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
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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