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The Hatter
Institute, Department of Academic & Clinical Cardiology, University
College London Hospitals & Medical School, Grafton Way, London
WC1E 6DB, UK
Correspondence to: Professor Yellon email: hatter-institute@ucl.ac.uk
Accepted 6 January 2000
| The first 150 words of the full text of this article appear below. |
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Introduction |
|---|
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
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