Review
Postinfarction left ventricular remodelling: where are the theories and trials leading us?
Z R Yousef, S R Redwood, M S Marber
Department of
Cardiology, The Rayne Institute, St Thomas' Hospital, King's College
London, London SE1 7EH, UK
Correspondence to: Professor Marber email: mike.marber@kcl.ac.uk
Accepted 21 July 1999
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Introduction |
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While mortality from overt ischaemic heart disease is falling, that from heart failure is increasing and reaching epidemic proportions.1 Although an aging population is partly responsible for this trend, recent observations showing persistently high mortality and morbidity rates following myocardial infarction further compounds the issue.2 An understanding of the pathophysiological processes leading to heart failure, and in particular the mechanisms underlying postinfarction heart failure (postinfarction ventricular remodelling) is therefore fundamental and forms the basis of this review.
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Acute myocardial infarction |
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Immediately after coronary artery occlusion, irreversible cell necrosis can occur within minutes. Factors affecting the amount of necrosis include the presence or absence of a preconditioning stimulus,3 the volume of ischaemic myocardium, and the amount of collateral blood flow.4 In addition, prompt reperfusion within a narrow time window, when myocytes are in a state of critical ischaemia and are prenecrotic/viable, has been shown to reduce cell death, limit infarct size, and increase survival.5
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