Key result
Atrial fibrillation was associated with significantly elevated CD40-L levels compared to healthy controls (401.0 vs 53.6 pg/mL, p=0.0034), which were significantly reduced following atrial ablation.
Why the study?
Does atrial ablation reduce circulating CD40-L levels in patients with atrial fibrillation?
Observational (n=105)
Does atrial ablation reduce circulating CD40-L levels in patients with atrial fibrillation?
Atrial fibrillation is associated with elevated levels of the inflammatory biomarker CD40-L, which are significantly reduced to normal levels following atrial ablation.
Supports inflammatory role of CD40-L in AF; hypothesis-generating for biomarker or ablation monitoring pending prospective trials.
Introduction Atrial fibrillation (AF) is currently the most common cardiac arrhythmia encountered in clinical practice and a major cause of morbidity and mortality among adults. Inflammation plays a crucial role in the development and progression of atrial fibrillation. CD40‐Ligand (CD40‐L) is a cellular mediator that is characteristically seen in inflammatory processes. CD40‐L can be expressed on platelets, leading to activation of endothelial cells and the release of cytokines during inflammation. The purpose of this study was to characterize and quantify the levels of the inflammatory biomarker CD40‐L to evaluate its relevance to AF both pre‐ and post‐ablation. Methods In a prospective study, plasma samples were collected from 55 AF patients at baseline prior to ablation, and at 1 and 3‐month follow‐up post‐ablation. Normal human plasma samples (n=50) were supplied by George King Biomedical Inc. (Overland Park, KS). ELISA kits were obtained to profile CD40‐Ligand (R&D Systems, Minnesota USA). Statistical analysis was performed using non‐parametric Mann‐Whitney t‐tests. Results There was a significant increase in the mean levels of CD40‐L at pre‐ablation baseline in patients with AF compared to normal (401.0±73.3 pg/mL vs. 53.6±4.74 pg/mL, p=0.0034). CD40‐L levels post‐ablation significantly decreased. At 1 month follow up, CD40‐L levels dropped (401.0±73.3 pg/mL vs. 40.6±6.86 pg/mL, p=<0.0001). At 3 months, the levels of CD40‐L remained decreased (43.3±7.98 pg/mL, p=<0.0001). There was no significant change between levels at 1 month and 3 months (p=0.8573). There was also no significant difference in post‐ablation levels of CD40‐L compared to normal human plasma levels (p=0.2095). Conclusion Inflammation plays an important role in the pathogenesis of atrial fibrillation. In our study, patients with atrial fibrillation have highly elevated levels of CD40‐L compared with normal healthy individuals. Contrary to previous reports, our study suggests that elevated levels of CD40‐L may play an important role in the pathogenesis of AF. It is also noted that the levels of this inflammatory mediator are modulated by atrial ablation as a medical treatment for AF. Support or Funding Information This project is supported by internal funds of Loyola University Medical Center.
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Otto et al. (2017) conducted an observational in Atrial Fibrillation (n=105). Atrial fibrillation vs. Healthy controls was evaluated on Mean CD40-L levels (p=0.0034). Atrial fibrillation was associated with significantly elevated CD40-L levels compared to healthy controls (401.0 vs 53.6 pg/mL, p=0.0034), which were significantly reduced following atrial ablation.
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