Impact of the ablation technique on release of the neuronal injury marker S100B during pulmonary vein isolation

S100B, a well-known damage-associated molecular pattern protein is released acutely by central and peripheral nerves and upon concomitant denervation in pulmonary vein isolation (PVI). We aimed to investigate whether the ablation technique used for PVI impacts S100B release in patients with paroxysmal atrial fibrillation (AF).

The study population consisted of 73 consecutive patients (age: 62.7 ± 10.9 years, 54.8% males) undergoing first-time PVI with either radiofrequency (RF; n = 30) or cryoballoon (CB; n = 43) for paroxysmal AF. S100B determined from venous plasma samples taken immediately before and after PVI increased from 33.5 ± 1.8 to 91.1 ± 5.3 pg/mL (P < 0.0001). S100B release in patients undergoing CB-PVI was 3.9 times higher compared to patients with RF-PVI (ΔS100B: 21.1 ± 2.7 vs. 83.1 ± 5.2  pg/mL, P < 0.0001). During a mean follow-up of 314 ± 186 days, AF recurrences were observed in 18/71 (25.4%) patients (RF-PVI: n = 9/28, CB-PVI: n = 9/43). Univariate Cox regression analysis indicated that an increase in S100B was associated with higher freedom from AF in follow-up (hazard ratio per 10  pg/mL release of S100B: 0.83; 95% confidence interval: 0.72–0.95; P = 0.007).

The ablation technique used for PVI has an impact on the release of S100B, a well-established biomarker for neural damage.