Catheterization and Cardiovascular Interventions 87:329–331 (2016)

Device Closure of Secundum Atrial Septal Defect in a 4.5 Kilogram Infant: Novel Use of the Amplatzer DuctOccluder II Device B.A. McCrossan,* MD, MRCPCH and K.P. Walsh, MD, FRCPI Modest secundum atrial septal defects (2 ASD) may cause significant pulmonary over perfusion during infancy, particularly in conjunction with left heart obstructive lesions. Amplatzer Septal Occluders are not ideal in this setting especially given recent concerns regarding device erosion. We report the first use of the Amplatzer Duct Occluder II device (ADO2) to close a 2 ASD in a 4.5 kg infant. VC 2015 Wiley Periodicals, Inc.

Key words: closure; ASD/PDA/PFO; congenital heart disease; pediatrics; pediatric intervention

INTRODUCTION

Device closure of secundum atrial septal defects (2 ASD) is a routine procedure in children three years and over. 2 ASDs morphologically suitable for device closure are usually well tolerated throughout early childhood and intervention may be deferred until preschool. There are particular circumstances in which a modest 2 ASD may be physiologically significant and catheter closure warranted [1]. However, concerns regarding wall erosion with nitinol ASD occluders necessitate further caution especially in smaller patients [2]. We report a novel technique for catheter closure of 2 ASD in an infant with the Amplatzer Duct Occluder II (ADO2) device (MN).

REPORT

The patient is a male infant born at full term by normal vaginal delivery, birth weight 3.5 kg. He presented to the Emergency Department during the first week of life in acute circulatory collapse. Initial echocardiography revealed a hypoplastic aortic arch with a discrete periductal coarctation and bicuspid aortic valve. There was a moderate muscular ventricular septal defect (VSD) and a moderate 2 ASD. Following stabilization, the patient underwent an extended end-to-end anastomosis repair of the aortic arch, via a left lateral thoracotomy, on day 9 of life. The post-operative course was slower than expected. The patient remained in intensive care. Multi-disciplinary input compiled a list of problems including pulmonary hypertension, dyspnoea, fluid overload, continuous positive airway pressure (CPAP) dependency, recurrent aspiration, parenteral feeding, C 2015 Wiley Periodicals, Inc. V

agenesis of the corpus collosum, and galactosaemia. The patient continued to receive six-hourly intravenous frusemide and spironolactone and a milrinone infusion. Serial echocardiography demonstrated mild left ventricular (LV) systolic and diastolic dysfunction along with continued atrial and ventricular shunts. The patient came forward for cardiac catheterization, at six weeks of age (weight 4.5 kg), with a view to device closure of VSD and assessment of suitability for 2 ASD closure. The procedure was performed under general anesthesia with FiO2 ¼ 0.25. Following intravenous access, heparin 100 units/kg and antibiotic prophylaxis (cefuroxime 30 mg/kg) were administered. Transesophageal echocardiography confirmed a moderate 2 ASD (maximal diameter ¼ 6 mm) with a further 2 mm fenestration enabling a significant left-to-right shunt, the left atrium was dilated. The anterior papillary muscle of the mitral valve was dominant but the valve appeared to function normally. The muscular VSD measured 6 mm. Department of Paediatric Cardiology, Our Lady’s Children’s Hospital, Crumlin, Dublin 12, Ireland Conflict of interest: Dr. Walsh is a Proctor for Amplatzer devices. Dr. McCrossan has no conflict of interest *Correspondence to: Dr. Brian McCrossan, Department of Paediatric Cardiology, Our Lady’s Children’s Hospital, Crumlin, Dublin 12, Ireland. E-mail: [email protected] Received 8 July 2014; Revision accepted 30 November 2014 DOI: 10.1002/ccd.25767 Published online 28 November 2015 in Wiley Online Library (wileyonlinelibrary.com)

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The right ventricle was dilated and moderately hypertrophied but biventricular systolic function was well preserved. Cardiac catheterization revealed two-thirds systemic right ventricular pressure and an acceptable left ventricular end diastolic pressure (12 mm Hg). The mean left atrial pressure was 4 mm Hg greater than right atrium. The calculated Qp:Qs was in excess of 4:1. The transverse aortic arch remained mild-to-moderately hypoplastic with an instantaneous doppler gradient ¼ 20 mm Hg but the left ventricular outflow tract was unobstructed. The VSD was crossed from the left ventricle via an antegrade approach with a 5 Fr Judkins right coronary guide catheter. This was exchanged for a 5 Fr Flexor sheath over an 0.03500 Rosen wire. The VSD was closed with an ADO2 6/6 mm device with no residual ventricular shunt. The left ventricular enddiastolic pressure (LVEDP) reduced slightly. Further transoesophageal echocardiogram (TOE) examination suggested a continuing significant atrial shunt (Fig. 1). Therefore an ADO2 6/4 mm device was positioned within the larger 2 ASD using the same Flexor sheath. Following careful echocardiographic evaluation, including interrogation of the pulmonary vein and mitral valve inflow Dopplers, the device was released in a stable position (Figs. 2 and 3). The smaller 2 ASD persisted. At the end of the procedure right ventricular systolic pressure remained at two-thirds systemic. The procedure was uncomplicated and well tolerated. The patient ceased non-invasive ventilation two days post-catheterization, weaned off milrinone two days later, and returned to the cardiac ward six days postprocedure. At most recent follow-up (six months postintervention), the patient is progressing satisfactorily. Current medication includes carvedilol and aspirin. Echocardiography demonstrates a normal sized left ventricle with good systolic contractility. There is no residual shunt at either atrial or ventricular level. The right ventricular dimensions are also within normal limits and the estimated right ventricular systolic pressure is approximately 35 mm Hg. DISCUSSION

Although 2 ASDs are usually well tolerated throughout infancy and early childhood, there are circumstances in which a modest 2 ASD may facilitate substantial shunting and significantly contribute to an infant’s poor clinical condition. For example, expreterm infants with broncho-pulmonary dysplasia (BPD) seem to be more susceptible to L-R shunting and have been shown to benefit from 2 ASD closure [3]. In particular, patients with left heart obstructive

Fig. 1. Secundum ASD pre-intervention. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

Fig. 2. ASD closed with ADO2 device. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

lesions can shunt massively across a 2 ASD in the face of high LVEDP/mitral stenosis, contributing to a vicious cycle of pulmonary engorgement, higher pulmonary vascular resistance, and increased pulmonary vascular return [4]. Beitzke et al. and Petit et al. describe cases of infants with multi-level left heart lesions who benefited significantly from device closure of 2 ASD [4,5]. Indeed device closure of 2 ASD during infancy is well described [1]. Lim et al. report 2 ASD occlusion in a 2.3 kg ex-preterm infant with BPD [6]. The vast majority of reported 2 ASD device closures in infancy are with the Amplatzer Septal Occluder (ASO, MN).

Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).

ADO2 to Close a 2 ASD

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bystander ASD) immediately following the procedure, this is not surprising given the absence of polyester in the ADO2 device compared with the ASO. However, it is gratifying that both shunts resolved within three months. The ADO2 was suitable for this patient because the defect was relatively small and, more importantly, was surrounded by apparently firm atrial septum. Otherwise there would have been a high risk of embolization given the smaller disc diameters (þ3 mm radius) compared with the ASO (þ6 mm radius). In these circumstances, the ADO2 seems an appropriate selection given its low profile, smaller disc diameter, and reduced rigidity which make it technically easy to deploy and retrieve but also theoretically less likely to erode. CONCLUSION Fig. 3. Fluoroscopy of ADO2 devices placed in the 2 ASD and muscular VSD.

However, there is increased awareness of the potential for wall erosion associated with the ASO. The proposed mechanism for wall erosion is a repetitive sawing interaction between the device rim and atrial wall which is made more likely by device over-sizing [7]. In relative terms, it seems difficult not to oversize ASOs in infants. Consequently, the ASO does not seem the ideal device but has been utilized due to familiarity and lack of an alternative. Dilber et al. report successful closure of a 2 ASD with the Amplatzer Duct Occluder I device (ADO1) in a 3.1 kg neonate following repair of common arterial trunk [8]. Morphologically, the ADO1 device does not seem appropriate for 2 ASD closure. The principal risks associated with ASD occlusion such as arrhythmia, effusions, vascular complications, and stroke may be attributed to larger, more rigid devices. Although the GOREV HELEX Septal Occluder has an excellent safety profile with respect to wall erosion, the sheath size required (9 Fr) was prohibitive for this patient. In this case, a 6/4 ADO2 device was selected as the maximal diameter of the 2 ASD measured 6 mm and a larger waist is not available. The shortest device is preferable in this situation to promote apposition of the two discs and enhance device stability. Although there was a residual atrial shunt (through device and R

Modest 2 ASDs with firm edges may be successfully closed using the ADO2 device. The ADO2 device is an attractive alternative to the ASO device in small infants. REFERENCES 1. Petit CJ, Justino H, Pignatelli RH, Crystal MA, Payne WA, et al. Percutaneous atrial septal defect closure in infants and toddlers: Predictors of success. Pediatr Cardiol 2013;34:220–225. 2. Crawford GB, Brindis RG, Krucoff MW, Mansalis BP, Carroll JD. Percutaneous atrial septal occluder devices and cardiac erosion: a review of the literature. Catheter Cardiovasc Interv 2012;80:157–167. 3. Wood AM, Holzer RJ, Texter KM, Hill SL, Gest AL, et al. Transcatheter elimination of left-to-right shunts in infants with bronchopulmonary dysplasia is feasible and safe. Congenit Heart Dis 2011;6:330–337. 4. Beitzke A, Zobel G, Nagel B, Koestenberger M. Transcatheter closure of an atrial septal defect in a newborn with aortic stenosis. Acta Paediatr 2009;98:582–583. 5. Petit CJ, Justino H, Fraser CD. Percutaneous closure of an atrial septal defect in an infant with Shone’s syndrome. Catheter Cardiovasc Interv 2012;80:188–191. 6. Lim DS, Matherne GP. Percutaneous device closure of atrial septal defect in a premature infant with rapid improvement in pulmonary status. Pediatrics 2007;119:398–400. 7. Tobis J, Shenoda M. Percutaneous treatment of patent foramen ovale and atrial septal defects. J Am Coll Cardiol 2012;60: 1722–1732. 8. Dilber D, Eicken A, Hess J. Early postoperative interventional ASD-closure for severe atrial right to left shunt in a neonate with common arterial trunk. Croat Med J 2013;54:394–396

Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).

Device closure of secundum atrial septal defect in a 4.5 kilogram infant: Novel use of the Amplatzer DuctOccluder II device.

Modest secundum atrial septal defects (2°ASD) may cause significant pulmonary over perfusion during infancy, particularly in conjunction with left hea...
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