The relevance of the association between inflammation and atrial fibrillation

心房颤动 炎症 混淆 医学 C反应蛋白 内科学 孟德尔随机化 心脏病学 人口 四氯化碳 胃肠病学 趋化因子 基因型 遗传变异 生物 基因 环境卫生 生物化学
作者
Josep M. Alegret,Gerard Aragonès,Roberto Elosúa,Raúl Beltrán‐Debón,Anna Hernández‐Aguilera,César Romero‐Menor,Jordi Camps,Jorge Joven
出处
期刊:European Journal of Clinical Investigation [Wiley]
卷期号:43 (4): 324-331 被引量:35
标识
DOI:10.1111/eci.12047
摘要

Abstract 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 ( CCL 2). Results Plasma CRP and CCL 2 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 CCL 2 was raised in both subgroups. Confounding factors were carefully considered, and multivariable analyses revealed that circulating CCL 2 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 CCL 2 polymorphisms, or any combinations. Conclusions Elevated plasma CRP concentration per se does not increase atrial fibrillation risk. Values obtained for CCL 2 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.

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