TY - JOUR
T1 - Atrial flutter/fibrillation in patients receiving transcatheter closure of atrial septal defect
AU - Chiu, Shuenn Nan
AU - Wu, Mei Hwan
AU - Tsai, Chia Ti
AU - Lai, Ling Ping
AU - Lin, Jiunn Lee
AU - Lin, Ming Tai
AU - Lu, Chun Wei
AU - Wang, Jou Kou
N1 - Publisher Copyright:
© 2016
PY - 2017/7/1
Y1 - 2017/7/1
N2 - Background/purpose Atrial flutter/fibrillation (AFL/Af) is a common late complication in atrial septal defect (ASD) patients even after occluder implantation. We try to delineate the risk factors of persistent AFL/Af. Methods From 1998 to 2010, all patients older than 18 years of age who received ASD occluder implantation in our hospital were enrolled, and their records were retrospectively reviewed. In addition, renin–angiotensin system gene polymorphisms including angiotensinogen gene, A1166C polymorphism on the angiotensin II type I receptor gene, and insertion/deletion (I/D) patterns on the angiotensin-converting enzyme gene were checked using direct sequencing. Results A total of 517 patients (male/female 127/390) were enrolled. The mean age of patients receiving occluder deployment was 41.5 ± 14.5 years. Prior to occluder deployment, 3.9% of patients had persistent Af, 3.1% of patients had paroxysmal Af, and 0.8% had AFL. After a follow-up of 1894 patient-years, 3.5% had persistent Af and 1.9% of patients had paroxysmal Af. The greatest risk factors of AFL/Af genesis included age, occluder size, presence of multiple ASDs, and underlying thyroid or mitral valve disorder (p < 0.001, p < 0.001, p = 0.033, p = 0.016, and p = 0.012, respectively). Preoperative AFL/Af status is the most important factor in determining AFL/Af resolution and progression after an intervention. The renin–angiotensin system gene polymorphisms had no association with AFL/Af genesis, and progression or resolution after intervention. Conclusion AFL/Af is common after ASD occluder implantation, and predisposed by older age, larger and multiple ASDs, and underlying disorders. Preoperative atrial arrhythmia status is the most important predictor of AFL/Af progression or resolution. Renin–angiotensin system gene polymorphisms had no association with AFL/Af.
AB - Background/purpose Atrial flutter/fibrillation (AFL/Af) is a common late complication in atrial septal defect (ASD) patients even after occluder implantation. We try to delineate the risk factors of persistent AFL/Af. Methods From 1998 to 2010, all patients older than 18 years of age who received ASD occluder implantation in our hospital were enrolled, and their records were retrospectively reviewed. In addition, renin–angiotensin system gene polymorphisms including angiotensinogen gene, A1166C polymorphism on the angiotensin II type I receptor gene, and insertion/deletion (I/D) patterns on the angiotensin-converting enzyme gene were checked using direct sequencing. Results A total of 517 patients (male/female 127/390) were enrolled. The mean age of patients receiving occluder deployment was 41.5 ± 14.5 years. Prior to occluder deployment, 3.9% of patients had persistent Af, 3.1% of patients had paroxysmal Af, and 0.8% had AFL. After a follow-up of 1894 patient-years, 3.5% had persistent Af and 1.9% of patients had paroxysmal Af. The greatest risk factors of AFL/Af genesis included age, occluder size, presence of multiple ASDs, and underlying thyroid or mitral valve disorder (p < 0.001, p < 0.001, p = 0.033, p = 0.016, and p = 0.012, respectively). Preoperative AFL/Af status is the most important factor in determining AFL/Af resolution and progression after an intervention. The renin–angiotensin system gene polymorphisms had no association with AFL/Af genesis, and progression or resolution after intervention. Conclusion AFL/Af is common after ASD occluder implantation, and predisposed by older age, larger and multiple ASDs, and underlying disorders. Preoperative atrial arrhythmia status is the most important predictor of AFL/Af progression or resolution. Renin–angiotensin system gene polymorphisms had no association with AFL/Af.
KW - atrial flutter/fibrillation
KW - atrial septal defect
KW - gene
KW - renin–angiotensin
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U2 - 10.1016/j.jfma.2016.09.005
DO - 10.1016/j.jfma.2016.09.005
M3 - Article
C2 - 27816405
AN - SCOPUS:85005773750
SN - 0929-6646
VL - 116
SP - 522
EP - 528
JO - Journal of the Formosan Medical Association
JF - Journal of the Formosan Medical Association
IS - 7
ER -