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Interventional cardiology
Healing and adverse remodelling after acute myocardial infarction: role of the cellular immune response
  1. Anja M van der Laan1,
  2. Matthias Nahrendorf2,
  3. Jan J Piek1
  1. 1Department of Cardiology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
  2. 2Centre for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, USA
  1. Correspondence to Professor Dr Jan J Piek, Department of Cardiology, Academic Medical Centre, University of Amsterdam, PO Box 22660, Amsterdam 1100 DD, The Netherlands; j.j.piek{at}amc.uva.nl

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After a myocardial infarction (MI), the damaged myocardial tissue is repaired and eventually replaced by scar tissue. In a substantial proportion of MI patients, the repair mechanisms induce profound structural and functional changes not only in the infarct zone, but also in the non-infarcted area. These patients show myocardial thinning and expansion of the infarct zone in the early phase after MI, and pathologic cardiomyocyte hypertrophy, apoptosis and extracellular matrix remodelling in the remote zone, a process that may continue for months. These underlying mechanisms induce alterations of the left ventricular (LV) shape, mass, volume, and function, which is also referred to as adverse LV remodelling (figure 1). Although some of these changes may be adaptive and physiological as short term compensation for the sudden loss of contractile function in the infarcted area, it may lead over time to heart failure and cardiac death.w1

Figure 1

Adverse Left ventricular (LV) remodelling after myocardial infarction (MI) is characterised by an altered LV shape and LV volume. Cardiovascular magnetic resonance (CMR) images of a 44-year-old male patient with a large acute anterior MI. Left panels show the vertical long axis end-diastolic cine image, 3 days (panel A) and 3 months after MI (panel C). The right panels demonstrate the corresponding late gadolinium enhancement images with the infarct zone and remote zone (panels B and D). At day 3 after MI, there was extensive microvascular obstruction (panel B, white asterisk) indicated by the black hypoenhanced areas within the hyperenhanced infarcted myocardium. At 3 months after MI, CMR demonstrated an increase …

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