Clin Res Cardiol (2023). https://doi.org/10.1007/s00392-023-02180-w

Procedural cardiac neuronal cell damage is associated with the success of pulmonary vein isolation
J. Hoffmann1, E. Waezsada2, L. K. Elsner3, J. S. Wolter4, S. Kriechbaum4, J. Sperzel4, C. Liebetrau5, M. Kuniss4, C. W. Hamm3, T. Neumann4, T. Keller6
1Justus-Liebig-Universität Giessen, Gießen; 2Innere Medizin, Bürgerhospital Friedberg, Friedberg; 3Medizinische Klinik I - Kardiologie und Angiologie, Universitätsklinikum Gießen und Marburg GmbH, Gießen; 4Abteilung für Kardiologie, Kerckhoff Klinik GmbH, Bad Nauheim; 5Kardiologie, CCB am AGAPLESION BETHANIEN KRANKENHAUS, Frankfurt am Main; 6Franz-Groedel-Institut (FGI), Justus-Liebig-Universität Giessen, Bad Nauheim;

Introduction and Aims: Atrial fibrillation (AF) has a high incidence in our society especially among elderly people resulting in a high individual and socioeconomic burden. Therefore improving therapy options is of utmost importance. Pulmonary vein isolation (PVI) is performed by electrically isolating the pulmonary veins ostially from the left atrium via cardiac catheterization aiming at termination of AF. In the course of PVI myocardial as well as neuronal cells in the atrium are ablated and thus destroyed. The enzyme neuron-specific enolase (NSE) is detectable in the peripheral circulation in case of neuronal injury whereas the biomarker cardiac troponin I (cTnI) reflects myocardial damage. The aims of the current investigation were to evaluate potential associations of procedural success after PVI with structural cardiac damage reflected by NSE and cTnI levels.

Methods and Results: The present analysis evaluates 134 patients (age 62; IQR 65-71years, 42.0% females) with clinical indication for PVI due to symptomatic paroxysmal or persistent AF that were enrolled in a prospective registry between 08/2014 to 11/2016. After a 3 months blanking period 104 patients showed a procedural longterm success within a 12 month follow-up free of AF. Blood samples were taken from peripheral veins at admission and one day after PVI. NSE and high sensitivity cTnI levels were measured in blood samples by commercial, automated assays.

Both investigational biomarkers, NSE and cTnI, showed increased levels on day one after the PVI with NSE rising from mean 11.6 ng/ml to 14.1 ng/ml (p<0.001) and sTnI rising from mean 4.0 pg/ml to 5149 pg/ml (p<0.001) after PVI. NSE levels measured one day after PVI were associated with procedural success (p=0.023) whereas cTnI levels observed one day after PVI showed no statistically significant difference with regard to procedural success (p=0.96). Day one cTnI levels were not able to predict freedom of AF with an area under the receiver operator characteristic curve (AUROC) of 0.496 whereas NSE concentrations determined one day after PVI predicted procedural success with freedom of AF within a 12 month follow-up with an AUROC of 0.676.

Conclusions: The PVI procedure in AF patients is associated with cardiac damage regarding myocardial and neuronal cell injury that is quantifiable by biomarkers such as cTnI and NSE. The amount of neuronal cell damage but not the amount of myocardial cell damage is associated with longterm procedural success.


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