Taking lizard saliva to heart

Abstract

This editorial refers to ‘Exenatide reduces reperfusion injury in patients with ST-segment elevation myocardial infarction’, by J. Lonborg et al. , doi:10.1093/eurheartj/ehr309 For patients presenting with an acute ST-segment elevation myocardial infarction (STEMI), the most effective therapy for reducing myocardial infarct (MI) size, preserving left ventricular (LV) systolic function, and improving clinical outcomes is timely myocardial reperfusion by primary percutaneous coronary intervention (PPCI). Although the process of myocardial reperfusion is critical for myocardial salvage, paradoxically it can also induce cardiomyocyte death, thereby mitigating the full beneficial effects of myocardial reperfusion in terms of MI size reduction and myocardial salvage—a phenomenon which has been termed ‘lethal myocardial reperfusion injury’.1 The fact that a therapeutic intervention administered solely at the time of myocardial reperfusion can reduce MI size by up to half suggests that lethal myocardial reperfusion injury may actually contribute up to 50% of the final MI size.1 Although the process of myocardial reperfusion has been further optimized by recent advances in antiplatelet (e.g. prasugrel and ticagrelor) and antithrombotic (e.g. bivalirudin) therapy, there is still no effective treatment for reducing lethal myocardial reperfusion injury in PPCI patients. Over the years a number of therapeutic strategies with proven efficacy for reducing lethal myocardial reperfusion injury in experimental studies [e.g. antioxidants, calcium channel blockers, anti-inflammatory agents, hypothermia, erythropoietin, protein kinase C (PKC)-δ inhibition] have produced disappointing results when investigated in the clinical arena as adjunctive therapy to PPCI. The reasons for this failure to translate cardioprotection into the clinical setting can be attributed to a number of factors including inappropriate animal MI models and poorly designed clinical studies.2 However, more recently, a number of novel therapeutic strategies (such as ischaemic postconditioning,3–5 atrial natriuretic peptide,6 cyclosporin-A,7 and remote ischaemic preconditioning8) have been reported in proof-of-concept clinical …