1. Introduction are closely related and do indeed both change after infarction, it is largely unknown what the exact structural It has been known for many years that infarction of the component is that causes the reduction in cardiac function heart induces prominent alterations of cardiac structure. after infarction. Also it is not clear which structural The most apparent is the scarring of the infarct. Structural component should be targeted for effective pharmacochanges after infarction are, however, not limited to the therapy after infarction. infarcted area, but also extend into the non-infarcted In this review we attempt to clarify the structural myocardium. Changes in the non-infarcted myocardium alterations after infarction. We and others have focused for include hypertrophy of the cardiomyocytes, growth of the many years on the potential importance of changes in the capillary network, and an increase in interstitial collagen. vital non-infarcted myocardium and, indeed, found several Cardiac structure is a major determinant of function, alterations in cardiac structure after infarction and effects which is depressed after myocardial infarction (MI). After thereon of drugs that improved cardiac function. However, infarction, both short term and long term compensatory or recent data in animal studies and humans point to the regulatory mechanisms are activated. Often these mecha- importance of the infarct itself as a potential target for nisms also affect cardiac structure. Although activation of intervention. The infarct appears to be more than just dead these compensatory mechanisms may be beneficial early tissue and infarct healing turns out to be an active and well after infarction, they may have adverse effects, when controlled process. Also, interventions in infarct healing activation is continued for a longer time. Indeed, pharma- appear to affect cardiac function. Therefore we hypothesize cological treatments that block the long term activation of that changes in the structure of the infarct may be of major these compensatory mechanisms, like angiotensin convert- importance for the maintenance of cardiac function. Future ing enzyme inhibitors (ACEI) that block the renin–an- pharmacological interventions should, for this reason, not giotensin system (RAS), have been shown to improve only be directed to the non-infarcted myocardium, but also cardiac function after infarction. to the mechanisms that control adequate infarct healing. Although we know that cardiac function and structure After describing the components of the normal heart, we will focus on the characteristics of cardiac wound healing and some of the control mechanisms involved, with special