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Many clinical scenarios leading to myocardial necrosis will lead to some form of cardiac symptoms such as chest pain and/or dyspnea. Depending on the etiology and extent there might be characteristic changes on the electrocardiogram.
Myocardial necrosis can be fast and reliably detected biochemically with serologic markers such as troponin I and troponin T, creatine kinase MB isoform 1.
Myocardial necrosis is a result of acute myocardial cell death or irreversible myocardial injury and leads to a leakage of intracellular components of the irreversibly damaged cardiomyocytes into the myocardial extracellular space 2-4, which will then increase if the damage is high enough and also lead to myocardial edema.
The necrotic myocardial zone will subsequently undergo a healing or remodeling process, starting with an inflammatory response, where the necrotic tissue is degraded and resorbed and will eventually be replaced by myocardial scar tissue 3,4.
Due to the excellent sensitivity and fast availability of serologic biomarkers, imaging methods have no real role in the detection of myocardial necrosis but the localization and the search for the etiology for non-ischemic or indeterminate cases.
Myocardial necrosis can be displayed with inversion recovery gradient echo images as a late gadolinium enhancement or in case of microvascular obstruction as void or lack of any enhancement 3,5. The enhancement is due to an increase of extracellular volume as a result of leakage of intracellular components into the extracellular space and hence increased volume of distribution for gadolinium-based contrast agents. It might be subendocardial, transmural, subepicardial or patchy depending on the etiology 5,6.