Arrhythmias can develop in various cardiac diseases, such as ischemic heart 
disease, cardiomyopathy and congenital heart disease. It can also contribute to 
the aggravation of heart failure and sudden cardiac death. Redox stress and 
Ca(2+) overload are thought to be the important triggering factors in the 
generation of arrhythmias in failing myocardium. From recent studies, it appears 
evident that Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) plays a 
central role in the arrhythmogenic processes in heart failure by sensing 
intracellular Ca(2+) and redox stress, affecting individual ion channels and 
thereby leading to electrical instability in the heart. CaMKII, a 
multifunctional serine/threonine kinase, is an abundant molecule in the neuron 
and the heart. It has a specific property as "a memory molecule" such that the 
binding of calcified calmodulin (Ca(2+)/CaM) to the regulatory domain on CaMKII 
initially activates this enzyme. Further, it allows autophosphorylation of T287 
or oxidation of M281/282 in the regulatory domain, resulting in sustained 
activation of CaMKII even after the dissociation of Ca(2+)/CaM. This review 
provides the understanding of both the structural and functional properties of 
CaMKII, the experimental findings of the interactions between CaMKII, redox 
stress and individual ion channels, and the evidences proving the potential 
participation of CaMKII and oxidative stress in the diverse arrhythmogenic 
processes in a diseased heart.