Among these cytokines, tumor necrosis factor (TNF) can directly alter Ca2+ handling in cardiomyocytes, which is crucial for the initiation of AF and atrial electrical remodeling[10,40,41]; platelet-derived growth factor (PDGF) can reduce the duration of action potentials and Ca2+ transients of cardiomyocytes[42]; and also C-reactive Protein is associated with an increased number of identified nonpulmonary vein ectopies and high-frequency sites in the left atrium[43,44]. Here, CRP is linked to atrial fibrillation.