Reperfusion arrhythmias and lethal reperfusion injury share the same pathophysiological basis of intracellular calcium overload, suggesting arrhythmias could serve as a marker for fatal injury.
Reperfusion does not only salvage ischaemic myocardium but can also cause additional cell death which is called lethal reperfusion injury. The time of reperfusion is often accompanied by ventricular arrhythmias, i.e. reperfusion arrhythmias. While both conditions are seen as separate processes, recent research has shown that reperfusion arrhythmias are related to larger infarct size. The pathophysiology of fatal reperfusion injury revolves around intracellular calcium overload and reactive oxidative species inducing apoptosis by opening of the mitochondrial protein transition pore. The pathophysiological basis for reperfusion arrhythmias is the same intracellular calcium overload as that causing fatal reperfusion injury. Therefore both conditions should not be seen as separate entities but as one and the same process resulting in two different visible effects. Reperfusion arrhythmias could therefore be seen as a potential marker for fatal reperfusion injury.
Weg et al. (Tue,) conducted a review in Reperfusion cardiac arrhythmias and reperfusion-induced cell death. Reperfusion arrhythmias was evaluated. Reperfusion arrhythmias and lethal reperfusion injury share the same pathophysiological basis of intracellular calcium overload, suggesting arrhythmias could serve as a marker for fatal injury.