Objectives This study compared the effects of amiodarone on ventricular electrophysiological properties in normal dogs and CHF dogs. Methods Dogs (n=44) were randomized into four groups: Group 1 (n=10) was the control. Group 2 (n=10) was given amiodarone orally 300 mg·d-1 for 4 to 5 weeks. Group 3 (n=12) was the congestive heart failure (CHF) models induced by right ventricular rapid pacing (240 pulses·min-1 for 4 to 5 weeks). Group 4 (n=12) was the CHF models given amiodarone orally 300 mg·d-1 for 4 to 5 weeks. The ventricular electrophysiological variables were evaluated by standard electric stimulation and monophasic action potential (MAP) recording. Results Amiodarone prolonged sinus cycle length (SCL), intra-ventricular conduction time (IVCT), MAP duration (MAPD90), ventricular effective period (VERP), ventricular activation time (VAT) and ventricular recovery time (VRT) without significant effects on the ratio of VERP to MAPD90 (VERP/MAPD90), ventricular fibrillation threshold (VFT), the dispersion of VRT (VRT-D), and ventricular late repolarization duration (VLRD) in normal dogs. However, amiodarone did not further prolong the prolonged SCL, MAPD90, VERP, VAT and VRT, but further prolonged IVCT in CHF dogs. Amiodarone normalized the abnormal ventricular electrophysiological properties in CHF dogs as manifested by increasing the decreased VERP/MAPD90 and VFT, shortening the prolonged VLRD, and decreasing the increased VRT-D. Amiodarone did not worsen the hemodynamic parameters in normal and CHF dogs. Conclusions Amiodarone had different effects on ventricular electrophysiological properties in normal and CHF dogs. The favorable effects of amiodarone in normalizing some abnormal cardiac electrophysiological properties in CHF models may have potential value on the prevention and treatment of ventricular arrhythmias and sudden cardiac death in CHF. Objectives This study compared the effects of amiodarone on ventricular electrophysiological properties in normal dogs and CHF dogs. Methods Dogs (n = 44) were randomized into four groups: Group 1 (n = 10) was the control. Group 2 Group 3 (n = 12) was the congestive heart failure (CHF) models induced by right ventricular rapid pacing (240 pulses · min-1 for 4 to 5 weeks Group 4 (n = 12) was the CHF models given amiodarone orally 300 mg · d-1 for 4 to 5 weeks. The ventricular electrophysiological variables were evaluated by standard electric stimulation and monophasic action potential (MAP) recording. Results Amiodarone prolonged sinus cycle length (SCL), intra-ventricular conduction time (IVCT), MAP duration (MAPD90), ventricular effective period (VERP), ventricular activation time (VAT) and ventricular recovery time (VRT) without significant effects on the ratio of VERP to MAPD90 (VERP / MAPD90), ventricular fibrillation threshold (VFT), the dispersion of VRT (VRT-D), and ventricular late repolarization duration (VLRD) in normal dogs. However, amiodarone did not further prolong the prolonged SCL, MAPD90, VERP, VAT and VRT, but further prolonged IVCT in CHF dogs. Amiodarone normalized the abnormal ventricular electrophysiological properties in CHF dogs as manifested by increasing the decreased VERP / MAPD90 and VFT, shortening the prolonged VLRD, and decreasing the increased VRT-D. Amiodarone did not worsen the hemodynamic parameters in normal and CHF dogs The favorable effects of amiodarone in normalizing some abnormal cardiac electrophysiological properties in CHF models may have potential value on the prevention and treatment of ventricular arrhythmias and sudden cardiac death in CHF.