Thermal preconditioning of targeted tissue enhances pulsed field ablation lesions

Pulsed field ablation (PFA) is a cardiac ablation modality that induces cell death via irreversible electroporation (IRE) rather than thermal injury. Intrinsic biophysical tissue properties - including temperature and conductivity- can influence PFA lesion formation, however, this phenomenon is not thoroughly characterized.

To evaluate the impact of thermal preconditioning on PFA lesion characteristics using a controlled in vitro model.

Twenty-millimeter-thick Solanum tuberosum potato slabs were assigned to one of five preconditioning groups: cold (7-10 °C), control (21.5-23 °C), room-temperature soaked (immersed in water at 21.5-23 °C), dry-heated (40 °C), and wet-heated (40 °C water-soaked). Pre-ablation surface temperature was recorded. A monophasic unipolar PFA application was delivered (1750 V, 20 µs pulses, 3 pulses, 1-second interval) using a 3.5 mm electrode catheter. Lesions were stained with 2,3,5-triphenyltetrazolium chloride (TTC) and measured.

Pre-heating the tissue to 40 °C produced markedly larger lesions than control. Dry-heated samples produced a mean lesion diameter of 34.1 ± 1.7 mm and wet-heated 35.0 ± 1.9 mm, vs. 25.3 ± 2.0 mm in controls (p < 0.001). Lesion depth was also greater in heated tissue (wet-heated 12.23 ± 0.76 mm vs. control 10.7 ± 1.3 mm, p = 0.017). In contrast, cooling the tissue to < 10 °C reduced lesion diameter (23.1 ± 2.3 mm) and depth (9.3 ± 1.0 mm), significantly smaller than controls (both p < 0.01). Room-temperature soaking (RT-soaked) alone did not produce significant change in lesion dimensions.

In this in vitro model, thermal preconditioning significantly alters PFA lesion formation. Increasing the tissue temperature prior to ablation markedly increases lesion diameter and depth, possibly by lowering the electroporation threshold. These findings suggest that tissue temperature is a tunable factor influencing PFA efficacy.