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Brief episodes of ischaemia/reperfusion in peripheral organs or limbs render the heart and other parenchymal organs more resistant to subsequent injury by more prolonged periods of ischaemia and reperfusion.1 Such remote ischaemic conditioning (RIC) has not only been demonstrated in experimental animals, but is also operative in humans. In proof-of-concept studies, RIC reduced infarct size in patients undergoing elective interventional2 or surgical coronary revascularization,3–5 as evidenced by reduced cardiac biomarker (creatine kinase, troponin I or T) release, and this effect translated into improved short-term5 and long-term4,6 clinical outcomes which were, however, analysed only as secondary endpoints from studies with reduced infarct size as primary endpoint. Also in patients suffering an acute myocardial infarction, RIC before interventional reperfusion still reduced infarct size, as evidenced by SPECT imaging,7 or improved salvage, as evidenced by MRI,8 and this protection again translated into improved short-term8 and long-term clinical outcome,9 again analysed as secondary endpoints only. Recently, it was shown that in patients with acute myocardial infarction infarct size was reduced when RIC was combined with thrombolysis.10 However, not all studies on RIC in humans have been positive, and the discrepancies have been largely attributed to confounding variables,11 such as co-morbidities or concomitant medications or, in case of surgery, anaesthetics12 which interfere with the protection by RIC. While infarct size is a most important determinant of remodelling, progression to heart failure, and ultimate prognosis,13 studies on RIC sufficiently powered for …

ERICCA and RIPHeart: two nails in the coffin for cardioprotection by remote ischemic conditioning? Probably not!