General

LGE is not disease specific and can be caused by ischaemic and non-ischaemic necrosis/fibrosis, inflammatory or infectious pathology or tumourous lesions. Gadolinium agents do not penetrate intact myocytes, they accumulate within the increased extracellular space or into ruptured myocytes. Left: normal myocardium, center: necrosis / fibrosis with increased extracellular space, right: Acute myocardial infarction.

Coronary pattern	Non-coronary pattern
From subendocardium to subepicardium (ischaemic wave front) with increasing coronary occlusion time	Subendocardium is typically spared
Circumferential extent related to size of perfusion bed and occluded coronary artery	Often more patchy distribution, localized in mid-wall and subepicardium
Acute reperfused MI can be associated with MVO	Global subendocardial LGE (uncommon even with diffuse CAD)

Coronary pattern

Subendocardial infarct LGE transmurality correlates with likelihood of recovery after revascularization LGE identifies arrhythmogenic substrate (mapping for ablation) Transmural myocardial infarct Degree of transmurality correlates inversely with viability Ischaemic cardiomyopathy Often also LV dilatation, differential diagnosis of DCM Coronary LGE pattern with subendocardial/transmural LGE LGE identifies arrhythmogenic substrate (mapping for ablation)

Non-coronary pattern

Cardiac amyloidosis Difficulty in nulling Global subendocardial distribution (non-coronary pattern) or patchy subendocardial or transmural LGE Base-apex LGE gradient, blood pool early darkening DD AL vs. ATTR amyloidosis AL: less extensive LGE, often (global) subendocardial pattern, QALE score < 13 ATTR: more extensive and diffuse LGE, often more diffuse and transmural pattern, QALE score ≥ 13 Dilated cardiomyopathy Pattern of fibrosis is related to underlying aetiology of DCM In most cases lack of LGE -> consider T1 mapping Diffuse mid-wall or subepicardial septal LGE (reflecting fibrosis and not matching a coronary perfusion bed) Often localized LGE of the inferoseptal wall Hypertrophic cardiomyopathy Focal (mid-wall) LGE of anterior and posterior RV insertion points (hinge points) and of hypertrophied segments LGE in HCM indicates replacement fibrosis but may also indicate necrosis/scarring Apical HCM: apical wall may develop ischaemia with wall thinning → LGE can be transmural (mimicking ischaemic injury in the absence of epicardial CAD) Systemic Sclerosis Basal to mid-interventricular septum and RV insertion points or diffuse patchy LGE Myocarditis Lateral, typically inferolateral or inferior wall with a mid-wall to subepicardial enhancement Atypical cases of myocarditis with transmural or diffuse LGE Often concomitant LGE involvement of the pericardium Anderson-Fabry Disease Mid-wall (or subepicardial) LGE of the inferolateral wall of mid to basal LV Consider T1-Mapping: low ECV and low native T1 value of septum Sarcoidosis Basal and mid-interventricular septum but also patchy LGE ARVC Diffuse LGE of RV (and occasionally LV) wall Endomyocardial fibrosis (Loeffler’s endocarditis) Restrictive CMP with endocardial fibrotic tissue deposition of inflow tract and apex of one or both ventricles “V sign” of LGE pattern at ventricular apex, characterized by a 3-layer appearance of dark myocardium, bright thickened fibrotic endocardium, and overlying dark thrombus

False positive LGE

Septal perforator (mimicking septal basal mid-wall enhancement) RV trabeculation (contrast extending underneath the muscle mimicking septal enhancement)

References

Friedrich MG, Sechtem U, Schulz-Menger J, et al. International Consensus Group on Cardiovascular Magnetic Resonance in Myocarditis. Cardiovascular magnetic resonance in myocarditis: A JACC White Paper. J Am Coll Cardiol. 2009 Apr 28; 53(17):1475-87. Vermes E, Carbone I, Friedrich MG, Merchant N. Patterns of myocardial late enhancement: typical and atypical features. Arch Cardiovasc Dis. 2012 May; 105(5):300-8. Satoh H, Sano M, Suwa K, et al. Distribution of late gadolinium enhancement in various types of cardiomyopathies: Significance in differential diagnosis, clinical features and prognosis. World J Cardiol. 2014 Jul 26; 6(7):585-601.