Ca2+-homeostatic proteins play an important role in Ca2+excitation–contraction coupling (ECC); however, the involvement of Ca2+calmodulin-dependent protein kinase II delta (CaMKII) in this process is less known. It has been suggested that CaMKII phosphorylates the key proteins for ECC including L-voltage Ca2+ channels (LTCC), which subsequently become longer in the open state. Such changes may initiate after depolarisations promoting arrhythmias and contractility disturbances.1 To test this hypothesis, KN-93 (0.5 μ/l), a CaMKII inhibitor, was administered into the perfusion solution before ischaemia and during the first 10 min of reperfusion. Incidence of ventricular fibrillation was decreased in the KN-treated rat hearts. Although the duration of arrhythmias did not differ between the groups, arrhythmia score was lower upon CaMKII inhibition. Likewise, the recovery of post-ischaemic contractile function was improved in the KN-treated hearts. On the other hand, no additive anti-arrhythmic effects of CaMKII inhibition were observed in the group treated with simvastatin (10 mg/kg, 7 days), which is known to suppress electrical instability.2 In the presence of CaMKII inhibitor in the simvastatin-treated group, the severity of arrhythmias was unchanged as compared with the group without treatment. However, CaMKII inhibitor reversed attenuation of post-ischaemic contractile dysfunction in simvastatin-treated rats. CaMKII and LTCC protein levels, which were lower in simvastatin-treated rats, were not influenced by KN treatment. In conclusion, CaMKII is involved in the mechanisms of ECC; however, it seems that under certain conditions, such as statins-mediated cardioprotection, it may have a distinct influence on excitation and contraction. Supported by VEGA 1/0620/10, 2/0173/08.