Research Paper Volume 12, Issue 9 pp 8423—8433
Inflammatory activation and endothelial dysfunction markers in patients with permanent atrial fibrillation: a cross-sectional study
- 1 U.O.C di Medicina Interna con Stroke Care, Dipartimento di Promozione della Salute, Materno-Infantile, di Medicina Interna e Specialistica di Eccellenza “G. D’Alessandro”, University of Palermo, Palermo, Italy
- 2 Dipartimento di Scienze e Tecnologie Biologiche Chimiche e Farmaceutiche, University of Palermo, Palermo, Italy
- 3 Dipartimento di Promozione della Salute, Materno-Infantile, di Medicina Interna e Specialistica di Eccellenza “G. D’Alessandro”Section of Public Health Epidemiology and Preventive Medicine, University of Palermo, Palermo, Italy
- 4 Molecular and Clinical Medicine PhD Programme, University of Palermo, Palermo, Italy
- 5 Unit of Nephrology and Hypertension, European Society of Hypertension Excellence Center, Dipartimento di Promozione della Salute, Materno-Infantile, di Medicina Interna e Specialistica di Eccellenza “G. D’Alessandro”, University of Palermo, Palermo, Italy
received: October 2, 2019 ; accepted: April 16, 2020 ; published: May 3, 2020 ;https://doi.org/10.18632/aging.103149
How to Cite
Copyright © 2020 Maida et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
In recent years a growing body of evidence supported the role of inflammation in the initiation, maintenance and outcome of atrial fibrillation (AF). Nevertheless, despite a large amount of information, whether AF or the underlying structural heart disease (SHD) is the cause of the inflammatory process is still under debate. We, therefore, sought to determine if the inflammatory process reflect an underlying disease or the arrhythmia ‘per se’. We evaluated plasma levels of soluble Interleukin 2 Receptor Alpha (sIL-2Rα), TNF-α and IL-18 in 100 consecutive patients with permanent AF, (43 with a SHD and 57 without a SHD) compared to 121 age and sex-matched controls which had normal sinus rhythm. We also evaluated the endothelial function in both groups of patients using reactive hyperemia index (RHI) values measured by Endo-PAT2000. Compared to controls, AF patients showed higher circulating levels of inflammatory markers and a lower mean value of RHI. At multiple logistic regression analysis, the inflammatory markers and RHI were significantly associated with AF presence, whereas ROC curve analysis had good sensitivity and specificity in inflammatory variables and RHI for AF presence. No significant association was observed in the group of permanent AF patients, between inflammatory markers and the presence of an underlying SHD. These findings could help to clarify the role of inflammation in subjects with AF and suggest that the markers of systemic inflammation are not associated with the underlying cardiovascular disease, rather with the atrial fibrillation ‘per se’.
AF: Atrial Fibrillation; SHD: Structural heart disease; LAF: Lone AF; CRP: C-reactive protein; TNF-α: Tumor necrosis factor α; IL: Interleukin; RH-PAT: Reactive hyperemia peripheral arterial tonometry; RHI: Reactive hyperemia index; LVH: Left ventricular hypertrophy; LAE: Left atrial enlargement; LAVI: Left atrial volume index; eNOS: Endothelial nitric oxide synthase.