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This editorial refers to ‘Postconditioning protects against human endothelial ischaemia–reperfusion injury via subtype-specific K ATP channel activation and is mimicked by inhibition of the mitochondrial permeability transition pore’[†][1], by M.I. Okorie et al. , on page 1266 Myocardial infarction is almost invariably a regional event which results from occlusion of a coronary artery secondary to atherosclerotic plaque rupture. In contrast to localized infarction, atherosclerosis is a generalized process which involves the entire vascular tree, albeit to a different extent and with different manifestations. It therefore seems logical to analyse phenomena in the peripheral vasculature, which is much easier and more feasible for non-invasive access than the coronary circulation or the myocardium, with the aim of predicting the risk of a coronary event. In fact, patients with peripheral arterial disease carry a higher risk of coronary artery disease.1 Also, vascular dysfunction in specific vascular territories is associated with increased risk of coronary artery disease; erectile dysfunction is an example.2The study by Okorie et al. 3 … [1]: #fn-2

european heart journal

Preservation of peripheral vasodilation as a surrogate of cardioprotection? The mechanistic role of ATP-dependent potassium channels and the mitochondrial permeability transition pore