Abstract

Background: Cardiac involvement sarcoidosis (CS) has increased risk of arrhythmia linked to sudden death. Cardiac sympathetic nervous (SNS) dysfunction may play an important role for these events. However, the association between the SNS dysfunction and active inflammation or tissue fibrosis has not been studied. The aim of this study was to evaluate the left ventricle (LV) SNS dysfunction measured by C-11 hydroxyephedrine (HED) positron emission tomography (PET)/CT and its association with tissue fibrosis measured by cardiac magnetic resonance (CMR) in patients with CS and active inflammation. Methods: Eleven patients with CS based on the JMHW guidelines (1993) were enrolled. CS (age 59±16 y) and preserved LVEF (64±14 %) underwent HED PET, FDG PET, and CMR. Ten healthy controls underwent HED PET. LV wall was divided into 17 segments. Reduced HED uptake, focal FDG uptake, and late gadolinium enhancement (LGE) on CMR were defined as positive for the visual assessment. In addition, whole LV and regional HED uptake was quantitatively assessed by retention index (RI). Standard uptake value (SUV) was measured in the FDG positive segments. Results: CS had reduced global LV HED RI compared to control (0.09±0.04 vs. 0.15±0.03 %/min, P<0.001). FDG positive group (n=7) had lower global HED RI than FDG negative group (n=4) (0.065±0.027 vs. 0.130±0.040 %/min, P=0.010). In contrast, there was no significant difference in LGE positive segments numbers between the two groups (3.14±2.79 vs. 1.25±0.96, P=0.46). In segmental analysis, the percentage of abnormal segments were trend to higher in HED than LGE (P=0.19). In addition, there was no correlation between regional FDG SUV and HED RI (n=42 segments, R=-0.11, P=0.50). Conclusions: Cardiac involvement sarcoidosis with active LV inflammation and preserved LVEF showed global LV cardiac sympathetic nervous dysfunction. Denervation area was tended to be larger than tissue fibrosis. Furthermore, no association was seen between FDG uptake and HED retention index in regional level. These findings may imply that multiple factors other than inflammatory process and tissue fibrosis may be involved in the cardiac sympathetic nervous dysfunction in cardiac involvement sarcoidosis.

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