Conduction Abnormality and Arrhythmia After Transcatheter Closure of Atrial Septal Defect

Abstract

Background: The aim of this study was to prospectively perform ambulatory 24-h ECG monitoring to assess the effects of transcatheter closure of atrial septal defect (ASD).

Methods and Results: A total of 235 consecutive subjects (female, n=163; male, n=72; age, 44.6±14.4 years) were enrolled in the study, who were due undergo ASD closure. Holter monitoring was performed before procedure and at 1, 6 and 12 months of follow-up. During the procedure transient supraventricular arrhythmia occurred in 8 patients (3.4%), and bradycardia in 3 (1.3%). In 3 patients (1.3%) an episode of atrial fibrillation occurred in the first hour after the procedure. In 8 patients (3.4%) transient first-degree atrioventricular block was noted. A significant increase in number of supraventricular extrasystoles (SVES)/24 h was noted 1 month after the procedure (P<0.001). On multiple forward stepwise regression analysis, device size and fluoroscopy time had an influence on increase in number of SVES seen 1 month after the procedure (P<0.001).

Conclusions: Transcatheter closure of ASD is associated with a transient increase in supraventricular premature beats and a small risk of conduction abnormalities and paroxysmal atrial fibrillation in early follow-up. Transcatheter closure of ASD does not reduce arrhythmia that appears prior to ASD closure. Larger device size and longer procedure time are associated with increased risk of supraventricular arrhythmia on early follow-up. (Circ J 2014; 78: 2415–2421)

Atrial septal defect (ASD) is, besides bicuspid aortic valve and mitral valve prolapse, the most common congenital heart defect (CHD) observed in adults.^1–3 ASD account for approximately 10% of all heart defects diagnosed after birth and up to 30–40% of CHD seen in patients >40 years of age.³ Rhythm disorders are one of the most prominent symptoms of the disease, especially in patients over 40.⁴ Surgical treatment of ASD, which had been the only treatment method for more than 45 years, may be associated with the occurrence of rhythm disorders such as atrial fibrillation (AF) or supraventricular tachycardia (SVT), although some authors noted a reduction in supraventricular arrhythmic burden after closure.⁴ Percutaneous ASD type II (ASD II) closure has lately become the primary treatment option and, according to European Society of Cardiology guidelines, should be the therapy of choice when anatomical conditions are favorable.⁵ On average around 70% of ASD II patients may be treated percutaneously.^5–7

The aim of this study was to evaluate the impact of percutaneous ASD II closure with the use of an Amplatzer septal occluder (ASO) on rhythm and conduction disorders over a period of 1 year.

Methods

A total of 235 adult patients (female, n=163, 69.4%; male, n=72, 30.6%) who were due to undergo ASD closure with the use of ASO in the last decade, were enrolled in the present study.

Mean patient age was 44.6±14.4 years (range, 18–69 years). Diagnosis of ASD II was based on clinical and transthoracic echocardiographic evaluation. Final qualification for the procedure was based on transesophageal echocardiography (TEE).

Eligibility criteria for percutaneous closure was the presence of a single ASD II located in the central part of the septum, encircled by at least a 5-mm rim (except aortic rim) and a significant left-to-right shunt measured on right heart catheterization (ratio of total pulmonary blood flow to total systemic blood flow, Qp/Qs >1.5:1) or shunt with signs of right ventricular volume overload, coexisting impairment of physical status, enlargement of right heart cavity or pulmonary hypertension.

In 2 cases there were 2 separate septal defects instead of a single one, but they were located close enough to each other to be available for closure with the use of one device.

In all patients ASO was implanted in typical fashion, under local anesthesia with continuous TEE (described elsewhere).⁸

Electrocardiography (ECG), consisting of a standard 12-lead ECG and 24-h ECG Holter monitoring, was conducted in each patient at 1, 6 and 12 months after the procedure. ECG indices taken for analysis included: leading cardiac rhythm, heart axis and the presence of any rhythm or conduction disturbances. Holter ECG monitoring was performed with the use of a 3-lead DelMar 563 recorder and analyzed on the DelMar Avionix software reporting the mean, minimum, maximum heart rate (HR) and the presence of any conduction or rhythm disorder, that is, supraventricular extrasystoles (SVES), SVT or ventricular extrasystoles (VES).

Results

Amplatzer devices were implanted without any major complication in all eligible individuals. The mean ratio of pulmonary to systemic blood flow or Qp:Qs was 1.54±0.9 (range, 1.1–2.5) on echocardiography.

Transient SVT was observed in 8 patients (3.4%) during the procedure and transient bradycardia to 30 beats/min in 3 (1.3%). The mean procedure time including preceding right heart catheterization was 33.1±9.5 min (range, 18–66 min) and the mean fluoroscopy time was 10.8±6.7 min (range, 5–26 min). Diameter of the implanted ASO devices ranged from 12 to 40 mm (mean, 21.8±7.5 mm). The ratio of ASO device size to ASD size was 1.09±0.06 (range, 1.2–1).

Sinus rhythm (SR) was detected in 210 patients (89.4%) before ASD closure. Persistent AF was observed in 25 (10.6%). Left axis deviation was seen in 20 patients (8.5%), right axis deviation in 65 (27.7%), complete or incomplete right bundle branch block in 49 (20.9%), and first-degree atrioventricular block (AVB) in 33 (14%).

After ASD closure SR was present in 210 patients (89.4%). Persistent AF, observed in 25 subjects (10.6%), remained unchanged over the entire observation period. In 3 patients (1.3%) with SR an episode of AF occurred in the first hour after the procedure and was successfully terminated by electrical cardioversion.

In some patients we found that isolated supraventricular ectopic beats initiated AF or supraventricular tachyarrhythmia (Figures 1,2).

Figure 1.

Incidence of supraventricular extrasystole, which then degenerates into atrial fibrillation. Red arrow, normal beat; green arrow, isolated supraventricular ectopic beat; black arrow, atrial fibrillation.

Figure 2.

Incidence of supraventricular extrasystole, which then degenerates into atrial fibrillation. Red arrow, normal beat; green arrow, isolated supraventricular ectopic beat, black arrow, atrial fibrillation.

In 8 patients (3.4%) a transient first-degree AVB was noted in the first hour after the procedure. Right and left axis deviation as well as first-degree AVB observed prior to ASD closure remained unchanged during follow-up. Table 1 lists ECG findings before and after ASD closure.

Table 1. Electrocardiographic Findings

	Before ASD closure	After ASD closure
		1 month	6 months	12 months
Sinus rhythm	210 (89.4)	210 (89.4)	210 (89.4)	210 (89.4)
Paroxysmal AF	33 (14)	36 (15.3)	33 (14)	33 (14)
Persistent AF	25 (10.6)	25 (10.6)	25 (10.6)	25 (10.6)
Right axis deviation	65 (27.7)	65 (27.7)	65 (27.7)	65 (27.7)
Left axis deviation	20 (8.5)	20 (8.5)	20 (8.5)	20 (8.5)
Incomplete RBBB	33 (14)	33 (14)	33 (14)	34 (14.5)
Complete RBBB	16 (6.8)	16 (6.8)	16 (6.8)	16 (6.8)
First-degree AVB	33 (14)	36 (15.3)	33 (14)	33 (14)
SVT	23 (9.8)	51 (21.7)*	25 (10.6)	23 (9.8)

Data given as n (%). *P=0.0021. AF, atrial fibrillation; ASD, atrial septal defect; AVB, atrioventricular block; RBBB, right bundle branch block; SVT, supraventricular tachycardia.

Mean and maximum HR significantly increased in the first month after the procedure as recorded on 24-h ECG monitoring (mean: before, 76.4±15.8 beats/min vs. after, 95.1±13.7 beats/min, P<0.05; maximum: before, 129.2±34 beats/min vs. after, 162.7±31.7 beats/min, P<0.001). Variations in mean, minimum and maximum HR are given in Table 2.

Table 2. Changes in HR/24 h After ASD Closure

	Mean HR/24 h	Maximum HR/24 h	Minimum HR/24 h
Before closure	76.4±15.8 (50–98)	129.2±34 (110–195)	50.4±16 (37–61)
At 1 month	95.1±13.7 (45–93)	162.7±31 (109–198)	50.7±11.7 (40–70)
At 6 months	79.2±16.9 (50–92)	146±30.1 (100–175)	52.9±11.9 (47–61)
At 12 months	75.8±21 (55–89)	132.5±39 (105–175)	51.9±11.6 (47–63)
P before vs. 1 month	P<0.05	P<0.001	NS
P before vs. 6 months	NS	NS	NS
P before vs. 12 months	NS	NS	NS

Data given as mean±SD (min–max). ASD, atrial septal defect; HR, heart rate.

As well as changes in HR, the prevalence of paroxysmal supraventricular rhythm disorders also increased in the first month after the procedure. SVES were recorded in 80 patients (34%) before and in 165 (70.2%) 1 month after ASO implantation (P=0.0019). Similarly, transient SVT were seen in 23 (9.8%) prior to and in 51 (21.7%) after the procedure (P=0.0021).

Table 3 lists changes in the number of SVES during the observation period. The mean number of SVES recorded on 24-h ECG monitoring increased in the first month compared to before ASD closure (204±210 vs. 4,347±4,876, respectively, P<0.0001). The number of SVES then gradually decreased. At 6 months the mean number of SVES was 951±2,065 and at 1 year it was no different to that before the procedure (204±210 vs. 211±220, respectively, P=NS).

Table 3. Change in No. SVES/24 h After ASD Closure

	SVES/24 h
	Mean	SD	Median	Minimum	Maximum
Before closure	204	210	90	1	857
1 month	4,347**	4,876	2,900	78	30,132
6 months	951	2,065	243	1	15,423
12 months	211	220	99	0	905

**P=0.0032. ASD, atrial septal defect; SVES, supraventricular extrasystole.

There were 45 patients (19.1%) who had rhythm disorders in the follow-up period, requiring verapamil to relieve symptoms. The therapy was only temporary, and the rhythm disorders were successfully terminated after 6 months at the latest (mean, 2.6±1.3 months; range, 0.5–6 months).

In contrast, no significant shift in the mean number of VES before and 1 month after ASD closure was found in the 24-h ECG recording (176±199; range, 1–746 vs. 196±211; range, 0–905), respectively, P=NS; Table 4). Six months after ASD closure the number of VES increased to 286±553 (range, 1–4,024; P<0.001), and at 1 year the number of VES decreased and was similar to that before the procedure (182±203 vs. 176±199, respectively, P=NS).

Table 4. Change in No. VES/24 h After ASD Closure

	VES/24 h
	Mean	SD	Median	Minimum	Maximum
Before closure	176	199	64	1	746
At 1 month	196	211	88	0	905
At 6 months	286**	553	147	1	4,024
At 12 months	182	203	78	0	903

**P=0.0095. ASD, atrial septal defect; VES, ventricular extrasystole.

In order to investigate a possible impact of the procedure on rhythm disturbances, 29 clinical, hemodynamic and procedural indices were analyzed. A significant correlation between the number of SVES 1 month after the procedure and fluoroscopy time was identified (r=0.75691; P<0.001; Figure 3). A further correlation between the number of SVES and implanted device size was found (r=0.71855; P<0.001; Figure 4). Canonical correlation analysis showed that the following parameters had an influence on increased SVES 1 month after the procedure: procedure time, fluoroscopy time and device size (P<0.05).

Figure 3.

Correlation between fluoroscopy time and the number of additional supraventricular arrhythmias on 24-h electrocardiography at 1-month follow-up. ASD, atrial septal defect; SVE, supraventricular ectopy.

Figure 4.

Correlation between device size and the number of additional supraventricular arrhythmias on 24-h electrocardiography at 1-month follow-up. ASD, atrial septal defect; SVE, supraventricular ectopy.

On multiple forward stepwise regression analysis, of all the echocardiography and procedural parameters, only device size (F(7.20)=9.1171; P<0.001, standard error, 2.110) and fluoroscopy time (F(6.11)=9.0370; P<0.001, standard error 2.210) had an influence on the increase in SVES seen 1 month after the procedure. No significant relationships were noted between rhythm disorders and patient age, size of the right atrium and ventricle, size of left atrium, size of the defect or significance of the left-to-right shunt.

Discussion

Percutaneous closure of interatrial septal defects has become a standard therapeutic approach in the last few years. Correction of the defect may prevent the development of pulmonary hypertension, rhythm disturbances or failure of the heart. ASOs have been commonly used for defect closure for 20 years. Other types of devices are used less frequently.^8–21 The present study shows that implantation of the Amplatzer device does not cause substantial rhythm disorders, although it may lead to a transient increase in supraventricular arrhythmia.

Earlier studies showed that surgical correction decreased the severity of “heart palpitations”.^4,22 It is now believed that in some patients defect closure may actually protect from the recurrence of paroxysmal SVT or atrial flutter.^4,23 Generally, however, correction of the defect does not restore SR in patients with persistent AF, nor prevent the occurrence of AF. This study implies, consistently with other publications, that arrhythmias already observed prior to ASD closure will persist after the procedure.^24,25

In the present study supraventricular tachyarrhythmias, such as paroxysmal AF and SVT, were observed in the preoperative period in most patients, and persistent AF in 25 (10.6%). One year after the procedure, the number and type of supraventricular tachyarrhythmias did not differ significantly as compared with the baseline data.

Numerous experimental and clinical studies show that AF in patients with CHD, including intracardiac shunts, is caused by the ongoing remodeling of the atrial walls. This leads to change of the atrial size and shape, but also results in disproportion of muscle and connective tissue size and structure, impairment of cardiomyocyte electrical features and metabolism. Persistence of arrhythmia despite closure of the defect may therefore be the effect of permanent remodeling of the atria exposed to the long-lasting increased pressure.^26,27 In the present study the persistence of arrhythmia may also be related to the very short follow-up period relative to the long antecedent period before closure.

Data evaluating the impact of ASD closure with an Amplatzer device on rhythm and conduction disorders are scarce. The most commonly described disturbances are supraventricular arrhythmias seen during the closure procedure. Transient AVB or ST segment elevation, which are associated with air microembolization in coronary arteries, are observed less frequently. In the present study ASD closure was associated with a small risk of AV conduction abnormalities, in 8 patients (3.4%) transient first-degree AVB was detected in the first hour after the procedure.

In the present study there was a transient increase in the mean and maximum HR 1 month after the correction, which was not seen at 6 or 12 months. Similarly, the mean number of SVES on Holter ECG increased at 1 month after defect closure and subsequently decreased at 6 months; and 12 months later there was no difference compared with baseline. Probably the changes in mean/maximum HR were accounted for by the increase in SVES. In contrast, there were no apparent changes in the number of ventricular arrhythmias 1 month after device implantation.

Hill et al, who analyzed Holter ECG recordings of 41 patients before and after percutaneous ASD II closure, drew similar conclusions.²⁶ They observed a significant increase in supraventricular tachyarrhythmia without changes in VES.

Exacerbation of supraventricular arrhythmia after defect closure may be related to the procedure itself. An invasive character of the intervention, instrumentalization and device implantation may provoke rhythm disturbances. Exacerbation of supraventricular arrhythmias after defect closure may trigger pathological automatism.

Injury and scars from device implantation or replacement fibrosis may also provide a substrate for reentry. The dense fibrosis creates conduction block that can define borders of reentry circuits. Fibrosis also contributes to the creation of slow conduction that is necessary for reentry.

At the microscopic level, fibrosis separates myocyte bundles, forcing the excitation wave front to take a circuitous course through the bundles. In addition, conductivity between cells can be diminished. This uncoupling of myocyte bundles, and to some extent the myocytes within the bundles, slows conduction, although action potentials and ion channels in the myocytes can be relatively normal. Slow conduction and fibrous anatomic barriers set the stage for reentry.

We showed a correlation between the number of SVES in the first month and fluoroscopy time. Fluoroscopy time may be regarded as an index of procedure complexity. Any difficulties during the intervention will prolong fluoroscopy time.

The more time that is needed for appropriate implantation of the device, the more harm may be done to the atrial wall and septum, which may evoke arrhythmia. An additional correlation between Amplatzer device size and number of SVES was also found. The size of the device, similarly to fluoroscopy time, may predict difficulties in the intervention. In contrast, a greater weight and size of the device solely may have an impact on atrial walls and provoke supraventricular rhythm disorders.

Transient supraventricular arrhythmia was also reported after surgical ASD correction.^22,23,27 Karwot et al compared the Holter ECG results of 91 patients before and after either surgical or percutaneous intervention.²⁸ They found that during 2.5–5.5 years of observation, supraventricular arrhythmia was more frequent after surgical than percutaneous intervention (35% vs. 2.1%, respectively; P<0.05).²⁸

In the present study, supraventricular arrhythmia occurring de novo after device implantation was transient and resolved over 1 year. The present results are consistent with previously published data.^29–33 None of the rhythm disorders recorded in the present patients had an impact on postoperative period. No additional hospitalizations or other clinical incidences were associated with arrhythmias.

In some patients, we found that isolated supraventricular ectopic beats initiated AF or supraventricular tachyarrhythmia. Mazzanti et al demonstrated that either long- or short-coupled extrasystolic beats initiated ventricular fibrillation,³¹ hence it is interesting that this happened for AF as well. Thus temporary use of anti-arrhythmia agents may be necessary after ASD closure to prevent AF.

In the present group 45 patients (19.1%) with new-onset rhythm abnormalities in the first month had to be given anti-arrhythmia medication (calcium channel blocker), which was discontinued after rhythm normalization at 2.6±1.3 months (range, 0.5–6 months) on average.

It is therefore advisable to conduct a thorough follow-up after ASD II closure, including ECG monitoring, especially in the early post-procedural period.

Conclusions

Transcatheter closure of secundum ASD is associated with a transient increase in supraventricular premature beats and a small risk of AV conduction abnormalities and paroxysmal AF in early follow-up. Transcatheter closure of secundum ASD does not reduce arrhythmia that appears prior to ASD II closure. Larger device size and longer procedure time are associated with increased risk of supraventricular arrhythmia on early follow-up.

Disclosures

Name of Grant: No grants obtained for the study.

References

• 1.    Dickinson  DF,  Arnold  R,  Wilkinson  JL. Congenital heart disease among 160 480 live born children in Liverpool 1960–1969: Implication for surgical treatment. Br Heart J 1981; 46: 55–62.
• 2.    Akagi  T. Catheter intervention for adult patients with congenital heart disease. J Cardiol 2012; 60: 151–159.
• 3.    Therrien  J,  Webb  D. Congenital heart disease in adult. In: Braunwald E, editor. Heart disease: A textbook of cardiovascular medicine, 6th edn. Philadelphia: WB Saunders, 2001; 44: 1592–1618.
• 4.    Berger  F,  Vogel  M,  Kramer  A,  Alexi-Meskishvili  V,  Weng  Y,  Lange  PE, et al. Incidence of atrial flutter/fibrillation in adults with atrial septal defect before and after surgery. Ann Thorac Surg 1999; 68: 75–78.
• 5.    Baumgartner  H,  Bonhoeffer  P,  De Grot  N,  de Haan  F,  Deanfield  JE,  Galie  N, et al. ESC guidelines for the management of grown-up congenital heart disease. Eur Heart J 2010; 31: 2915–2957.
• 6.    Saito  T,  Ohta  K,  Nakayama  Y,  Hashida  Y,  Maeda  A,  Maruhashi  K, et al. Natural history of medium-sized atrial septal defect in pediatric cases. J Cardiol 2012; 60: 248–251.
• 7.    Podolec  P,  Przewłocki  T,  Pieculewicz  M,  Hlawaty  M,  Tomkiewicz-Pajak  L,  Plazak  W, et al. Przezskórne zamykanie ubytków w przegrodzie międzyprzedsionkowej przy pomocy zapinki Amplatza: Wyniki i zmiany hemodynamiczne w obserwacji 6-miesięcznej. Przegląd Lekarski 2004; 61: 640–646 (in Polish).
• 8.    Ghosh  S,  Chatterjee  S,  Black  E,  Firmin  RK. Surgical closure of atrial septal defects in adults: Effect of age at operation on outcome. Heart 2002; 88: 485–488.
• 9.    Pedra  CA,  Pihkala  J,  Lee  KJ,  Boutin  C,  Nykanen  DG,  McLaughlin  PR, et al. Transcatheter closure of atrial septal defects using Cardio-Seal implant. Heart 2000; 84: 320–326.
• 10.    King  TD,  Mills  NL. Secundum atrial septal defects: Non-operative closure during cardiac catheterisation. JAMA 1976; 235: 2506–2509.
• 11.    Rashkind  WJ. Transcatheter treatment of congenital heart disease. Circulation 1983; 67: 711–716.
• 12.    Chan  KC,  Godman  MJ,  Walsh  K,  Wilson  N,  Redington  A,  Gibbs  JL. Transcatheter closure of atrial septal defect and interatrial communications with a new self expanding nitinol double disc device (Amplatzer septal occluder). Heart 1999; 82: 300–306.
• 13.    Ueda  H,  Yanagi  S,  Nakamura  H,  Ueno  K,  Gatayama  R,  Asou  T, et al. Device closure of atrial septal defect: Immediate and mid-term results. Circ J 2012; 76: 1229–1234.
• 14.    Kim  NK,  Park  SJ,  Shin  JI,  Choi  JY. Eight-French intracardiac echocardiography: Safe and effective guidance for transcatheter closure in atrial septal defects. Circ J 2012; 76: 2119–2123.
• 15.    Schräder  R. Indication and techniques of transcatheter closure of patent foramen ovale. J Interv Cardiol 2003; 16: 543–551.
• 16.    Levi  DS,  Moore  JW. Embolization and retrieval of the Amplatzer septal occluder. Catheter Cardiovasc Interv 2004; 61: 543–547.
• 17.    Krumsdorf  U,  Ostermayer  S,  Billinger  K,  Trepels  T,  Zadan  E,  Horvath  K, et al. Incidence and clinical course of thrombus formation on atrial septal defect and patent foramen ovale closure devices in 1000 consecutive patients. J Am Coll Cardiol 2004; 43: 302–309.
• 18.    Hildick-Smith  DJ,  Sullivan  M,  Wisbey  M. Amplatzer device closure of atrial septal defects in mature adults: Analysis of 76 cases. Heart 2004; 90: 334–335.
• 19.    Chessa  M,  Carminati  M,  Butera  G,  Bini  RM,  Drago  M,  Rosti  L, et al. Early and late complications associated with transcatheter occlusion of secundum atrial defect. J Am Coll Cardiol 2002; 39: 1061–1065.
• 20.    Wi  J,  Choi  JY,  Shim  JM,  Uhm  JS,  Hwang  HJ,  Kim  JY, et al. Fate of preoperative atrial fibrillation after correction of atrial septal defect. Circ J 2013; 77: 109–115.
• 21.    Brandenburg  RO Jr,  Holmes  DR Jr,  Brandenburg  RO,  McGoon  DC. Clinical follow-up study of paroxysmal supraventricular tachyarrhythmias after operative repair of a secundum type atrial septal defect in adults. Am J Cardiol 1983; 15: 273–276.
• 22.    Majewska  B,  Różański  J,  Baranowski  R,  Rydlewska-Sadowska  W. Long-term follow-up of supraventricular tachyarrhythmia in adult patients with secundum atrial septal defect before and after surgery. Pol Arch Med Wewn 1999; 102: 1077–1082 (in Polish).
• 23.    Gatzoulis  M,  Harris  L. Atrial arrhythmia after surgical closure of atrial septal defects in adults. N Engl J Med 1999; 340: 839–846.
• 24.    Morton  JB,  Sanders  P,  Vohra  JK,  Sparks  PB,  Morgan  JG,  Spence  SJ, et al. Effect of chronic right atrial stretch on atrial electrical remodeling in patients with an atrial septal defect. Circulation 2003; 107: 1775–1782.
• 25.    Szyszka  A,  Cieśliński  A. Migotanie przedsionków w wadach serca: Przyczyny, zasady postępowania. Kardiol Pol 1995; 42: 337–341.
• 26.    Hill  SL,  Berul  CI,  Patel  HT,  Rhodes  J,  Supran  SE,  Cao  QL, et al. Early ECG abnormalities associated with transcatheter closure of atrial septal defect using Amplatzer septal occluder. J Interv Card Electrophysiol 2000; 4: 469–474.
• 27.    Silversides  CK,  Siu  SC,  McLaughlin  PR,  Haberer  KL,  Webb  GD,  Benson  L, et al. Symptomatic atrial arrhythmias and transcatheter closure of atrial septal defects in adults patients. Heart 2004; 90: 1194–1198.
• 28.    Karwot  B,  Białkowski  J,  Szkutnik  M. Iatrogenic cardiac arrhythmias following transcatheter or surgical closure of atrial septal defect in children. Kardiol Pol 2005; 62: 35–43.
• 29.    Szkutnik  M,  Lenarczyk  A,  Kusa  J,  Białkowski  J. Symptomatic tachy- and bradyarrhythmias after transcatheter closure of interatrial communications with Amplatzer devices. Cardiol J 2008; 15: 510–516.
• 30.    Wilson  NJ,  Smith  J,  Prommete  B,  O’Donnell  C,  Gentles  TL,  Ruygrok  PN. Transcatheter closure of secundum atrial septal defects with the Amplatzer septal occluder in adults and children: Follow-up closure rates, degree of mitral regurgitation and evolution of arrhythmias. Heart Lung Circ 2008; 17: 318–324.
• 31.    Mazzanti  A,  Kanthan  A,  Monteforte  N,  Memmi  M,  Bloise  R,  Novelli  V, et al. Novel insight into the natural history of short QT syndrome. J Am Coll Cardiol 2014; 63: 1300–1308.
• 32.    Komar  M,  Przewlocki  T,  Olszowska  M,  Sobien  B,  Podolec  P. The benefit of atrial septal defect closure in elderly patients. Clin Interv Aging 2014; 9: 1101–1107.
• 33.    Komar  M,  Przewłocki  T,  Olszowska  M,  Sobień  B,  Tomkiewicz-Pająk  L,  Podolec  P. Is it worth closing the atrial septal defect in patients with insignificant shunt? Postepy Kardiol Interwencyjnej 2014; 10: 78–83.