Impact of atrial fibrillation on inflammatory and fibrinolytic variables in the elderly

Abstract

Purpose. Atrial fibrillation (AF) is associated with inflammation and a prothrombotic state; however, it is still unclear whether this is independent of ageing and comorbidity. The objective of this study was to investigate the impact of AF on circulating levels of inflammatory and fibrinolytic markers in a 75-year-old general population. Methods. All 75-year-old citizens in Asker and Baerum counties in Norway were invited to participate in a prevalence study of AF. Blood samples were collected from 63 subjects with AF and a gender-matched control group of 126 subjects in sinus rhythm. C-reactive protein (CRP), tumour necrosis factor α (TNFα), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), P-selectin, CD40 ligand, tissue plasminogen activator antigen (tPA ag), plasminogen activator inhibitor-1 (PAI-1), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase inhibitor 1 (TIMP-1) activity were analyzed using commercially available assays. Results. Subjects with AF had higher levels of IL-6 (median 3.07 pg/mL (interquartile range 2.11, 4.36) vs. 2.26 (1.70, 3.26); p = 0.002) and PAI-1 activity (12.9 U/mL (6.6, 17.1) vs. 9.0 (4.6, 14.0); p = 0.005). No difference was found for the other markers. The presence of AF was still significantly associated with higher levels of IL-6 and PAI-1 activity after adjusting for confounders (p = 0.028 and p = 0.007, respectively). Conclusion. AF was independently associated with higher levels of IL-6 and PAI-1 activity. Thus, there is evidence of a proinflammatory state and reduced fibrinolysis also in this stable, out-of-hospital group of 75-year-old AF patients.

Key Words::

• Atrial fibrillation
• cardiology
• inflammation mediators
• C-reactive protein
• interleukin-6
• plasminogen activator inhibitor 1

Declaration of interest: The authors report no conflict of interest. The authors alone are responsible for the content and writing of the article.

The ABAF study was sponsored by the Medical Research Foundation, Baerum Hospital, Norway, Center for Heart Failure Research, Oslo, Norway, and an unrestricted grant from AstraZeneca, Oslo, Norway.