Insertion point LGE favors cardiac sarcoidosis, while extensive right ventricular transmural LGE suggests giant cell myocarditis or ARVC; LGE patterns differ by disease.
Can cardiac magnetic resonance parameters and late gadolinium enhancement patterns differentiate between cardiac sarcoidosis, giant cell myocarditis, and arrhythmogenic right ventricular cardiomyopathy?
Cardiac magnetic resonance reveals distinct patterns of late gadolinium enhancement and structural changes that can help differentiate cardiac sarcoidosis, giant cell myocarditis, and arrhythmogenic right ventricular cardiomyopathy.
Absolute Event Rate: 0% vs 0%
Abstract Objective: Diagnosing cardiac sarcoidosis (CS), giant cell myocarditis (GCM), and arrhythmogenic right ventricular cardiomyopathy (ARVC) is difficult because all 3 cardiomyopathies can involve both the right and left ventricles, leading to arrhythmias and heart failure. Notably, the extent and pattern of late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) for each condition remain poorly characterized which further complicates their differentiation. This study aimed to evaluate the diagnostic efficacy of CMR parameters to improve the accuracy of their differential diagnosis. Methods: Twelve patients with CS, 8 with GCM, and 30 with ARVC in Fuwai Hospital who underwent CMR between July 2011 and May 2024 were retrospectively analyzed in this study. Cardiac structure, function, and scar quantification were performed on a post-processing software. LGE in the left ventricle was visually classified by layer: subepicardial, intramural, transmural, and subendocardial. Left ventricle segmentation followed the American Heart Association 17-segment model. Results: Patients with CS had the greatest left ventricular mass compared to those with GCM or ARVC (111.2 (84.7, 155.8)g vs . 77.3 (63.6, 103.5)g vs . 64.4 (54.3, 81.4)g, P = 0.002). Meanwhile, those with ARVC had the largest right ventricular dimension and outflow tract ( P < 0.001), along with the most extensive right ventricular global longitudinal strain impairment compared with the CS or GCM group (−6.1% ± 4.9% vs . −14.8% ± 7.3% vs . −11.9% ± 4.9%, P < 0.001). CS patients presented with more LGE in the insertion area and less LGE in the right ventricular free wall than GCM and ARVC (all P < 0.001). The left ventricular layers showing the greatest vulnerability varied by condition: subepicardial for CS, subendocardial for GCM, and transmural for ARVC (all P < 0.02). Patients with CS and GCM presented with more extensive LGE than those with ARVC in the septal and anterior wall segments at the basal (segments 1–3) and mid-cavity (segments 7 and 8) levels of the left ventricle (all P < 0.05). However, at the apical level, patients with CS had less fibrotic involvement in segment 14 than patients with GCM or ARVC ( P = 0.039). Conclusion: The 3 cardiomyopathies differed in the pattern and extent of lesion involvement. Insertion point enhancement favors a diagnosis of CS. More extensive right ventricular transmural LGE should prompt consideration of GCM or ARVC. At the basal and mid-cavity levels, the extent of LGE in anteroseptal segments was significantly reduced in patients with ARVC relative to that in patients with CS or GCM.
Tang et al. (Wed,) reported a other. Insertion point LGE favors cardiac sarcoidosis, while extensive right ventricular transmural LGE suggests giant cell myocarditis or ARVC; LGE patterns differ by disease.