Histopathologic Characterization of Chronic Radiofrequency Ablation Lesions for Pulmonary Vein Isolation

Objectives This study describes the histopathologic and electrophysiological findings in patients with recurrence of atrial fibrillation (AF) after pulmonary vein (PV) isolation who underwent a subsequent surgical maze procedure. Background The recovery of PV conduction is commonly responsible for recurrence of AF after catheter-based PV isolation. Methods Twelve patients with recurrent AF after acutely successful catheter-based antral PV isolation underwent a surgical maze procedure. Full-thickness surgical biopsy specimens were obtained from the PV antrum in areas of visible endocardial scar. Before biopsy, intraoperative epicardial electrophysiological recordings were taken from each PV using a circular mapping catheter. Results Twenty-two PVs were biopsied from the 12 patients 8 +/- 11 months after ablation. Eleven of the 22 specimens (50%) revealed transmural scar, and 11 (50%) showed viable myocardium with or without scar. Each biopsy specimen demonstrated evidence of injury, most commonly endocardial thickening (n = 21 [95%]) and fibrous scar (n = 18 [82%]). Seven of the 22 specimens (32%) showed conduction block at surgery. Transmural scar was more likely to be seen in the biopsy specimens from the PVs with conduction block than in specimens from the PVs showing reconnection. However, viable myocardium alone or mixed with scar was seen in 2 specimens from PVs with conduction block. Conclusions PVs showing electrical reconnection after catheter-based antral ablation frequently reveal anatomic gaps or nontransmural lesions at the sites of catheter ablation. Nontransmural lesions are noted in some PVs with persistent conduction block, suggesting that lesion geometry may influence PV conduction. The histological findings show that nontransmural ablation can produce a dynamic cellular substrate with features of reversible injury. Delayed recovery from injury may explain late recurrences of AF after PV isolation. (J Am Coll Cardiol 2012;59:930-8) (C) 2012 by the American College of Cardiology Foundation