Late gadolinium enhancement
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Late gadolinium enhancement is also known under the terms ‘late enhancement’ or ‘delayed enhancement’.
Late gadolinium enhancement is based on the shortening of T1 and different regional distribution patterns of gadolinium-based contrast agents within the extracellular space of the myocardium. It also depends on varying uptake and washout patterns within the normal myocardium and those different disease processes. This is depicted by applying an inversion pulse to null the inherent signal of the myocardium after a certain amount of time 1-4.
Image acquisition for late gadolinium enhancement is usually conducted with an inversion recovery prepared T1 weighted gradient echo and either manually adapted inversion time or as PSIR sequence with a phase-sensitive inversion-recovery based reconstruction algorithm 1-4.
Typically late gadolinium enhancement is measured around 10-20 min after administration of a gadolinium-based contrast agent.
Late gadolinium enhancement is a result of regional differences in myocardial extracellular volume and different uptake and washout patterns within the extracellular space and is seen in myocardial injury e.g. myocyte necrosis, myocardial edema, myocardial scar tissue, and focal areas of fibrosis, and can be related to different cardiac diseases regarding its distribution and other tissue properties and clinical parameters 6.
It is applied in the various clinical scenarios and can help to detect and characterize various myocardial diseases 1-9:
- myocardial infarction
- patchy mid myocardial and/or focal subepicardial enhancement as an expression of potentially irreversible injury (myocyte necrosis, fibrosis, edema) 2,5,6
- can represent one of two main criteria in the diagnosis of acute myocarditis 5
- patchy mid myocardial and/or focal subepicardial enhancement as an expression of potentially irreversible injury 6-8
- linked to cardiac arrhythmia even with preserved left ventricular function 6,7
- subendocardial enhancement in a non-coronary distribution and poor contrast difference between blood and myocardium due to abnormal blood-pool/tissue gadolinium kinetics 1-3,6,7
- detection of intramyocardial midwall fibrosis 6,7,9
- predictor of ventricular arrhythmia and sudden cardiac death (SCD) 6,7,9
- patchy/streaky intramyocardial patterns at the right ventricular insertion sites within the hypertrophied myocardium suggest fibrosis
- prognostic value: increased risk of sudden cardiac death 6,7 especially if extensive or diffuse (>15% wall mass) 10
- characteristic midwall or subepicardial enhancement in the basal inferolateral wall 7
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