Article Text

Download PDFPDF
Protecting the ischaemic and reperfused myocardium in acute myocardial infarction: distant dream or near reality?
  1. D M Yellon,
  2. G F Baxter
  1. The Hatter Institute, Department of Academic & Clinical Cardiology, University College London Hospitals & Medical School, Grafton Way, London WC1E 6DB, UK
  1. Professor Yellon email: hatter-institute{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Acute coronary occlusion is the leading cause of morbidity and mortality in the Western world, and according to the World Health Organisation will be the major cause of death in the world as a whole by the year 2020.1 Although the management of this epidemic will centre on the development of effective primary prevention programmes, the impact of these strategies may be limited, particularly in the developing countries. There is an urgent need for effective forms of secondary prevention and, in particular, treatments which will limit the extent of an evolving myocardial infarction during the acute phase of coronary occlusion—the death of myocardium represents a catastrophic event since dead myocytes are not replaced by division of surviving myocytes. Preserving the viability of ischaemic myocardium therefore presents a therapeutic target. Although appreciated for many years, this concept has so far failed to produce a clinically useful agent capable of protecting the ischaemic myocardium from infarction. The term “cardioprotection” has been used loosely during the last few decades to describe various therapeutic approaches, including antiarrhythmic, antianginal, antihypertensive, and antiplatelet treatments. In the present discussion, we apply the term “cardioprotection” very specifically to describe interventions that preserve or enhance the viability of myocardium during ischaemia and reperfusion and thus limit the extent of acute myocardial infarction. It is our contention that in the light of current understanding of the mechanisms of cell injury during both ischaemia and reperfusion, we are well placed to identify molecular targets which may provide the foundation on which rational therapeutic approaches can be based.

Who needs cardioprotection and when?

The prerequisite for salvage of myocardium under threat of infarction is the return of coronary flow to the tissue as quickly as possible.2 ,3 The major clinical approach to reperfusion is the use of thrombolytics. However, fibrinolysis is not instantaneous and …

View Full Text