In the recent years, Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) was 
suggested to be associated with cardiac hypertrophy and heart failure but also 
with arrhythmias both in animal models as well as in the human heart. This 
article focuses on the role of CaMKII for excitation-contraction coupling but 
more explicitly it highlights major CaMKIIdependent proarrhythmogenic mechanisms 
including SR Ca(2+) leak and late Na(+) current. Because a clinical significance 
of CaMKII is implied for both mechanisms, CaMKII inhibition is suggested to be a 
therapeutical approach in the near future.