Treating arrhythmias is a challenge for clinicians because pharmacological 
therapies are often ineffective or have severe side effects. Patients with heart 
failure frequently present with supreventricular and ventricular arrhythmias. 
New antiarrhythmic therapies are needed that modulate the specific 
pathomechanisms underlying the development of cardiac arrhythmias and may have a 
better safety-profile. The Ca-calmodulin dependent kinase II (CaMKII) seems to 
be involved in the development of heart failure and arrhythmias and may 
therefore be a promising target for the development of antiarrhythmic therapies. 
The current review aims at discussing some novel as well as known cytosolic and 
sarcolemmal mechanisms involved in CaMKII-dependent arrhythmias without being 
able to cover all aspects known in the field.