143 Table 2 Symptoms of patients with sarcoidosis analyzed for cardiac autonomic dysfunction subdivided in normal and abnormal [123I]-meta-iodinebenzylguadine ([123I]MIBG) scintigraphy. Total group (n=46) [123I]MIBG normal (n=26) [123I]MIBG abnormal (n=20) Abnormal ECG % (n) 47 (21) 58 (15) 30 (6) Palpitations % (n) 52 (24) 54 (14) 50 (10) Dizziness % (n) 44 (20) 46 (12) 40 (8) Pain on the chest % (n) 30 (14) 27 (7) 35 (7) Arrhythmia % (n) 17 (8) 23 (6) 10 (2) Collapse % (n) 9 (4) 4 (1) 15 (3) Abnormal ergometry % (n) 9 (4) 15 (4) 0 (0) Near collapse % (n) 7 (3) 8 (2) 5 (1) Autonomic dysfunction of other organs % (n) 4 (2) 4 (1) 5 (1) Syncope % (n) 2 (1) 4 (1) 0 (0) LVEF abnormal % (n) 2 (1) 0 (1) 5 (1) Orthostasis % (n) 2 (1) 4 (1) 0 (0) LVEF: left ventricular ejection fraction. Comparing abnormal vs normal [123I]MIBG scans all p’s were > 0.05 (not significant). Eighty percent (n=16) of patients with an abnormal [123I]MIBG scintigraphy indicative of SCAD started therapy with carvedilol, and 14 of these patients (88%) experienced a subjective improvement in their symptoms. However, of the patients taking carvedilol, 50% experienced side effects that required discontinuation of treatment. These side effects included dizziness, fatigue, nausea, dry mouth, headache and muscle ache. Discussion This retrospective study highlights the potential role of [123I]MIBG scintigraphy in identifying SCAD in patients with symptoms suggesting cardiac involvement. Our data demonstrated that while only 5% of a large cohort of patients analyzed for cardiac sarcoidosis also underwent [123I]MIBG scintigraphy, we were able to diagnose SCAD in 44% of patients in this particular group. This finding suggests that SCAD in sarcoidosis patients with cardiac symptoms may be underdiagnosed in routine clinical practice. Although current cardiac sarcoidosis guidelines highlight the significance of using FDG PET/CT and CMR in diagnosing patients suspected of cardiac sarcoidosis,7 they provide no clear recommendations for addressing unexplained functional symptoms when CMR and FDG PET/CT are unremarkable. This underlines the need for further studies to explore the therapeutic potential of addressing SCAD. In our study, we did not find differences between presenting symptoms in patients diagnosed with cardiac sarcoidosis, SCAD, or those who had normal findings on CMR, FDG PET/CT and [123I]MIBG scintigraphy. Even more intriguingly, we were able to diagnose SCAD in a small group of patients already diagnosed with cardiac sarcoidosis based on the current guidelines. In our opinion, this has two important implications for the management of patients with symptoms suggesting cardiac sarcoidosis. First, as symptoms cannot differentiate between cardiac sarcoidosis and SCAD, we should consider a diagnosis of SCAD in all patients screened for cardiac sarcoidosis with normal CMR and FDG PET/CT. Second, in patients with cardiac sarcoidosis and therapy-refractory symptoms, the presence of SCAD cannot be ruled out. The fact that, in almost half of all patients with a [123I]MIBG scintigraphy, a diagnosis of SCAD was established suggests that SCAD is underdiagnosed in daily clinical practice. 9 149 9
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