Characteristics of recurrent atrial tachycardia after radiofrequency catheter ablation in patients with congenital heart disease

Introduction

Radiofrequency catheter ablation (RFCA) has evolved as a potential curative treatment for atrial tachycardia (AT) in patients with congenital heart disease (CHD). AT recurrence rates, however, are high and typically occur early after the ablation procedure. The mechanism of recurrent AT in CHD remains unclear, and has been attributed to either recovery of previous ablative lesions, non-targeted substates or formation of new AT substrate as a result of progressive atrial myopathy.

Purpose

This multicenter study aimed to systematically analyze the substrates for recurrent AT after prior RFCA in CHD on an individual patient basis.

Methods

Consecutive CHD patients who presented with AT recurrence after AT ablation and subsequently underwent a redo RFCA procedure in three high volume European referral centers were included. For each patient, the (presumed) clinical AT, targeted AT substrate and outcome for each targeted AT were identified and compared during both the index and redo procedures.

Results

Ninety-four CHD patients (40±17y, 65% male, 75% moderate or severe CHD complexity) who underwent redo RFCA (irrigated tip catheters on 90%) for AT recurrence after a median of 13 months (IQR 5-35) after the index procedure were analyzed. Seventy-nine presumed clinical AT substrates could be identified (21 Cavotricuspid (mitral) isthmus (CT(M)I), 31 Incisional related intra-atrial reentry (IART) in the systemic venous atrium (SVA), 13 focal atrial tachycardia (FAT) in the SVA, 4 FAT in pulmonary venous atrium (PVA), 10 other), of which 50 (59%) were identical to the substrates targeted during the first procedure, including the (CT(M)I) in 28 (50%) the SVA incision to caval inferior connection in 14 (28%), and other previously targeted substrates in 8 (16%)). New targeted AT substrates were the CT(M)I in 5 (14%) or related to the SVA incision in 18 (51%) (figure panel A).

Conclusion

In a large cohort of CHD patients referred for re-ablation of AT: (1) the majority of recurrent AT substrates was identical to the initially targeted AT substrate and (2) new AT substrates were identified predominantly in either the CTI or were related to the SVA incision.

Our findings suggest that the most important mechanism of AT recurrence in CHD is recovery of previous lesion despite irrigated tip catheter ablation. Techniques to achieve durable lesions and in addition, preventive linear empiric substrate ablation of the CTI and the lateral SVA incision to caval inferior connection are likely to improve long-term freedom from AT (figure panel B).