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- Acute myocardial infarction
- left ventricular remodelling
- cellular immune response
- cardiac remodelling
- coronary collateral circulation
- myocardial ischaemia and infarction (IHD)
- acute coronary syndrome
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
This is a reprint of a paper that first appeared in Heart, 2012, Volume 98, pages 1384–90.
Funding This work was supported by a grant by the Graduate School for Medical Sciences of the Academic Medical Centre, Amsterdam, The Netherlands to AML, and a grant from the National Institutes of Health (R01HL096576) to MN.
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. JJP is member of the medical advisory board of Abbott Vascular and consultant for Miracor.
Provenance and peer review Commissioned; externally peer reviewed.
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