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Postinfarction left ventricular remodelling: where are the theories and trials leading us?
  1. Z R Yousef,
  2. S R Redwood,
  3. M S Marber
  1. Department of Cardiology, The Rayne Institute, St Thomas' Hospital, King's College London, London SE1 7EH, UK
  1. Professor Marber email: mike.marber{at}

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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.

Acute myocardial infarction

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

Myocardial infarction is followed by a complex and interrelated sequence of events termed postinfarction left ventricular remodelling (table 1) which describes the compensatory responses of the cardiovascular system when faced with an acute loss of myocardial contractile function.6 Morphologically, the end result of these responses can be quantified by imaging the infarcted ventricle as it progressively dilates and assumes a more spherical as opposed to elliptical contour.6

View this table:
Table 1

Components of postinfarction ventricular remodelling

In the early stages, ventricular dilatation can be considered beneficial as it maintains stroke volume through the Frank-Starling mechanism. At the same time, however, the dilating ventricle proves detrimental as it exerts further demands on the surviving myocardium through increases in wall tension (the law of Laplace, fig1).7 Long term, left ventricular volume is a sensitive marker of postinfarction ventricular dysfunction, left ventricular end systolic volume being one …

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