Key result
Myocardial reperfusion triggers tissue injury, driving arrhythmias, stunning, microvascular dysfunction, and accelerated necrosis.
Critically timed reperfusion is a prerequisite for survival of ischaemic myocardium. However, reperfusion may have an injurious component, which in experimental models appears to be mediated by reperfusion-induced augmentation of the inflammatory response and generation of reactive oxygen free radicals. Four expressions of myocardial reperfusion injury have been defined, i.e. reperfusion arrhythmias, post-ischaemic contractile dysfunction (myocardial stunning), coronary vascular and microvascular reperfusion injury, and acceleration of necrosis in irreversibly injured cells/precipitation of necrosis in reversibly injured cells. Mechanical and pharmacological reperfusion therapy is well established in clinical cardiology, and this article reviews the experimental data underlying the current view of myocardial reperfusion injury, and considers the clinical relevance of this phenomenon.
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Peter Riis Hansen (1995) conducted a review in Myocardial reperfusion injury. Myocardial reperfusion therapy was evaluated. Myocardial reperfusion can induce injury through inflammatory augmentation and free radicals, manifesting as arrhythmias, stunning, microvascular injury, and accelerated necrosis.
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