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Protracted CRP elevation after atrial fibrillation ablation
James M McCabe1, Lisa M Smith, Zian H Tseng
1Division of Cardiology, Electrophysiology Section, University of California, San Francisco, California, USA.
Insights
Atrial fibrillation (AF) ablation causes inflammation, indicated by increased C-Reactive Protein (CRP) levels. This inflammation may explain early AF recurrence after the procedure.
Area of Science:
- Cardiology
- Electrophysiology
- Inflammation Research
Background:
- Atrial fibrillation (AF) is associated with inflammation, with C-Reactive Protein (CRP) as a key biomarker.
- Early AF recurrence post-ablation (within 3 months) is common and not indicative of procedural success or failure.
- The study hypothesizes that ablation-induced inflammation contributes to early AF recurrence.
Purpose of the Study:
- To investigate C-Reactive Protein (CRP) levels following AF ablation.
- To determine if the inflammatory response post-ablation correlates with early AF recurrence.
Main Methods:
- Prospective enrollment of patients undergoing AF ablation and a control group undergoing supraventricular tachycardia (SVT) ablation.
- CRP levels measured pre-ablation and at two follow-up visits (median 49 and 147 days).
- Patient interviews and medical history review for AF recurrence prior to the first follow-up.
Main Results:
- CRP levels significantly increased from baseline to first follow-up in the AF ablation group (P = 0.0017), but not in the SVT group (P = 0.92).
- 45% of AF patients experienced recurrence before the first follow-up.
- Recurrent AF was associated with a significantly higher likelihood of increased CRP levels (OR 21, P = 0.045) after adjusting for confounders.
Conclusions:
- AF ablation triggers a sustained inflammatory response lasting several weeks.
- This post-ablation inflammation is a likely cause of early AF recurrence.
Background:
Atrial fibrillation (AF) has been linked to an inflammatory process detected through various biomarkers, including C-Reactive Protein (CRP). Early recurrence of AF within the first 3 months after curative AF ablation is not felt to reflect success or failure of the procedure. We hypothesized that this early recurrence is due to an inflammatory response to the ablation itself. We therefore sought to evaluate levels of CRP after AF ablation.
Methods:
We prospectively enrolled subjects undergoing AF ablation. A control group of patients undergoing ablation for supraventricular tachycardia (SVT) was also enrolled. Each patient had CRP drawn on the day of the procedure (prior to ablation) and during their first follow-up (median 49 days, interquartile range [IQR] 37-93) and second follow-up (median 147 days, IQR 141-257) clinic visits. Patient interviews were performed and medical histories reviewed for evidence of recurrent AF prior to the first follow-up.
Results:
CRP levels significantly increased from baseline to first follow-up in the AF ablation group (P = 0.0017). CRP did not significantly change after SVT ablation (P = 0.92). Seventeen (45%) of the AF subjects exhibited recurrence of AF prior to first follow-up. After adjusting for multiple potential confounders, AF ablation patients with recurrent AF prior to their first follow-up had a statistically significant greater odds of having an increase in CRP (OR 21, 95% CI 1.1-417, P = 0.045).
Conclusions:
AF ablation generates an inflammatory response that persists for several weeks. This inflammation may explain early recurrence of AF after curative ablation.
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