Reperfusion – the good, the bad, and the ugly

Reperfusion is mandatory to salvage ischemic myocardium from impending infarction. However, reperfusion also causes additional irreversible injury, not only to the myocardium, but also to the coronary microcirculation. Such reperfusion injury is the target of cardioprotective conditioning strategies. Such strategies include brief cycles of ischemia/reperfusion before (preconditioning), during (perconditioning), or after (postconditioning) the sustained myocardial index ischemia, either locally in the coronary circulation or remotely in limbs or other organs. Reperfusion injury is also the target of pharmacological cardioprotection therapies, eg, cyclosporine A, exenatide, or metoprolol, which engage parts of the signal transduction pathways involved in conditioning strategies. Acute myocardial stunning—fully reversible contractile dysfunction—during reperfusion after shorter episodes of myocardial ischemia is more paradigmatic than clinically relevant; however, long-term repetitive stunning initiates hibernation, ie, a state of prolonged contractile dysfunction, though with preserved viability such that contractile dysfunction is reversible upon eventual revascularization. Reperfusion arrhythmias are frequently observed, but are only rarely a clinical problem. L Heart Metab. 2016;70:4-7