© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
The infarcted myocardium
Simply dead tissue, or a lively target for therapeutic interventions
aDepartment of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Universiteit Maastricht, P.O. Box 616, 6200 MD, Maastricht, The Netherlands
bDepartment of Pharmacology, Cardiovascular Research Institute Maastricht (CARIM), Universiteit Maastricht, P.O. Box 616, 6200 MD, Maastricht, The Netherlands
* Corresponding author. Tel.: +31-43-387-6631; fax: +31-43-387-6613 jcl@lpat.azm.nl
Received 18 December 1998; accepted 12 April 1999
| The first 150 words of the full text of this article appear below. |
| 1 Introduction |
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It has been known for many years that infarction of the heart induces prominent alterations of cardiac structure. The most apparent is the scarring of the infarct. Structural changes after infarction are, however, not limited to the infarcted area, but also extend into the non-infarcted myocardium. Changes in the non-infarcted myocardium include hypertrophy of the cardiomyocytes, growth of the capillary network, and an increase in interstitial collagen.
Cardiac structure is a major determinant of function, which is depressed after myocardial infarction (MI). After infarction, both short term and long term compensatory or regulatory mechanisms are activated. Often these mechanisms also affect cardiac structure. Although activation of these compensatory mechanisms may be beneficial early after infarction, they may have adverse effects, when activation is continued for a longer time. Indeed, pharmacological treatments that block the long term activation of these compensatory mechanisms, like angiotensin converting enzyme inhibitors (ACEI) that block the
| 2 The structure of normal myocardium |
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| 3 The wound healing process after myocardial infarction |
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| 4 Changes in the non-infarcted myocardium after myocardial infarction |
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| 5 Effects of interventions on cardiac remodeling after myocardial infarction |
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| 6 Potential regulators of the formation of granulation tissue after infarction |
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| 7 Conclusions |
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