Aim of this review is to give an overview and discuss recent findings on the 
role of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in the heart. 
Special attention is drawn to excitation-contraction coupling (ECC) and 
excitation-transcription coupling (ETC). Because CaMKII expression and activity 
are increased in cardiac hypertrophy, heart failure, and during arrhythmias both 
in animal models as well as in the human heart a clinical significance of CaMKII 
is implied.