The multifunctional Ca$^2+$/calmodulin (CaM)-dependent protein
kinase II (CaMKII) has emerged as a proarrhythmic and procardiomyopathic
signal in a wide range of structural heart diseases. This review
discusses CaMKII structure and function and recent evidence implicating
CaMKII inhibition as a potential strategy for treating myocardial
dysfunction and arrhythmias in the setting of structural heart disease.