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Domain

Advanced Cardiac Imaging

Modules

Cardiac MRI

Tissue characterization is what CMR does that nothing else can.

How LGE Imaging Works

Gadolinium-based contrast agents are extracellular and do not enter viable myocytes with intact cell membranes, so they distribute preferentially into regions with an expanded extracellular space, such as fibrosis, scar, or infiltrative disease. The late gadolinium enhancement sequence uses an inversion recovery pulse timed to null (make black) normal myocardium, so that abnormal regions with delayed contrast washout and shortened T1 appear bright by comparison roughly 10-15 minutes after contrast administration. This is why LGE identifies structural fibrosis or scar rather than active ischemia per se, and why the inversion time must be adjusted individually to properly null normal myocardium.

Core Sequences

Cine (SSFP) for function/volumes. T1 mapping for diffuse fibrosis/infiltration. T2 mapping for edema/inflammation. Late gadolinium enhancement (LGE) for focal fibrosis/scar.

Ischemic vs. Non-Ischemic LGE

Late gadolinium enhancement cardiac MRI (4-chamber view) showing chronic inferior wall infarction/scar (Wikimedia Commons, CC BY-SA 4.0)Ischemic: subendocardial or transmural, in coronary distribution. Non-ischemic: mid-wall (DCM, myocarditis), epicardial (sarcoid, myocarditis), diffuse subendocardial (amyloid).

Key Indications

Myocarditis (Lake Louise). Cardiomyopathy characterization (HCM, ARVC, non-compaction, amyloid). Iron overload (T2*). Ischemia (stress perfusion). Congenital anatomy. Cardiac masses.

Tissue Characterization: LGE and Parametric Mapping

Late gadolinium enhancement pattern helps distinguish etiology — subendocardial-to-transmural enhancement in a coronary distribution suggests ischemic scar, while mid-wall or epicardial enhancement suggests a non-ischemic process such as myocarditis or sarcoidosis. T1 and T2 mapping add further tissue characterization for diffuse fibrosis and edema that LGE alone can miss.
Clinical pearls
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LGE ≥15% of LV mass in HCM is an SCD risk marker.
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CMR-detected myocardial edema in acute chest pain with normal coronaries is compatible with myocarditis, MINOCA, or takotsubo — T2 signal helps distinguish.
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LGE reflects an expanded extracellular space (fibrosis, scar, or infiltration) rather than direct gadolinium uptake by myocytes, since gadolinium chelates are extracellular agents.
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T1 mapping and extracellular volume (ECV) quantification can detect diffuse interstitial fibrosis even when conventional LGE imaging is negative.
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Stress perfusion CMR can assess for inducible ischemia without ionizing radiation and performs comparably to nuclear perfusion imaging for detecting obstructive CAD.