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Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia. Moreover, it is mentioned as one of the important causes of death due to heart disease, which imposes an undeniable financial burden on public health systems. Almost 1 out of 4 individuals aged 40 to 55 will experience AF at some point during their life. Increasing the pressure or the volume of the atria over time leads to the activation of fibroblasts, resulting in the accumulation of extracellular matrix and fibrosis. By disturbing electrical conduction, fibrosis creates microreentrant circuits, which can develop into AF. In this article, we evaluated the vital role of interleukins and inflammatory mediators in the pathogenesis, prognosis, and treatment of AF. We also discussed the importance of the broader use of interleukins in the clinical management of AF patients. Interleukins and inflammatory markers can be used as markers of diagnosis, cardiovascular events, and mortality in AF patients. Finally, the utilization of substances upregulating IL-10, such as resolvin D1 (RvD1), or applying IL-6 down-regulators and inhibitors, including anti-IL-6 antibodies, colchicine, and C1q/tumor necrosis factor-related protein-9 (CTRP9), are effective in the reduction of atrial interstitial fibrosis and treating AF patients.

The role of interleukins in pathogenesis and prognosis of atrial fibrillation