BACKGROUND: In patients late after surgical repair of congenital heart disease (CHD), areas with abnormal electrophysiologic properties may serve as slow conducting pathways within a macroreentrant circuit or may be the source of focal atrial tachycardia. OBJECTIVES: The purpose of this study was to evaluate the role of abnormal areas during focal atrial tachycardia prior to ablation. METHODS: Electroanatomic activation mapping of 62 atrial tachycardias was performed in 43 consecutive patients (37 +/- 12 years) after surgical repair of CHD. The mechanism of atrial tachycardia was scar related intra-atrial reentry (n = 27), cavotricuspid-related atrial flutter (n = 21), atrial fibrillation (n = 2), or focal atrial tachycardia (n = 10). During intra-atrial reentry, channels of slow conduction could be identified in all patients. Subsequent ablation was directed toward connecting two nonconductive borders. The site of origin during focal atrial tachycardia showed fractionated potentials and/or continuous electrical activity. RESULTS: Ablation directed at isolating the source area resulted in termination of focal atrial tachycardia in all cases. In two patients, ablation of an area showing continuous electrical activity giving rise to fibrillatory conduction resulted in termination of atrial fibrillation. Ablation of intra-atrial reentry was successful in 70%. Atrial flutter and focal atrial tachycardia were successfully ablated in all patients. No complications were observed. CONCLUSION: In patients with surgically corrected CHD, atrial tachycardia most often is caused by a macroreentrant mechanism but in some is the result of a focal mechanism. Areas of abnormal conduction may serve not only as a zone of slow conduction within a macroreentrant circuit but also as the site of origin of a focal atrial arrhythmia. Catheter ablation directed at "source isolation" is effective in eliminating focal atrial tachycardia in patients with CHD.
BACKGROUND: In patients late after surgical repair of congenital heart disease (CHD), areas with abnormal electrophysiologic properties may serve as slow conducting pathways within a macroreentrant circuit or may be the source of focal atrial tachycardia. OBJECTIVES: The purpose of this study was to evaluate the role of abnormal areas during focal atrial tachycardia prior to ablation. METHODS: Electroanatomic activation mapping of 62 atrial tachycardias was performed in 43 consecutive patients (37 +/- 12 years) after surgical repair of CHD. The mechanism of atrial tachycardia was scar related intra-atrial reentry (n = 27), cavotricuspid-related atrial flutter (n = 21), atrial fibrillation (n = 2), or focal atrial tachycardia (n = 10). During intra-atrial reentry, channels of slow conduction could be identified in all patients. Subsequent ablation was directed toward connecting two nonconductive borders. The site of origin during focal atrial tachycardia showed fractionated potentials and/or continuous electrical activity. RESULTS: Ablation directed at isolating the source area resulted in termination of focal atrial tachycardia in all cases. In two patients, ablation of an area showing continuous electrical activity giving rise to fibrillatory conduction resulted in termination of atrial fibrillation. Ablation of intra-atrial reentry was successful in 70%. Atrial flutter and focal atrial tachycardia were successfully ablated in all patients. No complications were observed. CONCLUSION: In patients with surgically corrected CHD, atrial tachycardia most often is caused by a macroreentrant mechanism but in some is the result of a focal mechanism. Areas of abnormal conduction may serve not only as a zone of slow conduction within a macroreentrant circuit but also as the site of origin of a focal atrial arrhythmia. Catheter ablation directed at "source isolation" is effective in eliminating focal atrial tachycardia in patients with CHD.
Authors: T Jared Bunch; Heidi M Connolly; Samuel J Asirvatham; Peter A Brady; Bernard J Gersh; Thomas M Munger; Win-Kuang Shen; Kristi H Monahan; Douglas L Packer Journal: J Interv Card Electrophysiol Date: 2007-10-20 Impact factor: 1.900
Authors: Róbert Pap; Mária Kohári; Attila Makai; Gábor Bencsik; Vassil Borislavov Traykov; Rodrigo Gallardo; Gergely Klausz; Kis Zsuzsanna; Tamás Forster; László Sághy Journal: J Interv Card Electrophysiol Date: 2012-07-27 Impact factor: 1.900