Background: The relevance of the association between inflammation and atrial fibrillation (AF) is not firmly established. The clinical importance is considerable because inflammation is usually not targeted as a treatment option, minimizing a probable benefit.
Materials and methods: We have used a case-control study with a Mendelian randomization rationale to assess whether proposed risk factors that have a genetic component and are readily detected in circulating blood are causally related to AF. The studied variables were C-reactive protein (CRP) and a representative of the chemokine system, the monocyte chemoattractant protein-1 (CCL2).
Results: Plasma CRP and CCL2 concentrations were significantly higher in AF patients than in the unaffected population. However, when segregated between paroxysmal and permanent, the difference for CRP was only observed in patients with a permanent condition. Plasma CCL2 was raised in both subgroups. Confounding factors were carefully considered, and multivariable analyses revealed that circulating CCL2 was significant and CRP was negligible to explain the presence of AF. The duration of the episode also bore a significant predictive value. Odd ratios for AF as a function of genotype did not differ from 1·0 for any of the individual CRP and CCL2 polymorphisms, or any combinations.
Conclusions: Elevated plasma CRP concentration per se does not increase atrial fibrillation risk. Values obtained for CCL2 suggest that inflammation is probably a consequence of AF. Our data also suggest that the effect of the duration of the episode should be further studied in the assessment of the actual role of inflammation.
© 2013 The Authors. European Journal of Clinical Investigation © 2013 Stichting European Society for Clinical Investigation Journal Foundation.