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Acute coronary syndromes
Infarct size reduction in acute myocardial infarction
  1. E McAlindon,
  2. C Bucciarelli-Ducci,
  3. M S Suleiman,
  4. A Baumbach
  1. NIHR Bristol Cardiovascular Biomedical Research Unit, Bristol Heart Institute, Bristol, UK
  1. Correspondence to Dr Andreas Baumbach, Cardiology Department, Level 7 Bristol Heart Institute, Bristol BS2 8HW, UK; andreas.baumbach{at}

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Learning objectives

  • To understand the pathophysiology of myocardial infarction.

  • To review the imaging and biochemical biomarkers that measure infarct size.

  • To review the pharmacological and mechanical treatments available that impact infarct size.

Coronary artery disease is the leading cause of death worldwide, with ST segment elevation myocardial infarction (STEMI) an important contributor. Infarct size following STEMI is a determinant of heart failure and death. This article provides an update on key modalities used to determine infarct size, and recent advances in interventions used to reduce infarct size.

Determinants of infarct size and their pathophysiology

The area at risk (AAR) is the region of the myocardial bed supplied by the infarct related artery (IRA). In the era of reperfusion, not all the AAR will become infarcted. Depending on time to reperfusion and the exact location of occlusion, there will be a proportion of the AAR (jeopardised but not infarctedw1) that can be salvaged by reperfusion therapy. This can be calculated as AAR−infarct size (figure 1).

Figure 1

Cardiovascular MRI short axis mid cavity slice of a left anterior descending ST segment elevation myocardial infarction (STEMI). The hyperintense area in panel A is the area at risk. The hyperintense area in panel B is the infarct size. The difference between these two areas is the myocardial salvage.

The cause of irreversible myocardial damage in STEMI can be divided into two categories: myocardial damage as a result of the myocardial ischaemic process itself; and myocardial damage as a result of reperfusion, termed reperfusion injury. It is difficult to separate out these two components (figure 2).

Figure 2

An illustration exhibiting the interaction of the effects on infarct size from time to reperfusion and reperfusion injury (RI) on infarct size. AAR, area at risk; MI, myocardial infarction. Reproduced with permission from Frőhlich et al.w6

Ischaemic cascade

Following a coronary occlusion, the myocardial bed supplied …

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  • Contributors EMcA: review of literature, writing of manuscript. CB-D: review of literature, editing of manuscript. MSS: writing of science paragraph, editing of the manuscript. AB: design of manuscript, review of literature, editing of manuscript.

  • Funding This research was supported by the National Institute for Health Research (NIHR) Biomedical Research Unit in Cardiovascular Disease at the University Hospitals Bristol NHS Foundation Trust and the University of Bristol. This article presents independent research funded by the NIHR. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health.

  • Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. The authors have no competing interests.

  • Provenance and peer review Commissioned; externally peer reviewed.

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