Focus on Autoimmune Myocarditis in Graves' Disease: A Case-Based Review

Figures

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  Figure 1. The changing trend of the high-sensitivity cardiac troponin I (hs-cTnI) during her hospitalization. The arrow indicates the times when the patient accepts glucocorticoid treatment.

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  Figure 2. (A) The 12-lead standard ECG only showed the poor progression of R waves in V1–V3. (B) A 24-h Holter ECG captured the occasional premature ventricular contractions.

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  Figure 3. (A) Representative late gadolinium enhancement (red arrow) in the left ventricular anterior wall under T1 imaging (long axis). (B) An enhancement signal (red arrow) appeared in the inferior wall and inferolateral wall of the middle segment of the left ventricle under T2 mapping (short axis). (C) An enhanced signal (red arrow) appeared in the interventricular septum in T2 black blood fat suppression sequences (short axis).

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  Figure 4. Overview of the possible mechanisms of hyperthyroidism-induced myocarditis. Both genomic and non-genomic actions contribute to the development of Graves' disease-induced myocarditis. Genomic actions mainly refer to binding to TH response elements in the promoter regions of TH-responsive genes. Non-genomic actions include high dynamic damage, ion channel alteration, and auto-attack from autoantibodies. All lead to a complex cascade of inflammation and sustained destruction of the heart muscle in the acute phases. In the chronic stage, fibrous repair, and structural remodeling are the main changes.

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  Figure 5. Representative heart sections of dexamethasone-treated autoimmune myocarditis induced by α-MHC immunization (α-MHC+). Establishment and treatment methods: in 0 and 7 days, respectively, 300 μg α-MHC (Ac-RSLKLMATLFSTYASADR-OH) was subcutaneously injected into BALB/C mice. Then, 0.75 mg/kg/day dexamethasone was given for intervention on the 16th to 20th day via intraperitoneal injection. The mice were sacrificed and their hearts were fixed with formalin for H&E staining on day 21.