Commentaries:
There a need for data , well-designed and blinded longitudinal studies.
The role of the post-cardioversion time course of hs-CRP levels in clarifying the relationship between inflammation and persistence of atrial fibrillation
Heart
E M Kallergis, E G Manios, E M Kanoupakis, H E Mavrakis, S G Kolyvaki, G M Lyrarakis, G I Chlouverakis, P E Vardas
Department of Cardiology, University Hospital of Heraklion, Crete, Greece
ABSTRACT
Objectives: Although recent studies suggest that inflammation is involved in the pathogenesis of atrial fibrillation (AF), it remains controversial whether it is a consequence or a cause of the arrhythmia.
Design: Prospective study.
Setting: Tertiary referral centre.
Patients and Interventions: In 52 patients with persistent AF lasting >3 months, high-sensitivity C-reactive protein (hs-CRP) was measured before and after electrical cardioversion.
Measurements and Results: All patients were successfully cardioverted to sinus rhythm (SR), but the recurrence rate was 23% at 1 month. Baseline hs-CRP was higher in patients with AF recurrence than in those who remained in SR (0.5 (SD 0.18) mg/dl vs 0.29 (SD 0.13) mg/dl, respectively, p<0.001). Similarly, arrhythmia recurrence was associated with greater left atrial diameters (45.4 (SD 3.3) mm vs 40.7 (SD 3.1) mm, respectively, p<0.001). However, logistic regression analysis showed that hs-CRP was the only independent predictor for AF recurrence (p<0.001). Additionally, patients who were in SR on final evaluation had significantly lower hs-CRP levels than at baseline (0.10 (SD 0.06) mg/dl vs 0.29 (SD 0.13) mg/dl, respectively, p<0.001), while those who experienced AF recurrence had similar values on final and on initial evaluation (0.56 (SD 0.24) mg/dl vs 0.50 (SD 0.18) mg/dl, respectively, p = 0.42).
Conclusion: High levels of hs-CRP are associated with an increased risk of AF recurrence after cardioversion. The restoration and maintenance of SR result in a gradual decrease of hs-CRP while AF recurrence has a different effect, suggesting that inflammation is a consequence, rather than a cause, of AF.
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