case_images: PMC10763246_01
case_images: LGE CMR frames in short-axis (A) and 4-chamber (B)-views demonstrating striated midwall fibrosis of the septal LV wall (arrows). Ejection fraction was mildly impaired (LVEF 47%). (C) Axial-view of 18FDG-PET follow-up revealing tracer uptake in the LV Septum (arrows). (D) 18FDG-PET follow-up under immunosuppressive therapy with glucocorticoids (GC) showing no more tracer uptake indicating no cardiac inflammation under GC.
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case_images: F1
case_images: A cardiovascular magnetic resonance (CMR) demonstrated a mildly impaired left ventricular ejection fraction (LVEF 47%) and striated intramyocardial fibrosis areas (Figures 1A,B), which was interpreted as pulmonary sarcoidosis with cardiac involvement in fibrotic, indolent stage. The 18FDG-PET follow-up scan after 6 months revealed tracer uptake in the LV septum (Figure 1C) and mediastinal lymph nodes, indicating active sarcoidosis despite the GC treatment. The subsequent 18FDG-PET scan showed a decreased lymph node inflammation and no cardiac inflammation (Figure 1D).
case_images: PMC10763246_02
case_images: ECG before (A) and after (B) Ajmalin provocation test unmasking coved-type ST segment elevation in V1 suggesting BrS. (C) Contrast-enhanced CT showing small, irregular foci in both lungs compatible with pulmonary sarcoidosis stage 3. LGE CMR frame in short-axis - view (D) revealing subendocardial to intramyocardial LGE in the basal septal and inferolateral LV wall and the entire right ventricular posterior wall (arrows), LVEF was mildly impaired (41%) with normal-sized heart chambers.
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case_images: PMC10763246_02_fcvm-10-1328802-g002.jpg
case_images: F2
case_images: T-waves (Figures 2A,B), suggesting the Brugada syndrome. To exclude the presence of structural heart disease, a CMR was performed 2 days after the Ajmaline provocation test was conducted, revealing an impaired LVEF of 41% with normal-sized heart chambers. Furthermore, late gadolinium enhancement (LGE) was observed in the subendocardial to intramyocardial regions of the basal septal and inferolateral LV wall, as well as the entire posterior wall of the right ventricle (Figure 2D). A contrast-enhanced CT showed small, irregular parenchymal foci dispersed in both lungs without evidence of mediastinal lymphadenopathy or fibrosis (Figure 2C).
case_images: PMC10763246_03
case_images: CMR showed simultaneously occurring edematous and fibrosing processes. (A) CMR, T2-weighted black blood imaging in short - axis view demonstrating regional edema of the LV anterolateral wall. (B) LGE CMR frame in 4-chamber view showing LV hypertrophy and anterolateral LGE, LVEF was mildly reduced (43%). 18FDG-PET coronal (C) and axial (D) views revealing intense FDG uptake in septal and lateral LV.
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case_images: F3
case_images: Repeated CMR scans confirmed the presence of concentric LV hypertrophy, reduced LVEF (43%), and anterolateral LGE (Figure 3B). T2 mapping demonstrated regional edema of the LV anterolateral wall (Figure 3A) and raised the suspicion of CS in (sub)acute inflammatory stage. The 18FDG-PET scan showed intense LV septal and lateral FDG uptake (Figures 3C,D), without evidences of extracardiac involvement. The coronary angiography ruled out relevant stenosis, and EMB were taken from the interventricular septum.
case_images: PMC10763246_04
case_images: CMR cine images in 4-chamber (A) and short-axis - views (B) revealing right ventricular dilatation with bulging (arrows) and regional dyssynchrony in end-systolic phase. Right ventricular systolic function was mildly reduced (RV EF 42%). CMR 3-chamber view of the RV (C) demonstrating fatty spots. (D) T1-weighted black blood spin CMR showing fatty replacement of the RV free wall.
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case_images: F4
case_images: The CMR revealed a dilated right ventricle with regional dyssynchrony and moderately decreased right ventricular ejection fraction of 42% (Figures 4A-D).