Influence of tissue thickness on thermal latency during high-power short-duration radiofrequency ablation with proactive esophageal cooling

Abstract

Abstract Funding Acknowledgements Type of funding sources: None. Background Thermal latency, or delayed heating, is increasingly recognized as an important factor in the formation of both intentional and unintentional lesions during radiofrequency (RF) ablation for the treatment of atrial fibrillation (AF). High-power short-duration (HPSD) ablation appears to have greater thermal latency than low or medium power ablation. Proactive esophageal cooling (PEC) has been shown to reduce esophageal lesion formation under a variety of conditions by directly reducing the effects of thermal latency, but the influence of anatomic dimensions on the protective efficacy of cooling during HPSD ablation has not been investigated. Purpose Determine the impact of changes in pericardial tissue thickness on thermal latency in order to quantify the protective efficacy of PEC across a range of anatomic dimensions. Methods We created a mathematical model of the left atrium undergoing HPSD ablation, both with and without a PEC device in place, using a range of pericardial tissue thicknesses (0.5, 0.75, and 1 mm). HPSD ablation was set at 50 W for 10 s, or 90 W for 4 s. We then examined the temperature dynamics at a range of thickness, focusing on the layer of mostly fatty tissue between the atrial and esophageal walls by varying the thickness of this layer while quantifying the degree of esophageal damage using the Arrhenius equation to determine the fraction of damage after peak heating has occurred. Results Under control conditions, the growth of lesions from RF ablation at both 50 W and 90 W was found to continue for greater than 10 seconds beyond the cessation of RF energy application. Esophageal lesion formation ranged from 71% to 96% transmurality after 50 W ablation for 10 s, and from 50% to 72% transmurality after 90 W ablation for 4 s. With PEC in place, esophageal lesion transmurality was markedly reduced, with a maximum transmurality ranging from 12% to 32% with 50 W ablation, and from 2% to 20% with 90 W ablation (Figure). Increasing thickness of pericardial tissue (with simulations of 0.5, 0.75, and 1 mm) resulted in decreasing esophageal lesion transmurality (67%, 74%, and 83% at 50 W power, and 72%, 82%, and 96% at 90 W power, respectively, with the 0.5, 0.75, and 1 mm simulations). Conclusions Thermal latency with HPSD ablation contributes to lesion growth and can cause esophageal injury. Proactive esophageal cooling counteracts this effect across a range of pericardial tissue thicknesses, and reduces esophageal lesion transmurality by an average of 79%.