To study the effect of Wendantang Huacaifang（WDTHCF）on atrial energy metabolic remodeling in paroxysmal atrial fibrillation（PAF）rats based on fatty acid metabolic pathway.

Male SD rats were selected and randomly divided into the normal group，the model group，the WDTHCF low，medium and high dose groups，and the amiodarone hydrochloride group，and the PAF model was induced by using Ach-CaCl_2.After the model was successfully established，the WDTHCF low，medium and high dose groups and amiodarone hydrochloride were given by gavage.The duration of atrial fibrillation was monitored using electrocardiography.The formation of atrial lipid droplets was detected by oil-red O staining.The contents of free fatty acid（FFA）and triglyceride（TG）of atrial tissues were detected.RT-qPCR was used to detect the mRNA expressions of aAMP-activated protein kinase（AMPK），acetyl coenzyme A carboxylase（ACC），carnitine palmitoyltransferase-1B（CPT-1B），fatty acid translocase/cluster of differentiation 36（FAT/CD36），fatty acid transport protein（FATP）and fatty acid binding protein 3（FABP3）.Western blot was used to detect the protein expressions of AMPK，p-AMPK，ACC，p-ACC and CPT-1B and immunohistochemistry method was used to detect myocardial translocation of atrial FAT/CD36.

Compared with the normal group，the rats in themodel group showed increased duration of AF（P<0.05），elevated contents of FFA and TG in the atria（P<0.05），significant lipid droplet formation in the atria，decreased mRNA expressions of AMPK，ACC，CPT-1B，FAT/CD36，FATP and FABP3（P<0.05），and decreased atrial tissue AMPK phosphorylation，ACC phosphorylation and relative protein expression of CPT-1B were significantly reduced（P<0.05），and the membrane translocation of FAT/CD36 in the atria was reduced（P<0.05）.After treatment with WDTHCF，PAF duration was shortened（P<0.05），and the contents of FFA and TG in the atria decreased（P<0.05），lipid droplet formation in atria decreased，the mRNA expressions of AMPK，ACC，CPT-1B，FAT/CD36，FATP and FABP3 in atrial tissues were elevated（P<0.05），and the relative protein expressions of AMPK phosphorylation，ACC phosphorylation and CPT-1B in atrial tissues were elevated（P<0.05），and the membrane translocation of FAT/CD36 in atria was increased.

WDTHCF improved atrial energy metabolic remodeling in phlegm-turbid and bloodstasis type of PAF rats through AMPK regulating the ACC/CPT-1Bmediated fatty acid metabolism pathway.