Aims: An increasing body of evidence has demonstrated the essential role of inflammation in the genesis and maintenance of atrial fibrillation (AF). The aim of the present study was to investigate whether success or failure of electrical pulmonary vein isolation (PVI) in patients with AF is related with the presence of a pre-ablative inflammatory state as determined by known clinical parameters and conventional markers of inflammation including high-sensitivity C-reactive protein, white blood cell (WBC) count, and fibrinogen. Methods and results: Seventy-two patients with paroxysmal (64%) or persistent AF (36%) underwent successful electrical PVI. The mean duration of arrhythmia was 5.5 ± 2.9 years. After a mean follow-up period of 12.5 ± 5.7 months, 44 patients (61%) were in sinus rhythm. In univariate Cox proportional hazard regression analysis, hypertension, body mass index (BMI), left ventricular ejection fraction, left ventricular end-diastolic diameter, left atrial diameter (LAD), WBC count, and high-sensitivity C-reactive protein were significantly associated with AF recurrence (P < 0.05). In multivariate Cox proportional hazard regression analysis, hypertension [hazard ratio (HR) 3.127; 95% confidence interval (CI) 1.269-7.706, P = 0.013], LAD (HR 1.077; 95% CI 1.014-1.144, P = 0.015), and WBC count (HR 1.423; 95% CI 1.067-1.897, P = 0.016) were independent pre-ablative predictors of AF recurrence following PVI. Conclusion: Conventional markers of the inflammatory cascade such as WBC count and high-sensitivity C-reactive protein as well as elements of the metabolic syndrome such as hypertension and increased BMI were significantly associated with AF recurrence. The impact of a pre-ablative inflammatory state in the overall success rate of PVI needs further elucidation. © The Author 2008.
CITATION STYLE
Letsas, K. P., Weber, R., Bürkle, G., Mihas, C. C., Minners, J., Kalusche, D., & Arentz, T. (2009). Pre-ablative predictors of atrial fibrillation recurrence following pulmonary vein isolation: The potential role of inflammation. Europace, 11(2), 158–163. https://doi.org/10.1093/europace/eun309
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