Objective To investigate the effect of allicin (All) on the delayed afterdepolarization (DAD), triggered activity (TA) and ion currents in the ventricular myocytes of rats with heart failure and the related mechanism. Methods Heart failure models were established in 20 SD rats by abdominal aortic ligation, and sham operation was performed in 10 SD rats as control. Enzymic digestion was used to isolate ventricular myocytes in the 2 groups. According to the experimental design, the model cells were divided into heart failure group (without administration, HF) and administration group (200.0 μmol/L All, HF+All). Patch clamp technique was used to observe the occurrence of DAD and TA and to record the associated changes of ion currents [the transient inward current (I_ti), L-type calcium current (ICa,L) and sodium-calcium exchanger current (INCX)] in the 3 groups. Flou-4AM fluorescence technique was used to detect the changes of intracellular calcium concentration. SPSS statistics 17.0 was used for statistical analysis. ANOVA and SNK-q test were used for comparison among groups. Results (1)The incidences of DAD and TA in the control group, HF group and HF+All group were [13.3%(2/15), 0.0%(0/15)], [60.0%(9/15), 26.7%(4/15)] and [40.0%(6/15), 13.3%(2/15)] respectively. Compared with the control group, the incidences of DAD and TA in the HF group increased significantly. Compared with the HF group, the incidences of DAD and TA in the HF+All group decreased significantly by 20.0% and 13.4% respectively (n=15, P<0.01). (2) Compared with control group, I_ti,INCX and ICa,L density increased in the HF group, but compared withHF group, they decreased in the HF+All group, in which I_ti peak inward current density decreased from(-1.05±0.06)pA/pF to(-0.53±0.05)pA/pF (n=10, P<0.01) and INCX inward current density from (-5.8±0.7)pA/pF to (-4.2±0.4)pA/pF (n=10, P<0.01). At the same time, All accelerated the steady-state inactivation of channel currents and decreased the peak current density of ICa,L from (-17.2+0.9) pA/pF to (-13.5+1.0) pA/pF (n=15, P<0.01). (3) Compared with the control group, the resting calcium concentration, transient calcium amplitude and time for intracellular calcium concentrations to reach 50% of maximum value in the HF group were significantly higher, but those parameters were significantly lower in the HF+All group than in the HF group (n=15, P<0.01). The intracellular calcium transient attenuation rate in the HF group was significantly lower than that in the control group, but it recovered significantly after the application of All (P<0.05). Conclusion All may reduce the occurrence of DAD and TA by reducing intracellular calcium and blocking I_ti and INCX currents in ventricular myocytes of rats with heart failure.