Atrial Fibrillation: Pathogenesis, Predisposing Factors, and Genetics

Abstract

Atrial fibrillation (AF) is the most frequent arrhythmia managed in clinical practice, and it is linked to an increased risk of death, stroke, and peripheral embolism. The Global Burden of Disease shows that the estimated prevalence of AF is up to 33.5 million patients. So far, successful therapeutic techniques have been implemented, with a high health-care cost burden. As a result, identifying modifiable risk factors for AF and suitable preventive measures may play a significant role in enhancing community health and lowering health-care system expenditures. Several mechanisms, including electrical and structural remodeling of atrial tissue, have been proposed to contribute to the development of AF. This review article discusses the predisposing factors in AF including the different pathogenic mechanisms, sedentary lifestyle, and dietary habits, as well as the potential genetic burden.

Keywords: Mediterranean diet; atrial fibrillation; diets; genetics; oxidative stress; pathogenesis; predisposing factors.

Figure 1

This graphical abstract summarizes the cellular mediators of atrial fibrosis. Following an insult, inflammatory mediators signal immune cells such as monocytes, CD4+ T-cells, and mast cells to infiltrate the atrial myocardium. These cells promote tissue fibrosis by secreting pro-fibrotic factors and regulatory molecules that enhance the activation and differentiation of fibroblasts to myofibroblasts. Additionally, the figure depicts the anti-fibrotic mediators that are secreted by Th1 cells in the early-insult stage and that are gradually overhauled by the products of pro-fibrotic Th2 cells. TGFβ, transforming growth factor beta; TNFα, tumor necrosis factor alpha; PDGF, platelet-derived growth factor; IL-1, interleukin 1; IL-4, interleukin 4; IL-6, interleukin 6; IL-10, interleukin 10; ROS, reactive oxygen species; IFNγ, interferon gamma; IGF-1, Insulin-like growth factor 1; Th1, t helper type 1; Th2, t helper type 2; PAR-2, protease activated receptor 2; Ang-II, angiotensin.

Figure 2

Graphical illustration of daily dietary habits that reduce (brown arrow) or increase (red arrow) the incidence of atrial fibrillation. n-3 PUFAs; polyunsaturated fatty acids.