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Delayed contrast enhancement on MR images of myocardium: past, present, future
Karen G Ordovas1, Charles B Higgins
1Department of Radiology, UCSF Medical Center, 505 Parnassus Ave, Room L308, Box 0628, San Francisco, CA 94143-0628, USA.
Differential enhancement of myocardial infarction was first recognized on computed tomographic (CT) images obtained with iodinated contrast material in the late 1970s. Gadolinium enhancement of myocardial infarction was initially reported for T1-weighted magnetic resonance (MR) imaging in 1984. The introduction of an inversion-recovery gradient-echo MR sequence for accentuation of the contrast between normal and necrotic myocardium was the impetus for widespread clinical use for demonstrating the extent of myocardial infarction. This sequence has been called delayed-enhancement MR and MR viability imaging. The physiologic basis for differential enhancement of myocardial necrosis is the greater distribution volume of injured myocardium compared with that of normal myocardium. It is now recognized that delayed enhancement occurs in both acute and chronic (scar) infarctions and in an array of other myocardial processes that cause myocardial necrosis, infiltration, or fibrosis. These include myocarditis, hypertrophic cardiomyopathy, amyloidosis, sarcoidosis, and other myocardial conditions. In several of these diseases, the presence and extent of delayed enhancement has prognostic implications. Future applications of delayed enhancement with development of MR imaging and CT techniques will be discussed.
Differential enhancement of myocardial infarction was first recognized on computed tomographic (CT) images obtained with iodinated contrast material in the late 1970s. Gadolinium enhancement of myocardial infarction was initially reported for T1-weighted magnetic resonance (MR) imaging in 1984. The introduction of an inversion-recovery gradient-echo MR sequence for accentuation of the contrast between normal and necrotic myocardium was the impetus for widespread clinical use for demonstrating the extent of myocardial infarction. This sequence has been called delayed-enhancement MR and MR viability imaging. The physiologic basis for differential enhancement of myocardial necrosis is the greater distribution volume of injured myocardium compared with that of normal myocardium. It is now recognized that delayed enhancement occurs in both acute and chronic (scar) infarctions and in an array of other myocardial processes that cause myocardial necrosis, infiltration, or fibrosis. These include myocarditis, hypertrophic cardiomyopathy, amyloidosis, sarcoidosis, and other myocardial conditions. In several of these diseases, the presence and extent of delayed enhancement has prognostic implications. Future applications of delayed enhancement with development of MR imaging and CT techniques will be discussed.
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