibited immediate VSD closure with no residual leakage. Of all 153 patients, 139 had perimembranous VSDs, 7 had muscular VSDs, and 7 had subpulmonic VSDs. Successful deployment was achieved in 123 (88.5 %) of the 139 patients with perimembranous VSDs. For various reasons, device deployment was impossible in 16 (11.5 %) patients with perimembranous VSDs: 5 had a persistent residual shunt, 3 had developed significant aortic regurgitation, 3 exhibited hemodynamic instability, 1 had transient complete heart block, 1 had multiple VSDs, and 3 developed device embolization. Among the patients who underwent successful device closure, five (4 %) had trivial aortic regurgitation that persisted even after release of the device, and two had a flow gradient of B20 mmHg across the right ventricular outflow tract. One patient developed a vascular complication during retrieval of the device from the aorta. This was our fourth patient, in whom we used a PDA device that became embolized because of the pigtail. Five of the seven patients with muscular VSDs underwent successful device closure. The procedure could not be performed in one patient because of the presence of multiple VSDs, and difficulty crossing the VSD was encountered because of its anterior location in the remaining patient.
Pediatr Cardiol (2015) 36:106–110
Successful device closure was only achieved in two of the seven patients with subpulmonic VSDs. The procedure could not be performed in four patients because of difficulty crossing the VSD and in one patient because of the development of significant aortic regurgitation after device deployment.
Discussion The VSDs in the present study ranged from 3 to 22 mm. We decided to close the VSDs based on the following clinical symptoms: recurrent respiratory tract infections, symptoms of heart failure, poor weight gain, and exertional dyspnea. Other indications to close the VSDs were cardiomegaly as shown by chest radiography, left ventricular hypertrophy as shown by electrocardiography, and left heart enlargement as shown by echocardiography. The cardiac output was evaluated in our patients by measuring the Qp/Qs ratio, which ranged from 1.3 to 4.0. Although some patients did not exhibit cardiomegaly or significant left-to-right shunting, we decided to close the VSDs based on the patients’ symptoms and echocardiographic evidence of aortic cusp prolapse. Patients with small VSDs showed remarkable improvement in their symptoms of recurrent respiratory tract infections after the VSD was closed. Our initial experience with the antegrade technique was associated with a long procedural time [3, 4]. We used a PDA device in one patient in the early period, but the device became embolized. We reattempted closure in this patient with a muscular VSD device using the retrograde technique, and deployment was successful. Since then, we have performed VSD closure using the retrograde technique almost exclusively. A low-profile muscular VSD device was chosen to avoid radial and clamping force tension on the conduction system. We found that the Lifetech muscular VSD device has a relatively lower profile than does the Amplatzer muscular VSD device [9, 11]. The radial force of the Lifetech muscular VSD device and ADO II device is lower than that of the Amplatzer muscular VSD device. We thought that the use of these devices might reduce the injury to the conducting system. Another factor associated with conducting system injury is the length of the device. The waist length of the muscular VSD device is 7 mm, which is longer than the 3-mm waist length of the asymmetrical PM VSD device [2, 6]. We thought that the use of a device with a longer waist might reduce the clamping force on the septum, thereby minimizing the injury to the conducting system. Although the waist of the muscular VSD device is longer than that of the PM VSD device, no device encroachment in either the right or left ventricular outflow tract occurred. We chose the retrograde technique for two reasons. In the antegrade technique, the shearing force on the VSD margins during catheter manipulation may be higher than
109
those in the retrograde technique. This excessive shearing force might be a potential cause of conducting system damage. In addition, the procedural and fluoroscopic times are significantly longer in the antegrade than in the retrograde technique. We could not deploy the device in five patients because of a persistent residual shunt. All of these patients exhibited an insufficient aortic rim as confirmed during surgical closure. Three patients developed frequent hemodynamic instability during delivery sheath manipulation, and the procedures were thus abandoned. Three patients developed significant aortic regurgitation after the device was deployed; these patients were also sent for surgery. One patient developed a complete heart block after the device was deployed. The block persisted for more than 1 min, and the procedure was thus abandoned. One patient developed a complete heart block, 5 days after the procedure. This patient was managed by placement of a temporary pacemaker and administration of an intravenous steroid for 5 days followed by administration of an oral steroid for 2 weeks. Her complete heart block entirely resolved 3 days after the initiation of steroid therapy. We thereafter modified our protocol to include the administration of an intravenous steroid, usually dexamethasone, immediately after the procedure, and to continue an oral steroid (prednisolone) for five more days. This treatment is likely to prevent edema-induced damage to the conducting system. We experienced three cases of device embolization. In one patient, the device was caught under the tricuspid valve and was retrieved with a snare. The other two patients underwent surgery because an attempt to retrieve the VSD device from the pulmonary artery had a risk of actually pushing the device further into the peripheral circulation, inducing vascular damage. Device closure was successful in five of the seven patients with muscular VSDs. Of these five patients, two underwent VSD closure through a jugular approach with AV looping, and the other three underwent VSD closure through the retrograde technique. We had to abandon the procedure in two patients because of difficulty in crossing the anteriorly located muscular VSD in one patient and the presence of multiple muscular VSDs in the other. Although we attempted to close the subpulmonic VSDs in seven patients, we succeeded in only two. We experienced difficulty crossing the VSD in four patients because the VSD was located more anteriorly, and another patient developed significant aortic regurgitation. Of all 139 attempted perimembranous VSD closures, 16 (11.5 %) failed. Inadequate aortic rims were identified in 11 cases, resulting in a residual shunt in 5, development of aortic regurgitation in 3, and embolization of the device in 3. Deficient aortic rims were confirmed during surgical closure of the VSDs in these failed cases. We experience
123
110
the most difficult challenge in crossing anteriorly located subpulmonic and anterior muscular VSDs. We failed to cross six of eight anteriorly located VSDs. Oversizing was the cause of complete heart block in one patients with a perimembranous VSD; the block was reverted to sinus rhythm with steroid therapy.
Pediatr Cardiol (2015) 36:106–110
5.
6.
Conclusion 7.
Device closure of perimembranous VSDs using the retrograde technique was far superior to that using the antegrade technique. Low-profile muscular or ADO II devices can be used for VSDs in a perimembranous location. The procedure and fluoroscopic times were significantly lower with the retrograde technique than with the antegrade technique. No permanent complete heart block has occurred during 4.5 years of follow-up [5, 7, 8]. Our preprocedural assessment results were incorrect in terms of evaluating the adequacy of the aortic rim in 8 % of patients.
8.
9.
10.
References 11. 1. Bass JL, Karla GS, Arora R et al (2003) Initial human experience with the Amplatzer perimembranous ventricular septal occluder device. Catheter Cardiovasc Interv 58:238–245 2. Fu YC, Bass J, Amin Z et al (2006) 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 47:319–325 3. Gu X, Han YM, Titus JL et al (2000) Transcatheter closure of membranous ventricular septal defects with a new nitinol prosthesis in a natural swine model. Catheter Cardiovasc Interv 50:502–509 4. Hijazi ZM, Hakim F, Abu Haweleh A et al (2002) Catheter closure of perimembranous ventricular septal defects using new
123
12.
13.
Amplatzer membranous VSD occluder: initial clinical experience. Catheter Cardiovasc Interv 56:508–515 Holzer R, de Giovanni J, Walsh KP et al (2006) Transcatheter closure of perimembranous ventricular septal defects using the Amplatzer membranous VSD occluder: immediate and midterm results of an international registry. Catheter Cardiovasc Interv 68:620–628 Kramoh E, Dahdah N, Fournier A et al (2008) Invasive measurements of atrioventricular conduction parameters prior to and following ventricular septal defect closure with the Amplatzer device. J Invasive Cardiol 20:212–216 Masura J, Gao W, Gavora P et al (2005) Percutaneous closure of perimembranous ventricular septal defects with the eccentric Amplatzer device: multicenter follow- up study. Pediatric Cardiol 26:216–219 Miro J, Hosking M, Lee KJ, et al (2005) Closure of perimembranous ventricular septal defects with the Amplatzer device: multicenter Canadian experience. Pediatric interventional cardiac symposium and emerging new technologies in congenital heart surgery (PICS/ENTICHS-2005), Buenos Aires, 15–18 September 2005 Pedra CAC, Pedra SRF, Esteves CA et al (2004) Percutaneous closure of perimembranous ventricular septal defects with the Amplatzer device: technical and morphological considerations. Catheter Cardiovasc Interv 61:403–410 Pinto RJ, Dalvi BV, Sharma S (2006) Transcatheter closure of perimembranous ventricular septal defects using Amplatzer asymmetric ventricular septal defect occluder: preliminary experience with 18-month follow up. Catheter Cardiovasc Interv 68:145–152 Rigby ML, Redington AN (1994) Primary transcatheter closure of perimembranous ventricular septal defects. Br Heart J 72:368–371 Thanopoulos BD, Rigby ML, Karanasios E et al (2007) Transcatheter closure of perimembranous ventricular septal defects in infants and children using the Amplatzer perimembranous ventricular septal defect occluder. Am J Cardiol 99:984–989 Yip WCL, Zimmerman F, Hijazi ZM (2005) Heart block and empirical therapy after transcatheter closure of perimembranous ventricular septal defect. Catheter Cardiovasc Interv 66:436–441
ORIGINAL ARTICLE
Retrograde Closure of Perimembranous Ventricular Septal Defect Using Muscular Ventricular Septal Occluder: A Single-Center Experience of a Novel Technique Kalyanasundaram Muthusamy
Received: 18 February 2014 / Accepted: 16 July 2014 / Published online: 20 August 2014 Ó Springer Science+Business Media New York 2014
Abstract We herein report the advantages of retrograde ventricular septal defect (VSD) closure using a muscular VSD device for perimembranous VSDs. Perimembranous VSDs are conventionally closed by an antegrade technique (arteriovenous looping technique) using a patent ductus arteriosus or asymmetric perimembranous VSD device. However, we used a symmetrical muscular VSD device in all cases described in this report. Use of the antegrade technique for the first few patients with VSD resulted in prolonged procedural and fluoroscopic times and frequent slippage of the device into the right ventricle. Subsequent use of the retrograde technique shortened the procedural time and allowed for easier closure of the perimembranous VSD. We performed retrograde closure of perimembranous VSDs using a symmetrical muscular VSD device in 130 patients. We obtained a high rate of successful deployment (88.5 %) and a low rate of complications (6.0 %). We also achieved shorter procedural and fluoroscopic times than those associated with the antegrade technique. Keywords Ventricular septal defect Amplatzer muscular VSD device Cera Lifetech muscular VSD device Antegrade technique Retrograde technique Arteriovenous looping
Introduction Transcatheter closure of atrial septal defects, patent ductus arteriosus (PDA), and ventricular septal defects (VSDs) has been regularly performed since the introduction of the K. Muthusamy (&) G. Kuppuswamy Naidu Memorial Hospital, Coimbatore, India e-mail: [email protected]
123
Amplatzer septal occluder (AGA Medical Corporation, Plymouth, MN) in 1996 [1, 3]. However, few design modifications have been performed for atrial septal defect and PDA devices. Attempts were made to change the design of PDA devices to better facilitate their use in small and lowweight children, but with limited success. VSD device closure was initially performed with great enthusiasm, but the number of such procedures later substantially decreased because of complex deployment procedures and a high incidence of complete heart block [10, 13]. The exact cause of complete heart block after VSD device closure remains unclear. Potential causes of complete heart block include a high clamping force due to a short waist length and high radial tension due to the effect of the use of a high-profile perimembranous VSD device on the conducting system. Another possible cause of conducting system injury is catheter manipulation during use of the arteriovenous (AV) looping technique (antegrade technique). Therefore, we modified our approach by using a device with a longer waist length and lower radial force that is deployed via a retrograde technique.
Materials and Methods VSD device closure was performed in 153 patients (74 male and 79 female patients) from February 2009 to January 2014. Of these 153 patients, 139 had perimembranous VSDs, 7 had muscular VSDs, and 7 had subpulmonic VSDs. The patients’ ages ranged from 7 months to 20 years [12], and their weights ranged from 3.7 to 62.0 kg. The indications for VSD closure were recurrent respiratory tract infections, heart failure, poor weight gain, exertional dyspnea, cardiomegaly as shown on chest radiographs, left ventricular hypertrophy as shown by
Pediatr Cardiol (2015) 36:106–110
electrocardiography, left heart enlargement as shown by echocardiography, and no aortic cusp prolapse as shown by echocardiography. The patients’ cardiac output was evaluated using the Qp/Qs ratio, which ranged from 1.3 to 4.0. 1 day prior to the procedure, all patients were given a loading dose of dual antiplatelet therapy (aspirin, 5 mg/kg with a maximum of 600 mg; clopidogrel, 3 mg/kg with a maximum of 300 mg). The first four patients successfully underwent the AV looping technique. Two of these four patients had muscular VSDs, and other two had perimembranous VSDs. We used a PDA device in one of the patients with a perimembranous VSD, and the deployment was successfully performed using the antegrade technique. However, the device became embolized when the pigtail was removed from the left ventricle following the completion of left ventricular angiogram to check the residual shunt. The embolized device was retrieved with a snare, and the VSD was closed with a muscular VSD device using a retrograde technique. We thereafter used muscular VSD devices in all patients, and the deployment was performed through the retrograde technique. We initially used Cook’s Mullein sheath for device deployment, but later switched to an Amplatzer delivery system (AGA Medical Corporation, Plymouth, MN) because of repeated kinking in the unbraided Cook’s sheath. Devices used in our cases were the Lifetech PDA device (no. 1) (Lifetech Scientific (Shenzhen) Co., Ltd., Shenzhen, China), Lifetech muscular VSD device (no. 88) (Lifetech Scientific (Shenzhen) Co., Ltd. Shenzhen, China), Amplatzer muscular device (no. 9) (AGA Medical Corporation, Plymouth, MN), and
107
Fig. 2 Patient in Fig. 1. A 10-mm Lifetech muscular ventricular septal defect device was deployed, and an angiogram showed no residual shunt
Fig. 3 Patient in Fig. 1. Immediately after release of device
Fig. 1 10-month-old male patient, 5.9 kg. A left ventricular angiogram in the left anterior oblique cranial 50/30 view showed an 8-mm perimembranous ventricular septal defect
Amplatzer ADO-II device (no. 32) (AGA Medical Corporation, Plymouth, MN). Left ventricular angiography was performed in the left anterior oblique cranial 50/30-degree plane with a 5-French pigtail catheter (Figs. 1, 4). The size of the device chosen was 0–2 mm greater than the actual size of the VSD. The device was upsized or downsized if any residual leakage was present or the device was oversized. An angiographic evaluation was performed using a Berman catheter from the right ventricular side in the left anterior oblique cranial 50/30-degree plane, and the levophase was used to check the device position and identify any residual
123
108
Fig. 4 13-month-old female patient, 7.3 kg. A left ventricular angiogram in the left anterior oblique cranial 50/30 view showed an 8-mm perimembranous ventricular septal defect
Pediatr Cardiol (2015) 36:106–110
Fig. 6 Patient in Fig. 4. Immediately after release of device
the day after the procedure and at the 1-month follow-up visit.
Results
Fig. 5 Patient in Fig. 4. A 10-mm Lifetech ventricular septal defect device was deployed, and an angiogram obtained showed no residual shunt
leakage (Figs. 2, 5). Transthoracic echocardiography was used during and after deployment of the device to check the position of the device and identify any residual leakage, right ventricular outflow tract obstruction, or significant aortic or tricuspid regurgitation. The electrocardiographic and hemodynamic parameters of the patients were checked before releasing the device (Figs. 3, 6). After 2–3 h of observation in the postcatheterization ward, the patients were moved to a hospital room. All patients were discharged the next day. Electrocardiography was performed
123
All patients who underwent successful device deployment exhibited immediate VSD closure with no residual leakage. Of all 153 patients, 139 had perimembranous VSDs, 7 had muscular VSDs, and 7 had subpulmonic VSDs. Successful deployment was achieved in 123 (88.5 %) of the 139 patients with perimembranous VSDs. For various reasons, device deployment was impossible in 16 (11.5 %) patients with perimembranous VSDs: 5 had a persistent residual shunt, 3 had developed significant aortic regurgitation, 3 exhibited hemodynamic instability, 1 had transient complete heart block, 1 had multiple VSDs, and 3 developed device embolization. Among the patients who underwent successful device closure, five (4 %) had trivial aortic regurgitation that persisted even after release of the device, and two had a flow gradient of B20 mmHg across the right ventricular outflow tract. One patient developed a vascular complication during retrieval of the device from the aorta. This was our fourth patient, in whom we used a PDA device that became embolized because of the pigtail. Five of the seven patients with muscular VSDs underwent successful device closure. The procedure could not be performed in one patient because of the presence of multiple VSDs, and difficulty crossing the VSD was encountered because of its anterior location in the remaining patient.
Pediatr Cardiol (2015) 36:106–110
Successful device closure was only achieved in two of the seven patients with subpulmonic VSDs. The procedure could not be performed in four patients because of difficulty crossing the VSD and in one patient because of the development of significant aortic regurgitation after device deployment.
Discussion The VSDs in the present study ranged from 3 to 22 mm. We decided to close the VSDs based on the following clinical symptoms: recurrent respiratory tract infections, symptoms of heart failure, poor weight gain, and exertional dyspnea. Other indications to close the VSDs were cardiomegaly as shown by chest radiography, left ventricular hypertrophy as shown by electrocardiography, and left heart enlargement as shown by echocardiography. The cardiac output was evaluated in our patients by measuring the Qp/Qs ratio, which ranged from 1.3 to 4.0. Although some patients did not exhibit cardiomegaly or significant left-to-right shunting, we decided to close the VSDs based on the patients’ symptoms and echocardiographic evidence of aortic cusp prolapse. Patients with small VSDs showed remarkable improvement in their symptoms of recurrent respiratory tract infections after the VSD was closed. Our initial experience with the antegrade technique was associated with a long procedural time [3, 4]. We used a PDA device in one patient in the early period, but the device became embolized. We reattempted closure in this patient with a muscular VSD device using the retrograde technique, and deployment was successful. Since then, we have performed VSD closure using the retrograde technique almost exclusively. A low-profile muscular VSD device was chosen to avoid radial and clamping force tension on the conduction system. We found that the Lifetech muscular VSD device has a relatively lower profile than does the Amplatzer muscular VSD device [9, 11]. The radial force of the Lifetech muscular VSD device and ADO II device is lower than that of the Amplatzer muscular VSD device. We thought that the use of these devices might reduce the injury to the conducting system. Another factor associated with conducting system injury is the length of the device. The waist length of the muscular VSD device is 7 mm, which is longer than the 3-mm waist length of the asymmetrical PM VSD device [2, 6]. We thought that the use of a device with a longer waist might reduce the clamping force on the septum, thereby minimizing the injury to the conducting system. Although the waist of the muscular VSD device is longer than that of the PM VSD device, no device encroachment in either the right or left ventricular outflow tract occurred. We chose the retrograde technique for two reasons. In the antegrade technique, the shearing force on the VSD margins during catheter manipulation may be higher than
109
those in the retrograde technique. This excessive shearing force might be a potential cause of conducting system damage. In addition, the procedural and fluoroscopic times are significantly longer in the antegrade than in the retrograde technique. We could not deploy the device in five patients because of a persistent residual shunt. All of these patients exhibited an insufficient aortic rim as confirmed during surgical closure. Three patients developed frequent hemodynamic instability during delivery sheath manipulation, and the procedures were thus abandoned. Three patients developed significant aortic regurgitation after the device was deployed; these patients were also sent for surgery. One patient developed a complete heart block after the device was deployed. The block persisted for more than 1 min, and the procedure was thus abandoned. One patient developed a complete heart block, 5 days after the procedure. This patient was managed by placement of a temporary pacemaker and administration of an intravenous steroid for 5 days followed by administration of an oral steroid for 2 weeks. Her complete heart block entirely resolved 3 days after the initiation of steroid therapy. We thereafter modified our protocol to include the administration of an intravenous steroid, usually dexamethasone, immediately after the procedure, and to continue an oral steroid (prednisolone) for five more days. This treatment is likely to prevent edema-induced damage to the conducting system. We experienced three cases of device embolization. In one patient, the device was caught under the tricuspid valve and was retrieved with a snare. The other two patients underwent surgery because an attempt to retrieve the VSD device from the pulmonary artery had a risk of actually pushing the device further into the peripheral circulation, inducing vascular damage. Device closure was successful in five of the seven patients with muscular VSDs. Of these five patients, two underwent VSD closure through a jugular approach with AV looping, and the other three underwent VSD closure through the retrograde technique. We had to abandon the procedure in two patients because of difficulty in crossing the anteriorly located muscular VSD in one patient and the presence of multiple muscular VSDs in the other. Although we attempted to close the subpulmonic VSDs in seven patients, we succeeded in only two. We experienced difficulty crossing the VSD in four patients because the VSD was located more anteriorly, and another patient developed significant aortic regurgitation. Of all 139 attempted perimembranous VSD closures, 16 (11.5 %) failed. Inadequate aortic rims were identified in 11 cases, resulting in a residual shunt in 5, development of aortic regurgitation in 3, and embolization of the device in 3. Deficient aortic rims were confirmed during surgical closure of the VSDs in these failed cases. We experience
123
110
the most difficult challenge in crossing anteriorly located subpulmonic and anterior muscular VSDs. We failed to cross six of eight anteriorly located VSDs. Oversizing was the cause of complete heart block in one patients with a perimembranous VSD; the block was reverted to sinus rhythm with steroid therapy.
Pediatr Cardiol (2015) 36:106–110
5.
6.
Conclusion 7.
Device closure of perimembranous VSDs using the retrograde technique was far superior to that using the antegrade technique. Low-profile muscular or ADO II devices can be used for VSDs in a perimembranous location. The procedure and fluoroscopic times were significantly lower with the retrograde technique than with the antegrade technique. No permanent complete heart block has occurred during 4.5 years of follow-up [5, 7, 8]. Our preprocedural assessment results were incorrect in terms of evaluating the adequacy of the aortic rim in 8 % of patients.
8.
9.
10.
References 11. 1. Bass JL, Karla GS, Arora R et al (2003) Initial human experience with the Amplatzer perimembranous ventricular septal occluder device. Catheter Cardiovasc Interv 58:238–245 2. Fu YC, Bass J, Amin Z et al (2006) 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 47:319–325 3. Gu X, Han YM, Titus JL et al (2000) Transcatheter closure of membranous ventricular septal defects with a new nitinol prosthesis in a natural swine model. Catheter Cardiovasc Interv 50:502–509 4. Hijazi ZM, Hakim F, Abu Haweleh A et al (2002) Catheter closure of perimembranous ventricular septal defects using new
123
12.
13.
Amplatzer membranous VSD occluder: initial clinical experience. Catheter Cardiovasc Interv 56:508–515 Holzer R, de Giovanni J, Walsh KP et al (2006) Transcatheter closure of perimembranous ventricular septal defects using the Amplatzer membranous VSD occluder: immediate and midterm results of an international registry. Catheter Cardiovasc Interv 68:620–628 Kramoh E, Dahdah N, Fournier A et al (2008) Invasive measurements of atrioventricular conduction parameters prior to and following ventricular septal defect closure with the Amplatzer device. J Invasive Cardiol 20:212–216 Masura J, Gao W, Gavora P et al (2005) Percutaneous closure of perimembranous ventricular septal defects with the eccentric Amplatzer device: multicenter follow- up study. Pediatric Cardiol 26:216–219 Miro J, Hosking M, Lee KJ, et al (2005) Closure of perimembranous ventricular septal defects with the Amplatzer device: multicenter Canadian experience. Pediatric interventional cardiac symposium and emerging new technologies in congenital heart surgery (PICS/ENTICHS-2005), Buenos Aires, 15–18 September 2005 Pedra CAC, Pedra SRF, Esteves CA et al (2004) Percutaneous closure of perimembranous ventricular septal defects with the Amplatzer device: technical and morphological considerations. Catheter Cardiovasc Interv 61:403–410 Pinto RJ, Dalvi BV, Sharma S (2006) Transcatheter closure of perimembranous ventricular septal defects using Amplatzer asymmetric ventricular septal defect occluder: preliminary experience with 18-month follow up. Catheter Cardiovasc Interv 68:145–152 Rigby ML, Redington AN (1994) Primary transcatheter closure of perimembranous ventricular septal defects. Br Heart J 72:368–371 Thanopoulos BD, Rigby ML, Karanasios E et al (2007) Transcatheter closure of perimembranous ventricular septal defects in infants and children using the Amplatzer perimembranous ventricular septal defect occluder. Am J Cardiol 99:984–989 Yip WCL, Zimmerman F, Hijazi ZM (2005) Heart block and empirical therapy after transcatheter closure of perimembranous ventricular septal defect. Catheter Cardiovasc Interv 66:436–441
