Open AccessImpact of the ablation technique on release of the neuronal injury marker S100B during pulmonary vein isolation
Author(s) -
Katharina Scherschel,
Katja Hedenus,
Christiane Jungen,
Paula Münkler,
Stephan Willems,
Omar Anwar,
Niklas Klatt,
Christian Eickholt,
Christian Meyer
Publication year - 2020
Publication title -
europace
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.119
H-Index - 102
eISSN - 1532-2092
pISSN - 1099-5129
DOI - 10.1093/europace/euaa159
Subject(s) - medicine , pulmonary vein , hazard ratio , ablation , atrial fibrillation , cardiology , denervation , confidence interval , biomarker , concomitant , catheter ablation , population , radiofrequency ablation , biochemistry , chemistry , environmental health
Aims 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). Methods and results 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). Conclusion The ablation technique used for PVI has an impact on the release of S100B, a well-established biomarker for neural damage.