Key result
Short-term discontinuation of vagal nerve stimulation did not significantly alter arterial wall 18F-FDG-uptake (SUVmax 1.8 vs 1.7, p=0.051), but significantly increased insulin levels.
Why the study?
Because vagus nerve activation impacts inflammation, the authors hypothesized that vagal nerve stimulation influenced arterial wall inflammation measured by 18F-FDG uptake.
Does short-term discontinuation of vagal nerve stimulation alter arterial wall inflammation measured by 18F-FDG uptake in patients with refractory epilepsy?
Does short-term discontinuation of vagal nerve stimulation alter arterial wall inflammation measured by 18F-FDG uptake in patients with refractory epilepsy?
Absolute Event Rate: 1.8% vs 1.7%
p-value: p=0.051
Short-term discontinuation of vagal nerve stimulation alters insulin and 18F-FDG blood levels, complicating the assessment of its direct effects on arterial wall inflammation using 18F-FDG PET/CT.
No consistent arterial 18F-FDG change after short-term VNS discontinuation; hypothesis-generating for VNS effects on vascular inflammation and glucose metabolism.
Background Vagus nerve activation impacts inflammation. Therefore, we hypothesized that vagal nerve stimulation (VNS) influenced arterial wall inflammation as measured by 18F-FDG uptake. Results Ten patients with left-sided VNS for refractory epilepsy were studied during stimulation (VNS-on) and in the hours after stimulation was switched off (VNS-off). In nine patients, 18F-FDG uptake was measured in the right carotid artery, aorta, bone marrow, spleen, and adipose tissue. Target-to-background ratios (TBRs) were calculated to normalize the respective standardized uptake values (SUVs) for venous blood pool activity. Median values are shown with interquartile range and compared using the Wilcoxon signed-rank test. Arterial SUVs tended to be higher during VNS-off than VNS-on [SUVmax all vessels 1.8 (1.5–2.2) vs. 1.7 (1.2–2.0), p = 0.051]. However, a larger difference was found for the venous blood pool at this time point, reaching statistical significance in the vena cava superior [meanSUVmean 1.3 (1.1–1.4) vs. 1.0 (0.8–1.1); p = 0.011], resulting in non-significant lower arterial TBRs during VNS-off than VNS-on. Differences in the remaining tissues were not significant. Insulin levels increased after VNS was switched off [55.0 pmol/L (45.9–96.8) vs. 48.1 pmol/L (36.9–61.8); p = 0.047]. The concurrent increase in glucose levels was not statistically significant [4.8 mmol/L (4.7–5.3) vs. 4.6 mmol/L (4.5–5.2); p = 0.075]. Conclusions Short-term discontinuation of VNS did not show a consistent change in arterial wall 18F-FDG-uptake. However, VNS did alter insulin and 18F-FDG blood levels, possibly as a result of sympathetic activation.
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Boswijk et al. (2019) studied Refractory epilepsy (n=10). Short-term discontinuation of vagal nerve stimulation vs. Active vagal nerve stimulation (VNS-on) was evaluated on Arterial wall 18F-FDG uptake (SUVmax all vessels) (p=0.051). Short-term discontinuation of vagal nerve stimulation did not significantly alter arterial wall 18F-FDG-uptake (SUVmax 1.8 vs 1.7, p=0.051), but significantly increased insulin levels.
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