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Exploring the Role of Presepsin in the Prediction of Atrial Fibrillation Recurrence: Results from the PLACEBO Study
Aristi Boulmpou1, Christodoulos Papadopoulos1, Theocharis Koufakis2
1Third Department of Cardiology, Aristotle University of Thessaloniki, Ippokratio General Hospital, 54 642 Thessaloniki, Greece.
Background:
Presepsin, a soluble CD14 subtype released during immune activation, has emerged as a marker of inflammation in cardiometabolic disorders. Given the links between inflammation, metabolic dysregulation, and atrial fibrillation (AF), presepsin may represent a novel biomarker for predicting AF recurrence.
Aims:
To evaluate whether presepsin levels, alone or in combination with other biomarkers and clinical parameters, are associated with paroxysmal AF (PAF) recurrence in a well-characterized cohort from the PLACEBO trial.
Methods:
This was a retrospective exploratory substudy of 62 patients from the PLACEBO cohort with available baseline presepsin measurements. All patients had a history of PAF and were in sinus rhythm at inclusion. Presepsin and other biomarkers were measured at baseline. Reduced multivariable Cox regression models, limited to two or three predictors, were constructed to avoid overfitting.
Results:
During 12 months of follow-up, 27 patients (43.5%) experienced AF recurrence. Across the reduced multivariable models, each containing a limited number of predictors, obstructive sleep apnea (OSA) consistently emerged as an independent predictor (HR 3.13-3.36, p < 0.05). The use of HR ranges reflects the inclusion of these variables in more than one model. Galectin-3 (GAL3) and standard deviation of R-R intervals (SDRR) did not retain statistical significance, and presepsin was not independently associated with recurrence (HR 1.00, 95% CI 0.92-1.10, p = 0.94).
Conclusions:
In this exploratory study, OSA emerged as the only independent predictor of AF recurrence. Presepsin was not significantly associated with recurrence in the present cohort; however, given the limited sample size and exploratory design, these results do not exclude a potential association. Larger, adequately powered studies are needed to clarify the role of presepsin in AF recurrence risk.
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