Search

Background: Recent data suggest that luminal esophageal temperature (LET) monitoring during high-power short-duration (HPSD) ablation may be inadequate to prevent esophageal thermal injury during radiofrequency (RF) ablation. This is due in part to delayed responses to thermal latency and the continued temperature rise that occurs in tissues even after the cessation of RF energy with HPSD settings. Proactive esophageal cooling has been shown to reduce severe esophageal thermal injury during medium-power medium-duration RF ablation, but less is known about the effects in HPSD ablation. Objective: We aimed to quantify the time course of esophageal damage in scenarios with and without proactive esophageal cooling, hypothesizing a reduction in the resulting tissue damage with proactive esophageal cooling. Methods: Using a computer model of RF ablation in the left atrium adjacent to the esophagus, we calculated temperature over time using ablation power of 50 W for 10 s and 90 W for 4 s. We then determined the fraction of resulting damage to esophageal tissue via the Arrhenius equation and by the percentage of tissue above lethal isotherm temperature of 50°C. Transmurality of injury was then plotted over time, and results were compared between ablation with and without proactive esophageal cooling. Results: Esophageal damage increased even after the cessation of RF energy, suggesting significant thermal latency effects under HPSD ablation. Lesion growth continued for >10 s after cessation of 50 W ablation energy, and for >12 s after cessation of 90 W ablation energy without cooling. With proactive cooling, lesion growth after cessation of ablation energy was essentially halted. Without esophageal cooling, maximum injury transmurality reached 79% with 50 W, and 58% with 90 W. With esophageal cooling, injury transmurality remained below 20% with 50 W, and 10% with 90 W, representing reductions of 75% and 83%, respectively. Conclusions: RF ablation using HPSD settings demonstrates significant latency of effect, with tissue damage and lesion growth continuing beyond the cessation of application of RF energy. Proactive esophageal cooling significantly dampens this effect, reducing esophageal injury by up to 83%.

Introduction: Atrioesophageal fistula (AEF) is a severe complication of left atrial ablation for the treatment of atrial fibrillation. Thermal injury is the proposed mechanism, and a potential pathway occurs through exceeding the lethal isotherm of esophageal tissue in contact with the left atrial posterior wall. Active cooling with a novel cooling device has been shown to significantly reduce thermal injury, with no AEFs encountered after more than 4200 treatments worldwide. We aimed to evaluate the effects of active cooling when specifically using newer high-power short-duration (HPSD) ablation settings to further estimate the protective mechanisms of this novel approach to reduce serious injury. Hypothesis: Active cooling may preclude attainment of a lethal isotherm in esophageal tissue under HPSD ablation. Methods: We developed a model of the left atrium and esophagus, and simulated radiofrequency (RF) ablation of the left atrium under HPSD settings. Tissue thickness was set to typical posterior-wall parameters (Figure). Power settings were evaluated at 50 W for 10 seconds, and 90 W for 4 seconds. Active cooling was set to a typical 4 °C coolant temperature. Lethal isotherm temperature was taken as 50 °C. Results: In both scenarios of HPSD ablation, the peak esophageal mucosal temperature reached 39° C in control conditions, using no active cooling. With active cooling in place, peak temperatures remained below 11 °C (Figure). Peak temperatures at the epi-esophageal region of esophageal tissue exceeded the lethal isotherm of 50 °C in control conditions, but remained at or below the lethal isotherm with active cooling in place. Conclusions: Based on our mathematical modeling, esophageal cooling significantly reduced temperature rise and prevented the achievement of temperatures thought to be lethal to esophageal tissue. This finding may offer a mechanistic rationale for the absence of serious esophageal injury encountered to date using this approach.