High levels of intermediate cd14++cd16+monocytes predict incident atrial fibrillation in the general population

Abstract Background Atrial fibrillation (AF) is associated with increased inflammation and recent evidence also links inflammation to the pathogenesis of AF. However, studies of circulating immune cells and their contribution to AF are sparse. In particular, prospective studies of monocyte subsets and risk of developing AF are lacking. These studies are important to identify individuals at high risk of AF and further understanding of the pathogenesis of the disease. Purpose In the current study we compared differences in circulating monocyte subsets and incidence of AF in a large community-based cohort. Methods The study included 666 randomly selected individuals from the cardiovascular arm of the Malmö Diet and Cancer study. Among these, 145 individuals experienced incident AF during the follow up of 18.6 (11.5-21.7) years. To enumerate monocyte subsets (classical CD14++CD16-, intermediate CD14++CD16+, and non-classical CD14+CD16++) mononuclear leukocytes frozen at baseline were analyzed with flow cytometry. Monocyte subsets were determined as total numbers and percentages of total monocytes. Results Percentages of classical CD14++CD16- monocytes or non-classical CD14+CD16++ monocytes did not differ in subjects who developed AF compared to subjects without AF. However, intermediate monocytes displayed a trend towards increased percentages in subjects with incident AF. In addition, the number of intermediate CD14++CD16+ monocytes and classical CD14++CD16- monocytes were increased in subjects with incident AF. Both percentages and numbers of intermediate monocytes were associated with increased risk of developing AF during follow-up after adjustment for common risk factors. Conclusions This study shows that intermediate CD14++CD16+ monocytes are associated with incident atrial fibrillation independently of other common risk factors in the general population, supporting a role of inflammatory cells in AF.Figure 1