ArticlePhysiological research2026
Physiological Tissue Response to Pulsed-Field Ablation for Atrial Fibrillation: Insights from Biomarker Kinetics.
Article in Physiological research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Pulsed-field ablation (PFA) has become an important non-thermal modality for pulmonary vein isolation in atrial fibrillation (AF), characterized by myocardial selectivity and reduced collateral tissue injury. However, the physiological biomarker response to PFA remains incompletely defined. This study assessed serial changes in myocardial (troponin T, creatine kinase - CK and its isoenzyme - CK-MB) and renal (urea, creatinine) biomarkers in patients undergoing PFA at a single center and compared these findings with current clinical evidence. The study cohort consisted of 52 patients undergoing PFA (73 % men, 27 % women), with 52 % presenting paroxysmal AF and 48 % persistent AF. The mean left atrial diameter was 45 ± 7 mm and the average left ventricular ejection fraction was 55 ± 7 % The mean ablation burden was 67 ± 23 applications per procedure. Biomarkers were measured before and after ablation. Repeated-measures ANOVA demonstrated significant time effects for all myocardial biomarkers (p < 0.001) and significant interactions with ablation burden. Troponin-T increased from near-zero baseline values to markedly elevated levels immediately and 24-hours after the procedure, while CK and CK-MB rose several-fold with only partial decline after the procedure. In contrast, urea and creatinine remained stable, indicating preserved renal function without acute kidney injury. The number of PFA applications correlated positively with late CK and CK-MB values, suggesting that myocardial biomarker load scales with procedural intensity. These findings align with current literature showing extensive myocardial biorelease after PFA but favorable extracardiac safety. By concurrently analyzing myocardial and renal markers, this study demonstrates that substantial biochemical myocardial injury induced by PFA does not translate into measurable renal dysfunction. Overall, PFA appears physiologically consistent with a profile of robust but targeted myocardial injury and preserved renal safety.
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