Atrial septal defects (ASD) are one of the most common congenital heart diseases, comprising 30% of adult congenital heart disease. Unlike a patent foramen ovale, this is an actual defect, and depending on its size can cause many pathophysiologic changes leading to atrial arrhythmia (AA), right heart failure, pulmonary hypertension, decreased exercise tolerance, and stroke.1 The leading cause of morbidity associated with ASDs is atrial tachyarrhythmias, especially as people age.2 Ostium secundum types of ASD are amenable to percutaneous closure, which reduces the risk of right ventricular failure and arrhythmia.
Atrial fibrillation is a common arrhythmia seen in adults, with its incidence increasing with age, obesity, hypertension, and other comorbidities. Echocardiographic parameters that predict the development of atrial fibrillation in adults without adult congenital heart disease include left atrial size, E/A ratio of <1, left ventricular hypertrophy, and moderate tricuspid regurgitation, along with other features of diastolic dysfunction.3 There is a known risk of atrial fibrillation and flutter after percutaneous closure of ASDs, which increases the risk of systemic embolism and stroke.4
In this issue of JSCAI, Burke et al5 set out to study the effects of age and other patient-specific factors on the incidence of AA postpercutaneous ASD closure in patients without previous AA at Cleveland Clinic from 2010 to 2022. Of the 177 patients meeting inclusion criteria, including postprocedural electrocardiogram or rhythm monitoring, there was an increase in AA within 1 week postprocedurally from 0.9% to 14%, following which it dropped to 3.4% at 6 months and peaked again at ∼6 years. AA increase was associated with age, diastolic dysfunction, and lower left ventricular ejection fraction. The sudden increase in left atrial and left ventricular volume return after ASD closure was a possible mechanism leading to left atrial stretch and increased AA. Older patients with higher systemic and pulmonary artery pressures and enlarged right- and left-sided chambers have less reverse remodeling, which maintains an arrhythmogenic substrate. This may explain the second peak in AA in patients who had ASD closures.
The study added to the existing knowledge that ASD closures are associated with an increased incidence of AA.6, 7, 8 Still, it showed that there may be a second spike later in life, especially in patients over 60 years of age, suggesting that ASDs should be closed before 60 years of age. This study is unique in that routine monitoring was performed on patients who underwent transcatheter ASD closure since 2018 at Cleveland Clinic. Therefore, AAs were recognized even when the patients were asymptomatic, while other studies looked for AA only when patients were symptomatic.
This study suggests that patients undergoing ASD closures should be screened and optimized for risk factors, such as diastolic dysfunction and left ventricular ejection fraction, which predispose to AA, which are not uncommon, and watched for AA both immediately and frequently thereafter. It raises questions about the need for anticoagulation and antiarrhythmic therapy in patients undergoing ASD closures to avoid embolic complications. More prospective clinical trials are needed to understand the incidence of AA after ASD closures, based on not just patient factors but structural, procedural, and device-related factors.
Acknowledgments
Declaration of competing interest
The author declared no conflict of interest with respect to the research, authorship, and/or publication of this article.
Funding sources
This work was not supported by funding agencies in the public, commercial, or not-for-profit sectors.
References
- 1.Geva T., Martins J.D., Wald R.M. Atrial septal defects. Lancet. 2014;383(9932):1921–1932. doi: 10.1016/S0140-6736(13)62145-5. [DOI] [PubMed] [Google Scholar]
- 2.Brida M., Chessa M., Celermajer D., et al. Atrial septal defect in adulthood: a new paradigm for congenital heart disease. Eur Heart J. 2022;43(28):2660–2671. doi: 10.1093/eurheartj/ehab646. [DOI] [PubMed] [Google Scholar]
- 3.Rosenberg M.A., Manning W.J. Diastolic dysfunction and risk of atrial fibrillation: a mechanistic appraisal. Circulation. 2012;126(19):2353–2362. doi: 10.1161/CIRCULATIONAHA.112.113233. [DOI] [PubMed] [Google Scholar]
- 4.Himelfarb J.D., Shulman H., Olesovsky C.J., et al. Atrial fibrillation following transcatheter atrial septal defect closure: a systematic review and meta-analysis. Heart. 2022;108(15):1216–1224. doi: 10.1136/heartjnl-2021-319794. [DOI] [PubMed] [Google Scholar]
- 5.Burke B.J., Goldar G., Rajeswaran J., et al. Dual-phase increase in atrial arrhythmia prevalence following percutaneous atrial septal defect closure. J Soc Cardiovasc Angiogr Interv. 2025;4 [Google Scholar]
- 6.Muroke V., Jalanko M., Haukka J., et al. Outcome of transcatheter atrial septal defect closure in a nationwide cohort. Ann Med. 2023;55(1):615–623. doi: 10.1080/07853890.2023.2178669. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Chiu S.N., Wu M.H., Tsai C.T., et al. Atrial flutter/fibrillation in patients receiving transcatheter closure of atrial septal defect. J Formos Med Assoc. 2017;116(7):522–528. doi: 10.1016/j.jfma.2016.09.005. [DOI] [PubMed] [Google Scholar]
- 8.Fujii Y., Akagi T., Nakagawa K., et al. Clinical impact of transcatheter atrial septal defect closure on new onset atrial fibrillation in adult patients: comparison with surgical closure. J Cardiol. 2020;76(1):94–99. doi: 10.1016/j.jjcc.2020.01.008. [DOI] [PubMed] [Google Scholar]