Figure 1
Twelve lead surface ECG showing sinus rhythm with low QRS voltage and QRS fragmentation, inverted T waves in V1–V2, aVL. Low-amplitude post-QRS deflections were observed in the precordial leads V4–V6, suggesting right ventricle involvement. ECG: Electrocardiogram.
Figure 2
Transthoracic echocardiography: (a) Parasternal long axis view and (b) parasternal short axis view showing localised hypertrophy in the basal IVS segment. (c) Global longitudinal strain—showing mild longitudinal dysfunction (−17.9% with a patchy distribution of abnormal areas. (d) RV-centred apical four chambers view showing diastolic RV area and (e) systolic RV area, with an RV fractional area change of 39%. (f) Tissue Doppler tricuspid S wave velocity of 10.5 cm/s showing a normal right ventricle longitudinal function.
Figure 3
Hybrid 18F-FDG PET–CMR (3 T system) prior to initiation of immunosuppressive therapy. (a) Whole-body maximum intensity projection image demonstrating heterogeneous myocardial FDG uptake, without significant extracardiac hypermetabolic foci apart from small mediastinal lymph nodes. (b) Four-chamber view cine CMR showing non-dilated left ventricle with preserved systolic function (LVEF 53%) and no regional wall motion abnormalities. (c) and (d) LGE imaging showing heterogeneous mid-wall and subepicardial enhancement involving the basal and mid-anterior and anterolateral segments, with additional involvement of the basal inferolateral wall and focal enhancement of the right ventricular free wall. (e) Parametric mapping demonstrating increased T2 values (52–53 ms) in the basal inferolateral and anterior segments, consistent with active myocardial inflammation. (f) Fused axial FDG PET–CMR images demonstrating intense, heterogeneous FDG uptake in the inferolateral and anterior walls, basal interventricular septum and right ventricular free wall, co-localising with regions of LGE, confirming active inflammatory cardiomyopathy. 18F-FDG, l8F-fluorodeoxyglucose; LGE: Late gadolinium enhancement; PET–CMR: Positron emission tomography–cardiac magnetic resonance.
Figure 4
Follow-up 18F-FDG PET/CT compared with baseline hybrid PET–CMR in biopsy-proven cardiac sarcoidosis. Upper panels: Follow-up FDG PET/CT performed after initiation of immunosuppressive therapy demonstrating marked reduction of previously observed heterogeneous myocardial FDG uptake, with near-complete resolution of focal hypermetabolic activity. Lower panels: Baseline hybrid FDG PET–CMR prior to treatment showing intense, heterogeneous myocardial FDG uptake involving the anterior, inferolateral, basal interventricular septal and right ventricular free wall segments. Structural abnormalities with LGE identified on baseline CMR persisted despite metabolic remission, consistent with residual myocardial fibrosis. 18F-FDG, 18F-fluorodeoxyglucose; LGE: Late gadolinium enhancement; PET–CMR: Positron emission tomography–cardiac magnetic resonance.