In our present study, although hypocapnia and hypoxemia were not attenuated after LLVS was administered, the sympathetic neural hyperactivation was modulated, and the systemic inflammation was inhibited, also improving the remodeling of myocardial tissue structure, ion imbalance, and abnormal Cx43 and Cx40 expression, while ultimately inhibiting AF occurrence (Figure 8). Here, GJA1 is linked to atrial fibrillation.