HPSD ablation for AF high-power short-duration RF ablation for atrial fibrillation: A review.

This manuscript reviews the literature for all in silico, ex vivo, in vitro, in vivo and clinical studies of high-power short-duration (HPSD) radiofrequency (RF) ablations. It reviews the biophysics of RF energy delivery applicable to HPSD and the use of surrogate endpoints to guide the duration of HPSD ablations. In silico modeling shows that a variety of settings in power, contact force and RF duration can result in the same surrogate endpoint value of ablation index and several HPSD combinations produce lesion volumes similar to a low-power long-duration (LPLD) RF application. HPSD lesions are broader with more endocardial effect and are slightly shallower but still transmural. The first 10 s of RF application is most important for lesion formation with diminishing effect beyond 20 s. The ideal contact force is 10-20 g with only a small effect beyond 30 g. In vitro and in vivo models confirm that HPSD makes transmural lesions that are often broader and shallower, and with proper settings, result in fewer steam pops than LPLD. One randomized trial shows better outcomes with HPSD and validates lesion size index as a surrogate endpoint. Clinical studies of HPSD using comparator groups of LPLD ablations uniformly show shorter procedure times and shorter total RF energy delivery for HPSD. HPSD generally has a higher first pass vein isolation rate and a lower acute vein reconnection rate than LPLD. Although not dramatically different from LPLD, long-term freedom from atrial fibrillation and complication rates seem slightly better with HPSD.

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.