An initial ex vivo evaluation of temperature profile and thermal injury formation on the epiesophageal surface during radiofrequency ablation.

INTRODUCTION

Few studies have examined heat transfer and thermal injury on the epiesophageal surface during radiofrequency application, or compared the risk of esophageal thermal injury between standard and high-power, short-duration (HPSD) ablation. We studied the thermodynamics of HPSD and standard ablation at different tissue interfaces between the left atrium and esophagus, focusing on epiesophageal temperature changes and thermal injury.

METHODS AND RESULTS

Fresh porcine heart and esophageal sections were secured to a custom holder and submerged in a temperature-controlled, circulating water bath. During ablation, thermistors recorded temperatures at the catheter tip-atrial interface, epiesophageal-atrial interface, and esophageal lumen. Samples were ablated in triplicate with the following parameters: contact force (15/25g), power (10/20/30 W standard; 40/45/50 W HPSD), and duration (10/20/30 s standard; 5/10/15 s HPSD). Epiesophageal and endoluminal temperature rises were greater in HPSD than in standard ablation (epiesophageal: 5.9 ± 5.6 vs. 2.2 ± 2.0°C, p < .01; endoluminal: 0.7 ± 0.5 vs. 0.4 ± 0.2°C, p < .01). Six of 30 HPSD ablations and 1 of 26 standard ablations caused esophageal injury. The delay between the peak epiesophageal and endoluminal temperatures was greater in HPSD than in standard ablation (24.2 ± 22.1 vs. 13.0 ± 11.0 s, p = .023). Likewise, the peak epiesophageal surface temperature differed more from the concurrent endoluminal temperature in HPSD ablation (5.1 ± 5.3 vs. 1.7 ± 2.0°C, p < .01).

CONCLUSION

Endoluminal temperature underestimates epiesophageal surface temperature substantially during HPSD ablation. Visible epiesophageal injury was associated with a 2.2 ± 2.1°C rise in endoluminal temperature, corresponding to a 10.2 ± 6.5°C rise in epiesophageal temperature.