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Acute ST-elevation myocardial infarction (STEMI) is characterised by unpredictable epicardial artery occlusion. The myocardium supplied by the vessel is rendered ischaemic and depending upon the degree of ischaemia and its duration, can be irreversibly injured, leading to necrotic cell death and myocardial infarction. With the recognition that restoration of blood flow to ischaemic myocardium can salvage ischaemic tissue before it is irreversibly injured, leading to improved residual ventricular function and clinical outcomes, the mainstay of treatment has been to achieve optimal reperfusion as quickly as possible. However, reperfusion itself initiates processes that cause cell death (called reperfusion injury) and so the final extent of myocardial infarction is a composite of the injury caused by ischaemia and reperfusion.
There are a multitude of experimental interventions that profoundly modify the degree of ischaemia–reperfusion injury in the research laboratory. A range of animal model systems are used to study ischaemia–reperfusion injury using different species, protocols and end points. However, very few of the interventions tested on the bench have translated into routine clinical practice. Nevertheless, recent advances have delivered some successful proof-of-principle studies. This review will therefore focus on our current understanding of the underlying mechanisms of ischaemia and reperfusion injury, recent observations in basic science and clinical studies which may provide the basis for future interventions applicable to management of acute STEMI.
Pathophysiology of ischaemia and reperfusion injury
Although the cellular pathophysiology of ischaemia has been closely investigated, until recently the existence of reperfusion injury as a separate entity remained controversial.1–4 This distinction between ischaemic and reperfusion injury is important since interventions targeting the reperfusion phase can be applied in patients presenting with acute infarction where there is already significant tissue ischaemia by the time of presentation.5 At a clinical level myocardial injury is manifest as combination of (i) myocardial cell death, (ii) contractile dysfunction, (iii) …
Funding RKK is funded by the NIHR Oxford Biomedical Research Centre.
Competing interests None.
Provenance and peer review Commissioned; externally peer reviewed.
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