Extensive work has been done regarding the impact of thiamine deprivation on nervous system. In cardiac tissue, chronic thiamine deficiency is described to cause changes in the myocardium that can be associated with arrhythmias. However, compared to the brain, very little is known about the effects of thiamine deficiency on the heart. Thus, this study was undertaken to explore whether thiamine deprivation has a role in cardiac arrhythmogenesis. We examined hearts isolated from thiamine-deprived and control rats. We measured heart rate, diastolic and systolic tension, contraction and relaxation rates. Whole-cell voltage clamp was performed in rat isolated cardiac myocytes to measure L-type Ca²⁺ current. In addition, we investigated the global intracellular calcium transients by using confocal microscopy in the line scan mode. The hearts from thiamine-deficient rats did not degenerate into ventricular fibrillation during 30 minutes of reperfusion after 15 minutes of coronary occlusion. The anti-arrhythmogenic effects were characterized by the arrhythmia severity index. Our results suggest that hearts from thiamine-deficient rats did not experience irreversible arrhythmias. There was no change in L-type Ca²⁺ channel current (I_Ca,L) density. Inactivation kinetics of ICa,L in Ca²⁺-buffered cells was retarded in thiamine-deficient cardiac myocytes. The global Ca²⁺ release was significantly reduced in thiamine-deficient cardiac myocytes. The amplitude of caffeine-releasable Ca²⁺ was lower in thiamine deficient myocytes. In summary, we have found that thiamine deprivation attenuates the incidence and severity of post-ischemic arrhythmias possibly through a mechanism involving a decrease in global Ca²⁺ release.