Long-term follow up after transcatheter closure of atrial septal defect and patent foramen ovale in adults Dolgoročno spremljanje odraslih bolnikov po transkatetrskem zapiranju okvare preddvornega pretina in odprtega ovalnega okna Dolenc Jure, Cerar Andraž, Cvijic Marta, Prokšelj Katja, Koželj Mirta Department of Cardiology, University Medical Centre Ljubljana, Slovenia Korespondenca/ Correspondence: Jure DoLenc, MD, Department of Cardiology, University Medical Centre Ljubljana, Zaloška 7, 1000 Ljubljana, Slovenia. E-maiL address: dr.jdoLenc@gmaiL.com Ključne besede: srčne okvare; eLektrokardiografija; ehokardiografija; zapLeti. Key words: heart defects; eLectrocardiography; echocardiography; compLications Citirajte kot/Cite as: Zdrav Vestn 2013; 82: 809-17 PrispeLo: 24. dec. 2012, Sprejeto: 23. juL. 2013 Izvleček Izhodišča: Namen raziskave je bil proučiti dolgoročne elektrokardiografske in ehokardiograf-ske spremembe ter opredeliti zaplete pri perku-tanem zapiranju okvare preddvornega pretina in odprtega ovalnega okna pri odraslih. Metode: Retrospektivno smo analizirali klinične, elektrokardiografske in ehokardiografske spremembe pri 137 zaporednih bolnikih v 10-le-tnem obdobju po perkutanem zapiranju okvare preddvornega pretina (51 bolnikov) in odprtega ovalnega okna (86 bolnikov). Rezultati: Pri skupini bolnikov z odprtim ovalnim oknom nismo zabeležili pomembnih sprememb po posegu. Pri obeh skupinah nismo zabeležili pomembnih sprememb srčne frekvence in ritma ter trajanja intervalov PR in QRS. Pri skupini z okvaro preddvornega pretina smo zabeležili premik srčne osi v levo (p = 0,017), zmanjšanje ocenjenega sistoličnega tlaka v pljučni arteriji (p = 0,024), zmanjšanje zgodnje diastolične dopplerske hitrosti na trikuspidalni zaklopki (p = 0,002), zmanjšanje desnih srčnih votlin (p = 0,0004) in normalizacijo gibanja prekatnega pretina (p < 0,0001). Večina zapletov, povezanih s posegom, je bila zgodnjih in blagih, zabeležili pa smo 3 resne zgodnje zaplete. Zaključki: Pri skupini z odprtim ovalnim oknom nismo zabeležili pomembnih elektrokar-diografskih in ehokardiografskih sprememb. Pri skupini z okvaro preddvornega pretina pride do pomembnega in hitrega izboljšanja morfoloških in hemodinamičnih sprememb srca. Zapleti, povezani s posegom, so večinoma blagi in zgodnji, možni pa so tudi resni pozni zapleti. Zato je potrebno te bolnike spremljati dolgoročno. Abstract Background: The aim of our study was to define long-term electrocardiographic and echocardiography changes and complications after trans-catheter closure of atrial septal defect and patent foramen ovale in adults. Methods: The clinical, electrocardiographic and echocardiography follow-up of 137 consecutive patients that underwent transcatheter closure of atrial septal defect (51 patients) or patent foramen ovale (86 patients) in a 10-year period was analyzed retrospectively. Results: In the patent foramen ovale group, we observed no significant postprocedural changes. There were no changes in heart rate, heart rhythm and PR or QRS duration in both groups. In the atrial septal defect group, we observed a leftward shift in the heart axis (p = 0.017), a decrease in the estimated systolic pulmonary artery pressure (p = 0.024), decreased tricuspid early diastolic flow velocity (p = 0.002), a decrease in the right chamber dimensions (p = 0.0004) and interventricular septal movement normalization (p < 0.0001). Most of the complications were mild and occurred early after the procedure. Three early serious complications were documented. Conclusions: No electrocardiographic or echocardiography changes occurred after patent foramen ovale closure. Atrial septal defect closure is related to significant early morphological and hemodynamic improvement. Postprocedural complications are usually early and mild but serious late complications can occur. For that reason, long-term follow up is recommended in these patients. Introduction Atrial septal defect (ASD) is one of the most common congenital cardiac lesions occurring in up to 10 % of patients with congenital heart disease at birth.1 Secundum type ASD is the most common type, occurring in up to 60 % of ASD patients. 1 Traditionally, the only treatment modality in patients with hemodynamically important secundum type ASD was open heart surgery. The first interventional transcatheter closure of ASD was described in 19762 and is now a widely available form of treatment for relevant lesions in pediatric and adult populations. Patent foramen ovale (PFO) is present in 25 to 27 % of the adult population3'4 and is usually an unimportant echocardiographic or autopsy finding. It is presumed that in one out of 1000 patients with PFO, a cryp-togenic embolic stroke occurs as a result of paradoxical embolism through PFO/'5 Though, the number could be a lot higher because it is often difficult to ascertain where the embolism originated from. In patients with doubtlessly proved paradoxical embolism, the transcatheter closure of PFO is the usual mode of treatment. On the other hand, there is no evidence that PFO closure is any better than medical therapy alone as was shown in a recently published CLOSURE I trial.6 In both subgroups of patients, the data on the long-term results of the transcatheter procedure is lacking. Most studies are small and only sporadic cases of complications, such as new-onset atrial fibrillation, conduction abnormalities, aortic and mitral regurgitation, device embolisation, pericardial effusion or tamponade, residual right-to-left cardiac shunt, recurrent stroke or transient ischemic attack, are described/-^ In both subgroups of patients, the electrocardio-graphic and echocardiographic changes after the procedure are not well defined.17-21 The aim of our study is to define these changes and immediate and long-term po-stprocedural complications after percutaneous transcatheter occlusion of either secun-dum type ASD or PFO. Patients and methods Patients. From January 2001 to December 2010, 137 consecutive adult patients with PFO (86 patients) or secundum type ASD (51 patients) were treated with percutaneous transcatheter defect occlusion at the Department of Cardiology of the University Medical Centre Ljubljana, Slovenia. Patient data was collected and analysed retrospectively. The inclusion criteria for PFO patients were age under 55 and cryptogenic embolic stroke verified by positive magnetic resonance imaging. The inclusion criteria for ASD patients were the presence of a hemodynamically significant defect with anatomy appropriate for percutaneous occlusion. Amplatzer septal occluder was used in all patients. We studied ASD and PFO patients in the same study because the procedure and the type of the closure device for both defects were very similar. Follow up. Patients were followed up at regular intervals. Clinical data before the procedure, six months after the procedure and later on at yearly intervals were collected. No patients were lost to follow up. Standard 12-lead electrocardiographs were recorded before the procedure, six months after the procedure and later on at yearly intervals. Heart rate, rhythm, axis, PR interval and QRS duration data were collected. Transthoracic echocardiography was performed before the procedure, one day after, one and six months after the procedure and later on at yearly intervals. The right atrial size, right ventricular size and function, and coronary sinus anatomy were assessed from the apical four-chamber view. The interventricular septal movement, left ventricular size and function, as well as the pericardial space, were observed from the parasternal views. We assessed the valvular function. The right heart chambers' size and function were estimated qualitatively.22 The systolic pulmonary artery pressure was estimated from the continuous wave Doppler measurements of the tricuspid regurgitant flow velocity. Transesophageal echocardiography was performed before and during the procedure. Before the procedure, the Figure 1: Distribution of right atrial size 1 day, 1 month, 6 months and > 1 year after atrial septal defect closure. presence of PFO and right-to-left shunt was confirmed using contrast echocardiography. In ASD patients, the size and anatomy of the defect was observed. During the procedure, the position of the occluder device was assessed in all patients. Statistical analysis. The Kolmogorov--Smirnov test was used to verify normal distribution. Normally distributed continuous variables were expressed as means and standard deviations. In non-normal distributed continuous variables, the data was expressed as a median together with the 25th and 75th percentiles (inter-quartile range). Categorical data were summarized as frequencies and percentages. For comparisons of continuous variables, the paired Student t-test was used for normally distributed variables and the Wilcoxon matched-pair test for non-normally distributed variables. The data for categorical variables were analyzed by using the Fisher exact test. For all tests, a two-tailed p value less than or equal to 0.05 was considered statistically significant. Data was analyzed with the Statistical Package for Social Sciences version 16 (SPSS Inc, Chicago, Illinois). Results The baseline patient characteristics are shown in Table 1. Electrocardiography. In the PFO group, the mean heart rate before the defect occlusion was 69 ± 11 beats per minute. Mean heart axis before the procedure was 43 ± 31°. Mean PR interval before the procedure was 152 ± 26 ms and mean QRS duration was 89 ± 10 ms. All these parameters did not change during follow-up. All PFO patients were in sinus rhythm before the procedure and remained in sinus rhythm during follow up. In the ASD group, the mean heart rate before the defect occlusion was 78 ± 13 beats per minute. Mean PR interval before the procedure was 147 ± 25 ms and mean QRS duration was 100 ± 17 ms. None of these parameters changed during follow-up. However, we observed a statistically significant change of heart axis from 80 ± 36° before the procedure to 58 ± 37° six months after the procedure (p = 0.017). Forty-six ASD patients (90 %) were in sinus rhythm before the procedure and remained in sinus rhythm throughout the follow-up period. Only one patient converted to sinus rhythm from atri-al fibrillation postprocedurally. Echocardiography. The baseline echo-cardiographic characteristics of both study subgroups are summarized in Table 2. In the PFO group, none of the measured echocardiographic parameters changed throughout the follow-up period. None of the PFO patients had pericardial effusion or coronary sinus abnormality pre- or postpro-cedurally. In the ASD group, we found a statistically significant decrease in the estimated systolic pulmonary artery pressure. From 35 ± 7 mmHg (+ central venous pressure) preprocedurally, the pressure decreased to 30 ± 12 mmHg (+ central venous pressure) one day after the procedure (p = 0.024). The decrease in pulmonary artery pressure remained statistically significant throughout the follow-up period. We also documented an increase in the early diastolic pulsed--wave Doppler velocity at the mitral orifice from 85 ± 19 cm/s before the procedure to 99 ± 24 cm/s one month after the procedure (p = 0.004). The early diastolic pulsed wave Doppler velocity at the tricuspid orifice decreased from 85 ± 33 cm/s before the procedure to 52 ± 19 cm/s one day after the procedure (p = 0.002). Both Doppler parameter differences remained statistically significant throughout the follow-up period. In ASD group we also found a postprocedural decrease in the right heart chamber dimensions and normalization of interventricular septal movement (Figs 1-3). None of the other me- Figure 2: Distribution of right ventricular size 1 day, 1 month, 6 months and > 1 year after atrial septal defect closure. asured echocardiography parameters changed throughout the follow-up period. In the ASD group, three patients had mild pericardial effusion on the first day after the procedure. Later on, we observed no new-onset pericardial effusions. None of the effusions were hemodynamically significant. None of the patients in the ASD group had coronary sinus abnormality throughout the follow-up period. Complications. The device implantation success rate was 98.6 %. In the PFO group, one patient suffered from hypotensive (vasovagal) reaction during the procedure. We observed two serious complications in two patients. After the procedure, one patient needed surgery because of arterioveno-us fistula on the femoral artery access site. Another patient suffered from epigastric artery rupture with mild hemorrhagic shock. We observed two early postprocedural device embolisations without serious consequences. In the ASD group, we observed one serious complication in a patient with the rupture of the pulmonary vein and left atrium with cardiac tamponade. After urgent surgical intervention, the patient underwent an uneventful recovery. No thromboembolic events or late device-related erosions were observed in either subgroup of patients. Also, no significant valvular regurgitation was detected postpro-cedurally. Discussion PFO group. No significant electrocardiographic changes were observed postpro-cedurally in the PFO group. There were no heart rhythm or heart axis changes and no conduction abnormalities, which suggests that the anatomical position of the PFO septal occluder does not interfere with the conduction system of the heart. On the other hand, Johnson et al. reports changes in atrial conduction postprocedurally but the incidence of the clinically significant heart block was low.23 Mareedu et al. observed paroxysmal atrial fibrillation in one patient postprocedurally.4 Similarly, no echocardiographic changes were found postprocedurally in the PFO group. This was expected because PFO is not a hemodynamic anomaly. ASD group. There were no significant changes in the heart rate, heart rhythm, PR interval or QRS interval pre- or postproce-durally. Interestingly, Mainzer et al. observed an improvement in the right bundle branch block pattern in 53 %o of adult patients after ASD closure/0 Some authors report a 2 to 7 % incidence of different degrees of atrioventricular block early postprocedu-rally.11'1^ Usually, atrioventricular blocks are transient and only rarely pacemaker implantation is needed.^ Some studies report a relatively high percentage of new-onset atrial fibrillation postprocedurally in up to 4.5 %% of patients9'n'i7 and other report increased supraventricular ectopy/4 In our study, only one patient converted from atrial fibrillation preprocedurally to sinus rhythm postprocedurally. However, we observed a significant leftward heart axis shift postpro-cedurally. We presume this change to be a consequence of hemodynamic relief of the right ventricle after the closure of the left-to-right shunt. A similar finding is reported by Dhillon et al/5 On the first day after the procedure, both right atrial and right ventricular chamber dimensions decreased significantly and remained significant throughout the fol- Figure 3: Distribution of interventricular septal motion 1 day, 1 month, 6 motnhs and > 1 year after atrial septal defect closure low-up period. The same right chamber dimension reduction was observed by other authors,19'21 but as late as six weeks after the procedure21 or even six months after the procedure.26 Dhillon et al. reports preserved right ventricular function after transcatheter ASD closure and impaired right ventricular function after surgical ASD repair/5 These observations support the potential for favorable right heart remodeling after ASD transcatheter closure, despite longstanding right chamber volume overload."^6 Also, in percutaneous ASD closure the patient does not suffer from negative influence of extra-corporeal circulation as in surgical ASD closure. Similarly, we observed normalization of the interventricular septal movement on the first day postprocedurally, which remained significant throughout the follow-up . period. Mainzer et al. observed interventri-cular septal movement normalization as late as one month after the procedure/0 We found no changes in the left ventricular dimensions postprocedurally, yet some authors report left ventricular enlargement after the ASD closure, probably due to normalization of the left ventricular load after the closure of the left-to-right cardiac shunt.19-21 We also found no changes in right or left ventricular function after the ASD closure, probably due to the early intervention in individuals with preserved ventricular function. However, some authors report left ventricular ejection fraction improvement after the procedure.21 In the present study, we observed a significant drop in the estimated systolic pulmonary artery pressure as early as on the first day after the ASD closure and the drop remained significant throughout the follow-up period. Other authors report a similar drop in systolic pulmonary artery pressu-9'17'18'20 We also found a significant drop re Table 1: Baseline characteristics of the study cohort (N = 137). PFO patients ASD patients N (%) 86 (62) 51 (38) Mean age, years 40.35 ± 8.88 40.35 ± 8.88 Male sex (%) 36 (41) 16 (31) Sinus rhythm (%) 100 84 Positive TCD (%) 98 Mean defect diameter (mm) (central position, %) 16.9 ± 5.9 (68) Mean occlusion device diameter (mm) 23.96 ± 5.09 26.96 ± 6.27 ASA at discharge (%) 97 95 clopidogrel at discharge (%) 56 36 Warfarin at discharge (%) 8 12 Median follow up (days) (inter-quartile range) 951 (624-1852) 1835 (660-2619) PFO, patent foramen ovale; ASD, atrial septal defect; TCD, transcranial Doppler; ASA, acetylsalicilic acid Zdrav Vestn | Atrial septal defect and patent foramen ovale 813 in the tricuspid early diastolic blood flow velocity on the first day after the procedure. On the other hand, mitral early diasto-lic flow velocity increased significantly as late as one month postprocedurally. Both changes of flow velocities remained significant throughout the follow-up period. We understand these changes as a consequence of the reduction of transtricuspid flow and as an increase in transmitral flow after ASD closure. In conclusion, we observed significant morphological and hemodynamic improvement that occurred already within the first day after the procedure and continued later on. These echocardiography changes reflect the physiological changes after ASD Table 2: Baseline echocardiography characteristics of study group. PFO patients ASD patients Right atrial enlargement (%) Normal 91 15 MiLd 9 39 Moderate 0 26 Severe 0 20 Interventricular septal movement NormaL 96 52 Intermediate 4 16 Abnormal 0 32 Right ventricular enlargement (%) normal 95 18 Mild 5 25 Moderate 0 37 Severe 0 20 Right ventricular function (%) normal 100 97 Mildly decreased 0 3 Left ventricular enlargement (%) normal 100 97 Moderate 0 3 Left ventricular function (%) normal 100 97 Moderatly decreased 0 3 Tricuspid valvular regurgitation (%) None 71 20 Mild 29 55 Moderate 0 20 Severe 0 5 Mitral valvular regurgitation (%) None 78 58 Mild 21 37 Moderate 1 5 Aortic valvular regurgitation (%) None 94 95 Mild 5 5 Moderate 1 0 PFO, patent foramen ovale; ASD, atrial septal defect. closure, and similar changes can be seen after surgical closure of the defect.25 Complications. The device implantation success rate in our study was as high as 98.6 %, and similar to other published series with success rates ranging from 90 to 100 %.4,7,9,11,15,18,19,21 These observations suggest that transcatheter closure of ASD or PFO can be performed with a high overall procedural implantation success rate in appropriately selected patients. Most complications in our study were mild and occurred within the first 24 hours after the procedure. In the PFO group, we observed no recurrent neurologic events. Other authors report a 0 to 4.4 % rate of recurrent neurologic events.7-9'i5 Cifarelli et al. defined age and atrial septal aneurysm as risk factors for recurrent neurological events8, while Fischer et al. observed a high recurrent neurologic event rate as a consequence of an inappropriate antiplatelet regimen postprocedural-ly.15 The low recurrent neurologic event rate in these studies suggests that a combined acetylsalicilic acid and clopidogrel antiplate-let regimen is optimal. In our cohort, some patients received single antiplatelet regimen at discharge because of a high risk of bleeding . Some patients received a single an-tiplatelet medication in combination with warfarin because of co-existing indication for anticoagulant treatment, in most cases due to coexisting atrial fibrillation. On the other hand, the CLOSURE I trial found no difference in the occurrence of recurrent neurologic events between patients treated with medical therapy alone and those treated with percutaneous closure of the defect.6 We observed no significant postprocedural aortic or mitral regurgitation, no throm-boembolic events and no coronary sinus abnormalities in either group of patients. There are some reports of sporadic cases of thrombus formation on the device early19 and late after the procedure.9 None of the PFO patients had pericar-dial effusion postprocedurally, while three ASD patients had pericardial effusion on the first day after the procedure (2.2 % in both groups). Effusions resolved spontaneously without any intervention. Other authors re- port a lower 0.8-1.2 % incidence of pericardial effusion postprocedurally.9'19 Three patients (2.2 %) suffered from serious complications. All of them occurred early after the procedure and were related to procedural technique and not to device-related thromboembolic events. All serious complications occurred early in the learning curve. Some authors report cases of serious late complications, such as pulmonary venous obstruction that occurred 3.5 years after transcatheter closure of ASDW, or late severe mitral valve insufficiency that occurred three months after ASD closure.^ Another life threatening late complication is device erosion of adjacent structures. The incidence of such erosions in the United States is 0.1 %, and patients at increased risk are those with deficient aortic rim and/or superior rim and patients with oversized devices/7 We observed none of such late complications. Nevertheless, because late complications can be serious, these patients should not be discharged completely. The most common surgical complications after ASD device implantation in a study reported by Sarris et al. also occurred mostly within 48 hours postprocedurally.28 In addition, some patients needed surgery as late as eight years after device implantation, thus imposing the need for lifelong follow-up of these patients. This overview of possible complications after percutaneous transcatheter ASD or PFO closure suggests that this procedure is a reasonably safe and feasible technique that can be performed in selected individuals. Recent studies suggest that in PFO patients careful risk and benefit evaluation should be performed before closing the defect since the procedure seems not to be more efficient that conservative medical treatment alone. Further larger studies should confirm or exclude these observations. Study limitations. The main disadvantage of our study is the retrospective study design. Also, the number of enrolled patients is relatively low. For this reason as well as the reasons mentioned earlier we included both PFO and ASD patients in the same analysis. To assess procedural success rate in PFO group more accurately, we should perform transcranial Doppler studies postprocedu-rally. Conclusions In a retrospective study, we analyzed rhythm, morphological and hemodynamic changes and complications after percutaneous transcatheter closure of PFO or ASD in adults. These changes were minimal in PFO patients. On the other hand, we observed References 1. Gatzoulis MA, Swan L, Therrien J, Pantely GA. Adult congenital heart disease: a practical guide. Blackwell publishing, Oxford (UK), 2005. 2. King TD, Thompson SL, Steiner C, Mils NL. Secundum atrial septal defects: nonoperative closure during cardiac catheterization. JAMA 1976; 235: 2506-2509. 3. McMahon CJ, Feltes TF, Fraley JK, Bricker JT, Grifka RG, Tortoriello TA, et al. Natural history of growth of secundum atrial septal defects and implications for transcatheter closure. Heart 2002; 87: 256-9. 4. Mareedu RK, Shah MS, Mesa JE, McCauley CS. Percutaneous closure of patent foramen ovale: a case series and literature review. Clin Med Res 2007; 4: 218-226. 5. Lock JE. Patent foramen ovale is indicted, but the case hasn't gone to trial. Circulation 2000; 101: 838. 6. Furlan AJ, Reisman M, Massaro J, Mauri L, Adams H, Albers GW, et al. Closure or medical therapy for cryptogenic stroke with patent foramen ovale. N Engl J Med 2012; 366: 991-9. 7. van de Wyngaert F, Kefer J, Hermans C, Ovaert C, Pasquet A, Beguin C, et al. Absence of recurrent stroke after percutaneous closure of patent foramen ovale despite residual right-to-left cardiac shunt assessed by transcranial Doppler. Arch Car-diovasc Dis 2008; 101 (7-8): 435-41. 8. Cifarelli A, Musto C, Parma A, Pandolfi C, Pucci E, Fiorilli R, et al. Long-term outcome of tran-scatheter patent foramen ovale closure in patients with paradoxical embolism. Int J Cardiol 2010; 141(3): 304-10. 9. Majunke N, Bialkowski J, Wilson N, Szkutnik M, Kusa J, Baranowski A, et al. Closure of atrial sep-tal defect with the Amplatzer septal occluder in adults. Am J Cardiol 2009; 103(4): 550-4. 10. Moiduddin N, Cheatham JP, Hoffman TM, Phillips AB, Kovalchin JP. Amplatzer septal occluder associated with late pulmonary venous obstruction requiring surgical removal with acquired aorta to left atrial fistula. Am J Cardiol 2009; 103: 1039-1040. 11. Kazmi T, Sadiq M, Asif-ur-Rehman, Hyder N, Latif F. Intermediate and long-term outcome of patients after device closure of ASD with special reference to complications. J Ayub Med Coll Ab-botabad 2009; 21: 117-121. significant and early morphological and he-modynamic improvement in ASD patients that continued throughout the follow up. Most of the complications in both groups of patients were mild and occurred peri- or early postprocedurally. In our cohort, no late complications were observed. Abbreviations ASD, atrial septal defect PFO, patent foramen ovale 12. Li W, Han W, Yu C, Zhang C, Tu Z, Wu S, et al. Severe mitral insufficiency after transcatheter atrial septal defect closure with the Amplatzer septal occluder: a device-related complication. J Card Surg 2009; 24(6): 672-4. 13. Piatkowski R, Kochanowski J, Scislo P, Kochman J, Opolski G. Dislocation of Amplatzer septal occlu-der device after closure of secundum atrial septal defect. J Am Soc Echocardiogr 2010; 23: 1007x1-2. 14. Al-Anani SJ, Weber H, Hijazi ZM. Atrioventricular block after transcatheter ASD closure using the Amplatzer septal occluder: risk factors an recommendations. Catheter Cardiovasc Interv 2010; 75: 767-772. 15. Fischer D, Haentjes J, Klein G, Schieffer B, Drexler H, Meyer GP, et al. Transcatheer closure of patent foramen ovale (PFO) in patients with paradoxical embolism: procedural and follow-up results after implantation of the Amplatzer occluder device. J Interv Cardiol 2011; 24(1): 85-91. 16. Luermans JG, Post MC, ten Berg JM, Plokker HW, Suttorp MJ. Long-term outcome of percutaneous closure of secundum-type atrial septal defects in adults. Eurointervention 2010; 6: 604-610. 17. Yalonetsky S, Lorber A. Comparative changes of pulmonary artery pressure values and tricuspid valve regurgitation following transcatheter atri-al septal defect closure in adults and the elderly. Congenit Heart Dis 2009; 4: 17-20. 18. Yong G, Khairy P, De Guise P, Dore A, Marcotte F, Mercier LA, et al. Pulmonary arterial hypertension in patients with transcatheter closure of se-cundum atrial septal defects: a longitudinal study. Circ Cardiovasc Interv 2009; 2(5): 455-62. 19. Jategaonkar S, Scholtz W, Schmidt H, Fassbender D, Horstkotte D. Cardiac remodelling and effects on exercise capacity after interventional closure of atrial septal defects in different adult age groups. Clin Res Cardiol 2010; 99: 183-191. 20. Mainzer G, Braver Y, Khoury A, Schwartz Y, Ga-lenter-Yaniv L, Yalonetsky S, et al. Morphologic, mechanical, conductive, and hemodynamic changes following transcatheter closure of atrial septal defect. Congenit Heart Dis 2010; 5(1): 25-31. 21. Khan AA, Than JL, Li W, Dimopoulus K, Spen-ce MS, Chow P, et al. The impact of transcatheter atrial septal defect closure in the older population: a prospective study. JACC Cardiovasc Interv 2010; 3(3): 276-81. 22. Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005; 18: 1440-63. 23. Johnson JN, Marquardt ML, Ackerman MJ, Asir-vatham SJ, Reeder GS, Cabalka AK, et al. Elec-trophysiologic changes and arrhythmias following percutaneous atrial septal defect and patent foramen ovale device closure. Catheter Cardiovasc Interv 2011; 78(2): 254-61. 24. Hill SL, Berul CI, Patel HT, Rhodes J, Supran SE, Cao QL, et al. Early ECG abnormalities associated with transcatheter closure of atrial septal defects using the Amplatzer septal occluder. J Interv Card Electrophysiol 2000; 4(3): 469-74. 25. Dhillon R, Josen M, Henein M, Redington A. Transcatheter closure of atrial septal defect preserves right ventricular function. Heart 2002; 87: 461-465. 26. Thomson JDR, Aburawi EH, Watterson KG, Van Doorn C, Gibbs JL. Surgical and transcatheter (Amplatzer) closure of atrial septal defects: a prospective comparison of results and cost. Heart 2002; 87: 466-469. 27. Amin Z, Hijazi ZM, Bass JL, Cheatham JP, Hellenbrand WE, Kleinman CS. Erosion of Amplatzer septal occluder device after closure of secundum atrial septal defects: review of registry of complications and recommendations to minimize future risk. Catheter Cardiovasc Interv 2004; 63(4): 496-502. 28. Sarris GE, Kirvassilis G, Zavaropoulus P, Belli E, Berggren H, Carrel T, et al. Surgery for complications of trans-catheter closure of atrial septal defects: a multi-insitutional study from the European Congenital Heart Surgeons Association. Eur J Cardiothorac Surg 2010; 37: 1285-90.