791 CAN ALARMINS BECOME A THERAPEUTIC TARGET FOR A PATIENTS WITH ATRIAL FIBRILLATION?


 The link between alarmins and atrial fibrillation is clear and well known in the literature. We performed a non-systematic review about role of alarmins in pathophysiological mechanism of AF, hypothesizing their role in potential novel therapeutic targets for arrhythmia.
 Several studies have shown a key role of HMGB1 in AF physiopathology. We have seen an almost direct correlation between HMGB1 and oxidative stress in the inflammatory process of AF. Wu et al. observed that HMGB1 is higher in patients with permanent AF, because they experienced a continuous inflammatory tissue damaging impulse. It was shown a prothrombotic and procoagulative role of HMGB1, increased in patients with AF and atrial thrombosis.
 Scherschel et al. showed higher concentration of S100β protein in AF patients undergoing catheter ablation. Neuronal injury by intrinsic cardiac autonomic nervous system (ICSN) upon catheter treatment released damage-associated molecular pattern proteins (DAMPs) as S100β protein. In vitro studies dealing with murine intracardiac neuros showed that S100β decreased potential action and increased neuronal cells growth.
 Many studies demonstrate HSP70 protective role when intracellular, at high concentrations in patients who do not develop arrhythmia after cardiac injury, such as bypass, and low concentrations preoperatively in patients who later develop arrhythmia. At the serum level, on the other hand, it becomes an important marker of cellular damage and oxidative stress, also related to increased IL-2 AND IL-4.
 
 
 These results could be considered for new therapeutic strategies, as inhibition of oxidative stress, novel therapeutic targets of anticoagulant drugs and considering alarmins as predictive or prognostic biomarkers of disease.
