Background　Although coronary reperfusion in ischaemic myocardium is the only prerequisite of heart salvage， but reperfusion may lead to reperfusion arrhythmias. Cytosolic Ca2+ overload is a significant mechanism for the severe life-threatening arrhythmias. Ca/calmodulin-dependent protein kinaseⅡ（CaMKⅡ）is a serine/threonine kinase， which can adjust the intracellular calcium concentration （［Ca2+］i） via various pathways.　Objective　To explore the structure and function of CaMKⅡ and the impact of CaMKⅡ-dependent phosphorylation of the target protein on reperfusion arrhythmias.　Content　CaMKⅡ is a main signal molecule for early reperfusion arrhythmias. CaMKⅡ dysfunction can lead to deregulation of intracellular calcium homeostasis， finally cause reperfusion arrhythmias.　Trend　The choice of appropriate drug on the CaMKⅡand its relevant target protein may be important therapeutic approach for reperfusion arrhythmias.