Outcome in Patients with Secundum Type Atrial Septal Defect Referred for Percutaneous or Surgical Closure: A Single-Center Experience

Abstract

This single-center, retrospective analysis presents data from 611 patients with a secundum type atrial septal defect (ASD II) closure. Included were patients >2 years of age. Patients presented at a median (range) age of 6.95 (2–86) years for interventional closure of ASD II. Out of 611 patients, 215 underwent intracardiac repair based on transthoracic echocardiography (ECHO) findings. Transcatheter device closure was attempted and successfully performed in 300 out of 396 patients (Amplatzer™ Septal Occluder [ASO], n = 290 patients). Follow-up was 3.3 years (1 day–21.8 years) in patients with interventional closure of ASD II and 0.7 years (3 days–14.7 years; p < 0.001; Mann–Whitney) in patients after surgical closure. There was no in-hospital mortality in both groups. One patient, after Amplatzer device closure with an absent aortic rim, developed erosion, which was treated by cardiac surgery and patch closure of ASD II. Two patients showed dislocation of the device. In 231 out of 396 patients, right ventricular dimension normalized completely as determined on the last follow-up visit. Six patients at a median age of 60 (49.4–68.7) years presented with atrial fibrillation, which persisted after ASD II closure. About 26 patients (6.6%) showed pulmonary hypertension (PH), with 1 presenting with coincidental ASD II and severe PH. Closure of ASD II can be accomplished safely by interventional catheterization and intracardiac repair. In most cases, perioperative transthoracic and transesophageal ECHO is sufficient to decide whether a surgical approach or interventional closure is the best option to close the defect.

Keywords

cardiac catheterization/intervention (includes PCI) - congenital heart disease - CHD - pulmonary arteries/veins

Introduction

Congenital heart defects show a prevalence of 1.08% in all liveborn neonates.[1] Secundum type atrial septal defect (ASD II) is observed at a rate of 1.65/1,000 live births.[2]

In patients with a left-to-right shunt, volume overload will lead to dilation of the right atrium and right ventricle. Later in life, this will lead to atrial arrhythmia, heart failure, and pulmonary hypertension (PH). The natural history of ASD II showed a decrease in life expectancy.[3]

Closure of ASD II is, therefore, recommended for all patients presenting with right ventricular volume overload due to a significant left-to-right shunt (ratio of pulmonary to systemic flow [Qp/Qs] >1.5). Historically, cardiac surgery using cardiopulmonary bypass was the first option to close ASD II. Transcatheter closure using different devices, such as the Amplatzer™ Septal Occluder (ASO) or the Gore® Septal Occluder (GSO), has been performed at a large scale since 1990. This has enabled interventional cardiologists to close up to 80% of all ASD II by cardiac catheterization.[4]

The definition of PH associated with congenital heart disease was recently modified by the Pediatric Task Force of the Seventh World Symposium on Pulmonary Hypertension,[5] as a mean pulmonary artery pressure (mPAP) >20 mm Hg and an increased pulmonary vascular resistance index (PVRi) of >3 U·m². The combination of both an increase in mPAP >20 mm Hg and a concomitant increase in PVRi >3 U·m² is rarely observed in patients <18 years of age with ASD II.

Haworth, in the early 1980s, published a series of nine children with severe pulmonary vascular disease and ASD II.[6] According to current opinion, such cases would be classified nowadays as “idiopathic pulmonary arterial hypertension”[7] or “coincidental” since the rapid development of severe pulmonary vascular disease cannot be explained by the pre-tricuspid left-to-right shunt.[5]

It is currently not known whether there is a “gray zone” of patients presenting with moderately elevated mPAP that—when treated with device closure or cardiac surgery—will later develop severe pulmonary arterial hypertension.

Another topic in the management of patients with ASD II is atrial arrhythmias that occur after ASD II closure. Only limited data exist concerning the question of whether there is a difference between surgical and interventional treatment with respect to the development of atrial arrhythmias.[8]

In this retrospective study, we therefore analyzed our data obtained in patients with ASD II, aiming to answer the following questions:

1. What is the outcome of patients treated in a single center either by cardiac intervention or cardiac surgery to close the ASD II? Is there a difference in mortality or morbidity?

2. How often is an elevated pulmonary artery pressure >20 mm Hg combined with an increased pulmonary vascular resistance >3 WU in ASD II patients?

3. Do patients after surgical or interventional ASD II closure develop symptomatic pulmonary vascular disease during short-term follow-up?

4. Is there a difference in the occurrence of atrial arrhythmias between patients after intracardiac repair versus device closure of ASD II?

Methods

The study was conducted as a retrospective data analysis. We searched our electronic patient data system (i.s.h.med, SAP Germany SE, Walldorf, Germany) for patients with ASD II using the following criteria:

Inclusion Criteria

• Age ≥2 years at the time of ASD II closure.

• Availability of hemodynamic data prior to ASD II closure.

• Time period of defect closure in the years 2005 to 2021.

Exclusion Criteria

• ASD II associated with additional cardiac malformations.

• Other types of ASD II, such as sinus venosus ASD II, etc.

Demographic, clinical, and hemodynamic data were obtained from all the patients. The time point of the last follow-up visit was recorded.

The following parameters were recorded:

• 1) At cardiac catheterization prior to defect closure

  • a) Size and location of defect by transesophageal echocardiography (ECHO)

  • b) Hemodynamic parameters: Systolic, diastolic, and mPAP, capillary wedge pressure, PVRi as calculated by oximetry using tabular oxygen uptake, Qp/Qs ratio, and cardiac index.

  • 2) At last follow-up

  • a. Survival

  • b. Functional class, according to Rosenthal score[9]

  • c. Need for specific pulmonary antihypertensive medication (prior to or after defect closure)

  • d. Prevalence of arrhythmia

  • e. Presence or absence of right ventricular dilation at last follow-up (right ventricular dilation is defined as an increase in right ventricular diameter above z-score +2 in parasternal long axes view).

  In addition to screening of our own database, we contacted all referring physicians, in writing, to provide us with the latest cardiac findings. We, therefore, could obtain information with respect to survival and cardiac findings.

Statistical Analysis

Testing for Distribution of Normality (Kolmogorov–Smirnov Test)

Age, body weight, height, body surface area, size of ASD II, systolic pulmonary artery (PA) pressure, mPAP, CI, PVRi, and Qp/Qs ratio did not show a normal distribution. For this reason, continuous variables are expressed as median (range) and categorical variables as numbers of patients and percentages.

Events after closure of ASD II were defined as death, rhythm disorders, need for cardiac surgery, or interventional procedures related to the ASD II.

A p-value of <0.05 was considered statistically significant. Logistic regression was used to study the correlation between the presence or absence of right ventricular dilation at the last follow-up and follow-up duration (years).

Data analysis was performed using SigmaStat 3.0 for Windows software (Copyright 1882-2003 SPSS Inc; IBM, Armonk, NY).

The study was approved by the institutional review board of our institution (S-619/2022).

Results

Patient Population

A total of 611 patients were included after screening our institutional patient record system (i.s.h.med).

The study flow diagram for the allocation of patients is given in [Fig. 1].

Fig. 1 Study flow diagram. ASD II, atrial septal defect.

Of those 611 patients, 215 underwent intracardiac repair on the basis of transthoracic echocardiography findings without prior hemodynamic evaluation by cardiac catheterization.

These patients (males = 75, females = 140) were 6.14 (2–69.2) years of age at the time of ASD II surgery.

In 396 patients, hemodynamic evaluation was performed, and transcatheter closure of ASD II was attempted during the same cardiac catheterization.

Demographic data of these 396 patients are given in [Table 1].

Table 1 Population baseline characteristics (n = 396)

Median (range)
Age, years	6.95 (2–86)
Sex
Female	232
Male	164
Weight, kg	23.7 (4.3–115)
Height, cm	123 (62–198)
Body surface area, m2	0.9 (0.27–2.7)
Extracardiac comorbidities
Trisomy 21	8
Other: Wolf–Hirschhorn syndrome	1

Follow-up was 3.3 years (1 day–21.8 years) in patients with interventional closure of ASD II, and 0.7 years (3 days–14.7 years; p < 0.001; Mann–Whitney) in patients after surgical closure.

The characteristics of ASD II anatomy are given in [Table 2]. The median diameter of ASD II as measured by the balloon occlusion technique was 13 (3.5–30) mm. Deficient rims were present in 102 out of 396 patients. A deficient aortic rim was the most frequent form of absent rim observed (n = 37).

Table 2 Transcatheter closure of atrial septal defect: Echocardiographic and procedural features

	Median (range)/Number of occurrences
Transesophageal echographic diameter (mm)	11 (3–27)
Balloon sizing diameter (mm)	13 (3.5–30)
Deficient rims[a]	102 out of 396 patients
Aortic	n = 37
Posterior	n = 32
Anteroinferior	n = 22
Posterosuperior	n = 0
Inferior	n = 36
Superior	n = 0
Mode of closure
Percutaneous intervention	n = 300
Cardiac surgery with cardiopulmonary bypass	n = 96
Device type[b]
Amplatzer™ Septal Occluder	290
GORE® Septal Occluder	17
GORE® CARDIOFORM Septal Occluder	2
GORE® HELEX® Septal Occluder	1
Fluoroscopy time (minutes)	11.5 (1.5–90)

^a Deficient rims: Multiple absent rims present in some patients. No data on deficient rim: n = 16.

^b Multiple devices were used in some patients.

ASO was the occluder system most often used for transcatheter closure of the defect. GSO was used in 17 patients ([Table 2]).

Some patients presented with multiple ASD IIs. These patients were treated with multiple devices ([Table 3]).

Table 3 Multiple atrial septal defects—transcatheter device closure

Patient number	Sex	Age at first intervention (years)	Device size and type	Number of procedures	Follow-up (years)
1	F	15.3	6 mm Amplatzer™ Septal Occluder + 30 mm GSO	1	0.1
2	F	44.4	4 mm + 13 mm Amplatzer ASD II occlude	1	1
3	F	61.7	13 mm Amplatzer™ Septal Occluder + 25 mm GSO	2	11.2
4	F	59	30 mm Amplatzer multifenestrated ASD II device + 30 mm GSO	2	8.6
5	F	55	10 mm Amplatzer™ Septal Occluder + 25 mm GSO	2	3.8
6	F	30.9	30 mm GSO + 8 mm Amplatzer™ Septal Occluder + 8 mm Amplatzer ASD II occlude	3	1.2
7	M	68	16 mm Amplatzer™ Septal Occluder + 25 mm GSO + 10 mm Amplatzer™ Septal Occluder	3	6.5
8	F	71	8 mm + 18mm Amplatzer™ Septal-Occluder	1	3.14
9	M	16.3	6 mm Amplatzer™ Septal Occluder + 30 mm GSO	2	3.51
10	M	62.1	30 mm GSO + 30 mm Amplatzer multifenestrated ASD II occluder	2	1.15
11	F	51	30 mm GSO + 30 mm GSO	2	10.1

Abbreviations: ASD II, atrial septal defect; GSO, GORE® Septal Occluder.

Acute Complications after Device Closure

Device Erosion

Device erosion occurred in a 16-year-old patient with an anteriorly located ASD II and an absent aortic rim. This defect was 25 mm in diameter on balloon sizing. The defect was closed with a 26-mm ASO, which was positioned in a “Y” shape towards the ascending aorta. Twelve hours after the procedure, the patient complained about chest pain. An ECHO examination revealed pericardial effusion, and a pericardial drain was inserted, and hemorrhagic pericardial effusion was drained effectively. Despite cessation of pericardial effusion and hemodynamic and respiratory stability, it was decided to surgically remove the device and close the ASD II. The further course of this patient was uneventful.

Dislocation of Device

Dislocation of the device occurred in two patients:

1. A 6-year-old girl presenting with a 12-mm ASD II and aneurysmatic fossa ovalis, a 12-mm ASO was placed. At routine echocardiography performed on the following day, the device was not visible anymore. X-ray of the chest showed a dislocation into the transverse aortic arch. Surgical removal of the device was performed using extracorporeal bypass with deep hypothermic cardiac arrest.

   The ASD II was closed with a direct suture. Recovery was uneventful.

2. In another case, a 16-year-old boy presented with a 12-mm ASD II; a 30-mm GSO was implanted without prior balloon sizing. Several hours later, the patient complained about chest pain, and a chest X-ray showed dislocation of the GSO into the right PA. The patient was referred to the cath lab again, and the device was retrieved using a “lasso” and a long sheath. Thereafter, the defect was re-evaluated, and two defects could be found. Balloon sizing of the larger defect was performed and revealed a defect size of 22 mm. In addition, an ASD II of 6 mm could be found. The decision was made to close the smaller defect with a 6-mm ASO first. In order to stabilize the situation, an interval of 14 months was used before the other (larger) ASD II was closed. Again, balloon sizing showed a diameter of defect of about 15 mm, and a 30-mm GSO was placed successfully.

   On Transesophageal Echocardiography (TEE) 2 years later, there were no signs of residual shunt.

Mortality

There was no in-hospital mortality in both study groups.

The survival of patients—as evaluated by active contacting patients/parents and their referring physicians—led to the reported data on survival as documented by the above mentioned last follow-up data.

In patients treated with interventional ASD II closure, there were two deaths during the follow-up period.

1. A 2.7-year-old girl presented with ASD II and elevated right ventricular pressure on echocardiography. Cardiac catheterization revealed a mPAP of 52 mm Hg, left-to-right shunt of Qp/Qs = 1.96, PVRi = 15.7 U·m², and Rp/Rs = 0.32. There was clearly an out-of-proportion PH in this case, and a tentative diagnosis of idiopathic PH with associated ASD II was made. We decided to perform surgical ASD II closure with a 3-mm fenestration of the pericardial patch, and the patient was treated with pulmonary antihypertensive medication thereafter. Unfortunately, the girl died after a follow-up of 13.6 years from severe pulmonary vascular disease.

2. A 68-year-old man presented with multiple ASD IIs and right ventricular dilatation. Comorbidities included severe obesity (body mass index [BMI] = 37 kg/m²), arterial hypertension, and type II diabetes mellitus. The ASD IIs were closed by percutaneous intervention. The patient died 6.5 years later at the age of 74 years in another hospital after admission for severe congestive heart failure.

Freedom from Reintervention, Survival of Patients

One patient in the group who was treated by intracardiac repair needed reoperation after 2 weeks due to tearing of the pericardial patch. The recovery was uneventful.

The follow-up period was significantly shorter in patients who underwent surgical closure of ASD II on the basis of echocardiography findings. For this reason, a meaningful evaluation using a Kaplan—Meier survival analysis could not be performed.

Rhythm Disorders

Most patients presented with a normal sinus rhythm at the time of interventional or surgical ASD II closure.

Two patients presented with a pacemaker prior to closure of ASD II, one patient with cardiomyopathy and associated ASD II, and another with sick sinus syndrome prior to ASD II closure (see [Table 4]).

Table 4 Rhythm disorders in patients with atrial septal defect

Patient number	Age at ASD II closure (years)	Type of rhythm disorder before intervention or surgery	Follow-up duration (years)	Type of rhythm disorder at follow-up
1	4.26	Sick Sinus Syndrome—post-pacemaker implantation	4.2	Sick Sinus Syndrome—pacemaker VVI
2	68.7	Atrial fibrillation	8.26	Atrial fibrillation
3	51	Atrial fibrillation	1.15	Atrial fibrillation
4	49.36	Atrial fibrillation	6.84	Atrial fibrillation
5	75	Atrial fibrillation	0.56	Atrial fibrillation
6	1.93	Complete AV block—cardiomyopathy pacemaker	5.23	Complete AV block—cardiomyopathy pacemaker VVI
7	62.11	Atrial fibrillation	1.15	Atrial fibrillation
8	53.6	Atrial fibrillation	8.27	Atrial fibrillation
9	72.08	AV-node re-entry tachycardia	4.16	Sinus rhythm—after radiofrequency ablation

Abbreviation: ASD II, atrial septal defect.

Six patients at a median age of 60 (49.4–68.7) years presented with atrial fibrillation before the procedure, which persisted after ASD II closure at the last follow-up date.

Right Ventricular Dimension and Atrial Septal Defect Closure

At the last follow-up, right ventricular dilatation normalized in 231 patients. Persistent right ventricular dilatation was present in 120 patients. In 45 patients, no M-Mode data were available in order to analyze the right ventricular dimension.

Patients with persistent right ventricular dilation were slightly older at the time of closure of their defect (median 8.1 [2.0–86] years) compared to patients that showed a normal right ventricle on follow-up (median age at closure: 6.7 [2–72] years; Mann–Whitney p = 0.045).

The follow-up period in patients with normal right ventricular dimensions at follow-up was longer compared to patients with dilation of the right ventricle on follow-up (median follow-up 4.6 years vs. 1.7 years; Mann–Whitney p ≤ 0.001).

A logistic regression was calculated with the dependent variable “presence or absence of right ventricular dilation” and the independent variable “time after closure of ASD II.” The result of this statistical analysis showed a weak but present correlation between the presence of right ventricular dilation and the duration of follow-up (p = 0.08). In other words, in most patients, right ventricular dimension returned to normal during follow-up.

Pulmonary Hypertension

In 396 patients, the hemodynamic data were available. An elevated mPAP >20 mm Hg was measured in 67 patients (16.9%). An additional elevation in PVRi >3 U·m² was calculated in 26 out of 67 patients (6.6% of all patients with hemodynamic measurements).

Presence of PH was not related to age: There was no difference between the group of patients with normal PA pressure compared to the group of patients with PH (Mann–Whitney rank-sum test; p = 0.196).

The development of elevated indexed pulmonary vascular resistance (PVRi) in patients with mPAP >20 mm Hg showed a trend to increase with age, but this difference did not reach statistical significance in this series ([Fig. 2]).

Fig. 2 Age of patients in relation to increased PVRi. (Median = line within the box; boundaries = 25th percentile, 75th percentile). Whiskers (error bars) above and below the box indicate the 90th and 10th percentiles. Outliers given as single points. mPAP, mean pulmonary artery pressure; PVRi, pulmonary vascular resistance index.

With the exception of one patient presenting initially with severe PH (mPAP = 52 mm Hg, PVRi = 15.7 U·m²), none of the patients with mPAP >20 mm Hg and PVRi >3 U·m² showed signs of persistent PH on follow-up.

Discussion

Our data confirm that closure of ASD II by cardiac surgery or percutaneous intervention is a safe procedure, which can be performed with zero mortality.

ASD II closure by a transcatheter device emerged as the preferred treatment. O'Byrne and co-workers published a series of 6,392 cases with ASD II from 39 centers in the United States.[4] The success rate of percutaneous closure was reported as 82%. Our data confirmed this finding, although this was feasible in about 49% of our patients. The difference may be explained by differences in the study cohorts and in-house policies in decision-making for surgical or percutaneous closure.

Acute complications of percutaneous device closure are erosion and pericardial bleeding, as well as device embolization. In this patient series, erosion and pericardial effusion were observed in one patient with the ASO and a missing anterior rim. In this patient, a Y-shape configuration of the occluder below the aorta was observed. In 2004, Amin and co-workers published a study addressing the risk of erosions after percutaneous device closure with the ASO.[10] As a consequence of this report, Y-shaped placement of the ASO below the ascending aorta was avoided. Potential risk factors for erosions associated with the ASO were suggested as a deficient aortic rim and/or a superior rim and oversizing the occluder in relation to the dimensions of the defect.[10] However, this issue is unresolved, as other groups have found no such correlation.[11] [12] [13]

Device embolization is an issue when using percutaneous ASD II closure devices and, therefore, percutaneous ASD II closure requires postinterventional observation of the patients, as well as access to immediate cardiac surgery. Device embolization can be addressed frequently by catheter-interventional procedures to retract the embolized device, but in our series, the device had to be removed from the transverse aortic arch by cardiac surgery. This is consistent with recent findings published by Garre and co-workers, who reported about 30 cases of device embolization. Seventeen out of 30 patients needed cardiac surgery to remove the device, and—consistent with our findings—1 patient with embolization into the aorta needed a period of total circulatory arrest for retrieval of the device.[14]

Young children weighing ≤15 kg and patients presenting with defect size >20 mm are prone to more complications after transcatheter device closure than other patients.[11] In our opinion, we would still prefer surgical closure of such defects. Therefore, in this series, only patients older than 2 years of age were included.

Olejnik and co-workers recently published a single-center study comprising 803 patients who underwent transcatheter defect closure using ASO.[15] They reported a >5-year follow-up in 651/803 patients (81%). As in our series, the rate of complications was low: Device embolization (n = 1), thrombus formation at the occluder surface (n = 1), and cardiac erosion (n = 1).

Consistent with these findings, our data confirm that transcatheter defect closure of ASD II can be performed with low morbidity, but device erosion remains an issue during follow-up of these patients.

Surgical approaches for closure of ASD II and outcome have been recently reviewed.[16] Mortality is low in contemporary series: de Beco and co-workers reported the outcome in 120 children with a mortality of 0.8%.[17] Perioperative complications such as revision surgery, pericardial drainage, and thromboembolism were reported in 6.7% of their patients. A meta-analysis demonstrated that transcatheter closure of ASD II was superior to SC for all-cause mortality and total complications.[18] Ooi and co-workers reported a series of 4,606 transcatheter procedures and 3,159 surgeries for ASD II closure with no mortality in both groups.[19] The costs for transcutaneous closure of ASD II were found to be lower than the costs for surgical closure.[19] However, it should be taken into account that the decision for surgical or transcatheter device closure of ASD II must not be guided by cost efficiency, as Bacha commented.[20] Late complications of transcatheter closure of ASD II may also include fatal events due to device erosion, even years after a successful closure with various devices such as the ASO,[21] but also the Occlutech Figulla Flex device,[22] the Nit Occlud ASD II-R® device,[23] and pericardial tamponade due to perforation of fractured wire has been reported for the Gore Cardioform Occluder®.[24]

Therefore, surgical closure of ASD II remains a valid option and is the procedure of choice in small children and in patients with insufficient rims to perform transcatheter device closure. Parents and patients must be thoroughly informed about the advantages and risks of complications of both methods.

Mortality during follow-up was low in this series (two patients) and related to senescence and multimorbidity in one patient and severe pulmonary vascular disease in an adolescent presenting with ASD II and severe PH 13.6 years after ASD II closure. This child clearly presented with pulmonary vascular disease of unknown origin and associated ASD II. These patients are categorized according to the current classification for patients with PH as “Group C: Coincidental defects, including all (isolated) ASD IIs in childhood.”[5]

Surgical closure with a fenestrated pericardial patch has been successfully performed in these patients,[25] leading to improvement of symptoms.

Of note, the presence of PH has been reported even in children with ASD II.[6] At present, however, it is unclear whether the development of pulmonary vascular disease in children with ASD II is caused by the pulmonary volume overload in a subset of patients or—more likely—whether patients with pulmonary vascular disease and PH present with a coincidental ASD II. Wacker and co-workers[26] reported the data from the TOPP-1 registry and pointed out that 43 out of 62 patients with PH classified as Group C: “Coincidental shunts,” presented with an ASD II. On the basis of our findings, we cannot resolve this issue. We can, however, provide an estimate of the frequency of the association of ASD IIs with severe PH: In only 1 of 611 patients presenting with ASD II, severe pulmonary vascular disease was present.

PH at initial presentation, defined as mPAP >20 mm Hg and PVRi >3 U·m², was present in 26 patients.

Of note, with the exception of the single patient presenting with severe PAH at the initial presentation (mPAP = 52 mm Hg, PVRi = 15.7 U·m²), none of the other 26 patients showed signs of progressive vascular disease after intracardiac repair or device closure of their defect during follow-up. This demonstrates that normalization of pulmonary blood flow in these patients has a positive effect on pulmonary circulation, with the limitation that follow-up was 3.3 years (1 day–21.8 years).

Limitations

Due to the limited follow-up duration, we cannot provide data on the long-term outcomes with respect to survival and the development of pulmonary vascular disease.

In this series, most patients presenting for ASD II closure were young children (6.95 [2–86] years) when referred for transcatheter ASD II closure.

Follow-up was significantly shorter in patients who underwent surgical ASD II closure without prior cardiac catheterization. This can be explained by the fact that patients after surgical ASD II closure were more often referred to their local specialist for congenital heart disease, whereas patients after transcatheter device closure were re-evaluated more often in our outpatient clinic.

Rhythm Disorders

Current data suggest that new-onset atrial fibrillation (AF) is observed at a younger age in patients with an ASD II compared with the general population.[8]

AF is the most common rhythm complication observed in these patients with advancing age.[27] Berger and co-workers reviewed available studies addressing ASD II and atrial arrhythmias.[28] They concluded that older patients with AF rarely reverted to sinus rhythm after ASD II closure, whereas patients with atrial flutter clearly had a benefit from closure of their defect.

This is consistent with our findings. None of the six patients presenting with atrial fibrillation reverted to sinus rhythm during follow-up ([Table 4]).

No clear correlation between the method of ASD II closure and AF was found in a series of 173 patients with a follow-up of 43 (29–59) years.[8] We can confirm that the method of closure of ASD II (transcatheter vs. surgical) did not influence the occurrence of AF. As a limitation, the follow-up in our study population was much shorter.

In conclusion, this single-center, retrospective study demonstrates that closure of ASD II can be accomplished safely by interventional catheterization and intracardiac repair. Surgical closure can be performed with almost zero mortality, with the disadvantage of being more invasive. Transcatheter closure offers a safe option for most patients, but radiation exposure and the potential for early (device embolization) and even late complications caused by erosion demand a very careful approach when deciding which option is best for a given patient.

In most cases, preoperative transthoracic and transesophageal echocardiography is sufficient to decide whether a surgical approach or interventional closure is the best option to close the defect. PH, as defined by the new criteria, is present in a low proportion of patients referred for ASD II closure and does not influence short-term outcome, whereas severe PH with coincidental ASD II is of poor prognostic outcome. AF is observed only in older patients and does not revert to sinus rhythm in these patients after closure of their defect.

Conflict of Interest

The authors declare that they have no conflict of interest.

Contributors' Statement

J.G.: contributed to conceptualization, data curation, formal analysis, writing–original draft, writing–review and editing. V.Z. contributed to conceptualization, data curation, formal analysis, investigation, methodology, supervision, writing–original draft, writing–review and editing. M.F. contributed to data curation, formal analysis, writing–original draft. T.L. contributed to conceptualization, project administration, validation, writing–review and editing. M.G. contributed to conceptualization, data curation, formal analysis, methodology, project administration, resources, writing–original draft, writing–review and editing.

^‡ These authors contributed equally to this article.

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Publication History

Received: 05 July 2025

Accepted: 11 January 2026

Accepted Manuscript online:
19 January 2026

Article published online:
02 February 2026