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The acute restoration of blood flow to the ischaemic myocardium during reperfusion therapy for ST-segment elevation myocardial infarction (STEMI) may induce further injuries to the myocardium. This phenomenon, reperfusion injury, can paradoxically reduce the beneficial effects of myocardial reperfusion. Studies using various animal models have reported that the reperfusion injury can account for up to 50% of the total size of myocardial infarction.1 As such, minimising reperfusion injury could have significant clinical implications. In clinical practice, the mortality rate for STEMI has reached a plateau with a 1-year mortality of 10%, with approximately 25% patients developing heart failure, despite an early and successful reperfusion.1 2 Thus, there is a need for further improvements in the treatment of STEMI. The prevention of reperfusion injury may help to improve outcome following the most widely applied form of reperfusion therapy, primary percutaneous coronary intervention (PCI).
There are four categories of reperfusion injury in STEMI: stunning, reperfusion arrhythmia, no reflows/slow reflow by a microvascular obstruction (MVO) and lethal reperfusion injury.1 Different types of reperfusion injury may occur at the same time and ultimately determine the infarct size.1 3 Different methods have been examined to prevent reperfusion injury (figure 1).1 3 No reflow/slow reflow and lethal reperfusion injury often occur simultaneously. These two types of reperfusion injury can result in irreversible myocardial necrosis.1 It is unknown which one of the two reperfusion injuries contribute more to the final myocardial infarct size. It is suspected that the contribution of each reperfusion injury to final infarct size might depend on the nature of the lesions and is expressed roughly by the sum of the two types of reperfusion injury in clinical practice. Efforts to reduce these two reperfusion injuries have focused on thrombectomy, ischaemic postconditioning (IPC) and pharmacological conditioning and …