Myocardial Late Gadolinium Enhancement (LGE) in Cardiac Magnetic Resonance Imaging (CMR)-An Important Risk Marker for Cardiac Disease

Abstract

Cardiovascular magnetic resonance (CMR) has significantly revolutionized the comprehension and diagnosis of cardiac diseases, particularly through the utilization of late gadolinium enhancement (LGE) imaging for tissue characterization. LGE enables the visualization of expanded extracellular spaces in conditions such as fibrosis, fibrofatty tissue, or edema. The growing recognition of LGE's prognostic capacity underscores its importance, evident in the increasing explicit recommendations within guidelines. Notably, the contemporary characterization of cardiomyopathies relies on LGE-based scar assessment by CMR to a large extent. This review describes the pattern and prognostic value of LGE in detail for various cardiac diseases. Despite its merits, establishing LGE as a reliable risk marker encounters challenges. Limitations arise from the fact that not all diseases show LGE, and it should always be analyzed in the context of all CMR sequences and the patient's medical history. In summary, LGE stands as a robust indicator of adverse outcomes in diverse cardiovascular diseases. Its further integration into routine practice is desirable, necessitating widespread availability and application to accumulate both individual and scientific experience.

Keywords: cardiac magnetic resonance imaging; cardiomyopathy; late gadolinium enhancement; myocardial vitality; review; risk stratification.

Figure 1

Scheme of typical LGE patterns in short axis view, T1-weighted inversion recovery sequence; black: myocardium without LGE, white: LGE. Please note: the distribution pattern may vary within certain limits and should only be assessed in the context of patient’s history and the whole CMR examination. (A): Transmural ischemic scar with myocardial thinning as consequence of RCA-Infarction. (B): Non-transmural ischemic scar as consequence of LAD-infarction. (C): Myocarditis with subepicardial inferolateral LGE. (D): Classical hypertrophic cardiomyopathy with LGE at the RV insertions and in the area of greatest hypertrophy. (E): Dilated cardiomyopathy with a fine line of intramural septal LGE. (F): Non-dilated cardiomyopathy with ring-like LGE and a septal intramural and lateral epicardial distribution. (G): Classical ARVC with right ventricular dilatation and aneurysms with LGE. (H): Cardiac amyloidosis with strong LGE originating from the subendocardium in the hypertrophied LV and RV myocardium. (I): Anderson–Fabry disease with mild intramural to subepicardial inferolateral LGE and hypertrophy. Note: relatively frequent, unspecific pattern, also possible with increasing pressure load or as post-inflammatory residual. Additional T1 mapping sequences required for differentiation. (J): Endomyocardial fibrosis with LGE in the thickened endocardium, here without thrombosis. (K): Cardiac sarcoidosis with patchy subendocardial, subepicardial or transmural distribution, anterior “Hook-sign” and inferior “Triangle sign” in place of the RV insertions. (L): Cardiac involvement in muscular dystrophy Duchenne with subepicardial lateral LGE in thinned myocardium. Note: also possible in DCM of other origin.

Figure 2

Illustrative examples of LGE in important cardiac diseases: (A): Patient with s/p ST-Elevation myocardial infarctions in anterior and inferolateral location with LGE >50% of myocardial wall thickness. (B): Patient with s/p non-ST-Elevation myocardial infarction in anterior location with subendocardial LGE < 50% of myocardial wall thickness. (C): Patient with viral myocarditis and patchy lateral LGE. (D): Patient with hypertrophic cardiomyopathy (HCM) and septal LGE in the area of greatest hypertrophy.