Elucidation of inflammatory network underlying the pathogenesis of atrial fibrillation

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Endothelin-1 (ET-1) is profoundly involved in the activation of mast cells in hemodyamically stressed atria. ET-1-induced secretion of monocyte chemotactic protein-1 (MCP-1) from activated mast cells enhances migration of macrophages, and consequently promotes atrial remodeling. HMG-CoA reductase pitavastatin inhibits ET-1-triggered activation of mast cells and up-regulation of fibrogenic PDGF-A in atria, and thereby prevents atrial remodeling and inducibility of atrial fibrillation. These results suggest that application of statins may be a promising approach to achieve upstream prevention of atrial fibrillation in stressed hearts.