LAUSR

To date, worldwide, atrial fibrillation is the most common cardiovascular disease in adults, with a prevalence of 2% to 4%. The trigger of the pathophysiological mechanism of arrhythmia includes several factors that sustain and exacerbate the disease. Ectopic electrical conductivity, associated with the resulting atrial mechanical dysfunction, atrial remodeling, and fibrosis, promotes hypo-contractility and blood stasis, involving micro endothelial damage. This causes a significant local inflammatory reaction that feeds and sustains the arrhythmia. In our literature review, we evaluate the role of HMGB1 proteins, heat shock proteins, and S100 in the pathophysiology of atrial fibrillation, offering suggestions for possible new therapeutic strategies. We selected scientific publications on the specific topics “alarmins” and “atrial fibrillation” from PubMed. The nonsystematic review confirms the pivotal role of molecules such as S100 proteins, high-mobility group box-1, and heat shock proteins in the molecular pattern of atrial fibrillation. These results could be considered for new therapeutic opportunities, including inhibition of oxidative stress, evaluation of new anticoagulant drugs with novel therapeutic targets, molecular and genetic studies, and consideration of these alarmins as predictive or prognostic biomarkers of disease onset and severity.