Several studies have reported that inflammatory markers are associated with atrial
fibrillation (AF). The white blood cell (WBC) count is a widely available and broadly
used marker of systemic inflammation. We sought to investigate the association between
an increased WBC count and incident AF and whether this association is mediated by
smoking, myocardial infarction, and heart failure. We examined the participants in
the Framingham Heart Study original cohort. Cox proportional hazard regression analysis
was used to examine the relation between the WBC count and incident AF during a 5-year
follow-up period. We adjusted for standard AF risk factors, smoking, previous myocardial
infarction, and interim myocardial infarction and heart failure before the incident
AF. Our sample consisted of 936 participants (mean age 76 ± 6 years and 61% women).
The median WBC count was 6.4 × 109/L (25th to 75th percentile 5.6 × 109/L to 7.8 × 109/L). During a median 5-year follow-up period, 82 participants (9%) developed new-onset
AF. After adjusting for standard risk factors for AF, an increased WBC count was significantly
associated with incident AF, with a hazard ratio per SD (0.26 × 109/L) increase of 2.22 (95% confidence interval 1.10 to 4.48; p = 0.03). We found no
substantive differences adjusting for smoking, previous myocardial infarction, interim
myocardial infarction, or heart failure. In conclusion, in our community-based sample,
an increased WBC count was associated with incident AF during 5 years of follow-up.
Our findings provide additional evidence for the relation between systemic inflammation
and AF.
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Article info
Publication history
Published online: November 21, 2011
Accepted:
September 29,
2011
Received in revised form:
September 29,
2011
Received:
June 22,
2011
Footnotes
The Framingham Heart Study is supported by grant N01-HC-25195 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland and by Boston University School of Medicine, Boston, Massachusetts. Dr. Rienstra is supported by Rubicon grant 825.09.020 from The Netherlands Organization for Scientific Research, The Hague, The Netherlands; Dr. Magnani is supported by American Heart Association Award 09FTF2190028 (Dallas, Texas). Dr. Sinner is supported by the German Heart Foundation (Frankfurt, Germany). This work was supported by grant 1R01HL092577 from the National Institutes of Health, Bethesda, Maryland to Drs. Benjamin and Ellinor, grants 1RC1HL101056, 1R01HL102214, and R01AG028321 and support via grant 6R01-NS 17950 to Dr. Benjamin, and grants 5R21DA027021, 5RO1HL104156, 1K24HL105780 to Dr. Ellinor. This study was partially supported by the Evans Center for Interdisciplinary Biomedical Research ARC on Atrial Fibrillation Initiative (Boston University, Boston, Massachusetts).
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© 2012 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
