Noninvasive Vagus Nerve Stimulation in Postural Tachycardia Syndrome, 2023, Stavrakis et al

Noninvasive Vagus Nerve Stimulation in Postural Tachycardia Syndrome: A Randomized Clinical Trial

Stavros Stavrakis et al

"Abstract

Background
Low-level transcutaneous stimulation of the auricular branch of the vagus nerve at the tragus is antiarrhythmic and anti-inflammatory in animals and humans. Preliminary studies show that transcutaneous vagus nerve stimulation (tVNS) is beneficial in animal models of postural tachycardia syndrome (POTS).

Objectives
We conducted a sham-controlled, double-blind, randomized clinical trial to examine the effect of tVNS on POTS over a 2-month period relative to sham stimulation.

Methods
tVNS (20 Hz, 1 mA below discomfort threshold) was delivered using an ear clip attached to either the tragus (active; n = 12) or the ear lobe (sham; n = 14) for 1 hour daily over a 2-month period. Postural tachycardia was assessed during the baseline and 2-month visit. Heart rate variability based on 5-minute electrocardiogram, serum cytokines, and antiautonomic autoantibodies were measured at the respective time points.

Results
Mean age was 34 ± 11 years (100% female; 81% Caucasian). Adherence to daily stimulation was 83% in the active arm and 86% in the sham arm (P > 0.05). Postural tachycardia was significantly less in the active arm compared with the sham arm at 2 months (mean postural increase in heart rate 17.6 ± 9.9 beats/min vs 31.7 ± 14.4 beats/min; P = 0.01). Antiadrenergic autoantibodies and inflammatory cytokines were lower in the active arm compared with the sham arm at 2 months (P < 0.05). Heart rate variability was better in the active arm. No device-related side effects were observed.

Conclusions
Our results support the emerging paradigm of noninvasive neuromodulation to treat POTS. Mechanistically, this effect appears to be related to reduction of antiautonomic autoantibodies and inflammatory cytokines, and improvement in autonomic tone. Further studies are warranted. (Autoimmune Basis for Postural Tachycardia Syndrome; NCT05043051 )."

https://www.sciencedirect.com/science/article/abs/pii/S2405500X2300806X

 

Vagus Nerve Stimulation Reduces Orthostatic Tachycardia in Women

https://www.neurologyadvisor.com/to...imulation-orthostatic-tachycardia-women-pots/

 

Can't read this, but I'd like to know how they measured antiadrenergic autoantibodies since for Celltrend at least it's known there's no difference in the levels of POTS patients and healthy controls.

Isn't it also kind of obvious whether you're getting the placebo or the real thing since one is applied to the ear lobe and the other to the tragus. Wouldn't that destroy the purpose of the trial?

 

If participants were aware that only the tragus was suppose to have vagus nerve fibres then yes the whole thing is a nonsense. There is no sham if the sham is recognisable as the sham.

 

The authors say "The ear lobe, which is devoid of vagal innervation, was chosen as the site of stimulation in the sham group. Patients were unaware which site provides active stimulation to achieve blinding of treatment allocation." Seems like any participant with the ability to search the internet could have figure it out the treatment placement though.

The average heart rate increase in the baselines for both the control and active groups was less than 30 bpm. Based on the definition of POTS it seems like most participants did not in-fact fulfill POTS criteria. Why would they have chosen patients who didn't fulfill all the criteria on their baseline tests?

 

Agree and I know they're looking at "POTS", but I think the physiology of orthostatic intolerance is inadequately understood and being suboptimally assessed. This probably relates to the current insistence by cardiologists seeing LC/ME patients, that exercise is the cure for POTS in all cases. They don't seem to recognise the possibility of PEM. What's actually going on in the cardiovascular system as a whole needs to be much better understood. This leads to statements such as "Of course you're feeling fatigued, your heart is beating too fast. If you increase your exercise and reduce your heart rate the fatigue will go away." When talking to amateur or professional athletes that now can't climb up their own stairs, this is ridiculous.

Any study into orthostatic intolerance needs to focus on the more important physiological parameter: cerebral blood flow. Heart rate would seem to be a poor proxy for this in sufficient cases to limit the usefulness of the results.

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Cerebral blood flow is reduced in ME/CFS during head-up tilt testing even in the absence of hypotension or tachycardia: A quantitative, controlled study using Doppler echography (2020, Clinical Neurophysiology Practice)

Worsening Symptoms Is Associated with Larger Cerebral Blood Flow Abnormalities during Tilt-Testing in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome ME/CFS (2023, Medicina)

Cerebral Blood Flow Is Reduced in Severe Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients During Mild Orthostatic Stress Testing: An Exploratory Study at 20 Degrees of Head-Up Tilt Testing (2020, Healthcare)

Cerebral blood flow remains reduced after tilt testing in myalgic encephalomyelitis/chronic fatigue syndrome patients (2021, Clinical Neurophysiology Practice)

 

This has always been bizarre to me. When I first got sick I had a Vo2 max in the mid to high 70s (as a lightweight rower). Now that I have ME and POTS my cardiologist asked me to get on the rowing machine for a few minutes a day even though I had an elite level of fitness when I first got sick and that didn't seem to help.

The obsession with heart rate itself is also puzzling. Its clearly not the fact that my heart rate is elevated that is the issue. When training my heart rate would often be above 150 for a couple hours and I felt far less fatigued after that than I do now. Given I'm on ivabradine I'm sure my heart rate on average is actually lower now than it was before but I still have both ME and POTS. It is a little amusing seeing the Cardiologist torn between his beliefs regarding POTS and my presentation of the condition