PMC9887667_01
Comparison of electrocardiographic findings at the time of diagnosis (A/B) and approximately one year after initiation of combined steroid and immunosuppressant therapy (C/D). Limb (A) and precordial leads (B) of a 12-lead electrocardiogram at the time of diagnosis showing a normal heart rate (70 b.p.m.), sinus rhythm with first-degree atrioventricular block, right bundle branch block, and left anterior hemi-block. Approximately one year after initiation of combined steroid and immunosuppressant therapy, as well as implantation of a dual-chamber pacemaker-defibrillator, the limb (C) and precordial leads (D) of a follow-up electrocardiogram show a normal heart rate (67 b.p.m.), sinus rhythm with persistence of the right bundle branch block but recovery of the first-degree atrioventricular block and left anterior hemi-block.
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Preceding admission to our clinic, an electrocardiogram performed by her cardiologist revealed complex conduction abnormalities, including a right bundle branch block, left anterior hemi-block, and atrioventricular block 1 (Figure 1A and B). However, partial recovery of our patient's conduction abnormalities, including the  1 AV-block and left anterior hemi-block, could be noted in an electrocardiographic follow-up approximately one year after initiation of treatment (Figure 1C and D).
Course of the disease as monitored by sequential 18F-FDG-PET-CT scans. Maximum intensity projection (MIP) images (A-C) illustrate the overall 18F-FDG uptake of different organs. At time of diagnosis, (A) hypermetabolic lesions, showing as darker areas on MIP images, were identified in the myocardium, pulmonary trunk, lung, liver, spleen, various lymph nodes, and the spine. Consequential 18F-FDG-PET-CT scans indicate minimal response to treatment with prednisolone and cyclophosphamide after 4 months (B) but an almost full regression after 9 months (C). Hypermetabolic myocardial lesions, indicative of cardiac sarcoidosis, were found along the septum (D-F), as well as the anterior wall of the heart (G-I) and exhibited a similar response to treatment, with almost full regression reached after 9 months of treatment. In contrast, full regression could be reached after only 4 months of treatment in the hypermetabolic lesions found in proximity to the pulmonary trunk (J-L).
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Subsequently, positron emission tomography with 18F-fluorodeoxyglucose integrated with computed tomography (18F-FDG-PET-CT) was performed to screen for hypermetabolic lesions, which indicate active inflammation (Figure 2A, D, G, and J). In contrast, a control 18F-FDG-PET-CT indicated that most sarcoid lesions remained morphologically and metabolically unchanged at that time point (Figure 2B, E, H, and K). Eventually, a second control 18F-FDG-PET-CT performed 9 months after treatment initiation (Figure 2C, F, I, and L) indicated good overall response with full regression of lymph node and osseous lesions and slight residual activity at most in anteroseptal regions of the heart and in the liver.