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Mannose-binding lectin: an ancient molecule with new implications in myocardial infarction

Sebastian Grundmann, Christoph Bode, Martin Moser
DOI: http://dx.doi.org/10.1093/eurheartj/ehq070 1163-1164 First published online: 16 March 2010

This editorial refers to ‘Influence of functional deficiency of complement mannose-binding lectin on outcome of patients with acute ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention’, by M. Trendelenburg et al., on page 1181

The earliest possible revascularization of the occluded vessel and reperfusion of the ischaemic tissue is currently the most effective therapy for ST-segment elevation myocardial infarction (STEMI). Prompt reperfusion is a key determinant of infarct size, which again is a major predictor of morbidity and mortality in STEMI patients.

Advances in percutaneous coronary intervention (PCI) technology and especially in peri-interventional anticoagulation strategies have significantly improved the outcome of these patients in the past years. However, still ∼6% of patients do not survive to hospital discharge, and the identification of such patients at increased risk remains difficult and the necessary therapeutic consequences unclear.1 However, it becomes increasingly evident that early reperfusion alone is insufficient to prevent myocardial damage and prevent STEMI-related mortality. Furthermore, interventional revascularization after temporary ischaemia itself causes additional tissue damage and cell death, an important phenomenon referred to as myocardial ischaemia/reperfusion (I/R) injury. Despite restoration of epicardial flow, reperfusion triggers endothelial and cardiomyocyte damage that impairs myocardial perfusion and cardiac function, and may eventually contribute more to myocardial damage than the ischaemic event itself.2 The principles of I/R injury were first described by Jennings et al. in the …

*Corresponding author. Tel: +49 761 270 3441, Fax: +49 761 270 3200, Email: christoph.bode{at}uniklinik-freiburg.de