Mitochondrial care in acute myocardial infarction.

Abstract

This editorial refers to ‘Effect of intravenous TRO40303 as an adjunct to primary percutaneous coronary intervention for acute ST-elevation myocardial infarction: the MITOCARE study results’[†][1], by D. Atar et al. on page 112 Rapid restoration of blood flow has the greatest impact on reducing infarct size and improving patient prognosis in patients with ST-elevation myocardial infarction (MI). However, reperfusion itself can exacerbate myocardial damage on top of the initial ischaemic damage.1 Lethal reperfusion injury develops when sudden restoration of blood flow causes necrosis of myocytes that—albeit injured by the preceding ischaemia—were potentially salvageable at the time of reperfusion. In animal models, reperfusion injury may account for up to 50% of the final infarct size.1 Reperfusion injury is modifiable. Pre-infarct angina and repetitive episodes of ischaemia before ST-elevation MI reduce final infarct size, and are thought to be innate forms of pre-conditioning that reduce reperfusion injury.2 Hence, reperfusion injury is a target for improving outcomes in patients with acute MI undergoing optimal revascularization. Pre-conditioning by mechanical intervention, with repeated cycles of brief ischaemia and reperfusion before extended ischaemia, cannot be applied in acute MI due to its unpredictable nature. Repeated cycles of re-occlusion and reperfusion of the coronary artery within the first minute of reflow (post-conditioning) and repeated cycles of brief ischaemia and reperfusion in a distant organ (remote conditioning), typically the upper arm, can protect from lethal reperfusion injury and reduce infarct size by 30–70% according to experimental animal studies. Although the initial promising results with post-conditioning, which ultimately confirmed a specific intervention against reperfusion injury,3 have not been quite consistent in more recent studies,4,5 … [1]: #fn-2