Objectives: Atrial fibrillation (AF) itself alters atrial electrophysiological properties in a manner that favors the ease of inducing and maintaining AF. The purposes of this study were as follows: (1) Expression status of the channels associated with action potential was evaluated to analyze the changes developed in the molecular remodeling process in AF. (2) Correlations of molecular remodeling and structural/hemodynamic parameters were studied to evaluate the effects of mechanical factors on the expression of the channels. Methods: Total of 17 patients undergoing open heart surgery were included. There were 8 men and 9 women with a mean age of 57 짹 14 years (range 19 to 77). Twelve patients had sinus rhythm (SR) and five patients had AF. Echocardiographic data were obtained within one week and cardiac catheterization data within 1 month were used for this study. A piece of right atrial appendage tissue of 0.5 to 1.0 g was obtained during the surgical procedure. RT-PCR and western blot analysis were performed for the evaluation of the following molecules: L-type Ca2+ channel, ryanodine receptor (RyR2), sarcoplasmic reticular Ca2+-ATPase (SERCA2), HERG, Kv4.3, Kv1.5, HCN2, and SCN5A. Results: Reduced expression of L-type Ca2+ channel, RyR2, SERCA2, and Kv1.5 were observed in AF group. Borderline increased expression of HCN2 was observed in AF, however the expression levels of HERG, Kv4.3, and SCN5A were not changed. LA diameter was negatively correlated with RyR2 (p = 0.010, r2 = 0.979). FAS of the left atrium was positively correlated with RyR2 (p = 0.023, r2 = 0.954). Conclusions: (1) Molecular remodeling observed in AF would be related with the atrial action potential to favor initiation and maintenance of AF. (2) RyR2 had correlation with structural/hemodynamic parameters. The expression status of L-type Ca2+ channel and SERCA2 would be more related with underlying heart disease rather than the structural/hemodynamic parameters.