Does anyone know more about this study? From the description it sounds as if the change in endothelial function is seen quickly, unlike the 2-day CPET where a delay of 24 hours is required to see changes on the second test. This would make repeated EndoPET with exercise in between a superior diagnostic test, that is probably also much better tolerated. https://twitter.com/user/status/1595891804280233984
Bateman Horn centre are currently researching this with OMF https://www.s4me.info/threads/usa-news-from-the-bateman-horne-center.24836/#post-448585
This does need to be researched. I am glad someone seems to be doing that. However we don't know how reliable it is in ME for most patients. Yet. I hope it works. I expect most such tests, investigations etc. will fail. Until one doesn't, and then passes more extensive trials. Will that be this one? Now it does raise a possibility it shows something is wrong in a subset of us. Is it 1%, 50%, 99%? That is why we need testing. We also need the underlying physiological changes to be further investigated. Other studies have shown results suggestive of endothelial dysfunction, including NO synthesis deficits and if I recall correctly an enhanced acetylcholine response. Endothelial function is not fully covered by a single test. Also the current test might be better than the old test, presuming its been updated.
But I haven't heard many people going for a 2-day CPET. They go for an ICPET instead, which does not require 24 hours. I do not think a repeated EndoPAT test would give you more information than an ICPET does. If you are going to require exertion from the patient anyway, may as well as capture everything. As far as endothelial function tests go, I find the EndoPAT interesting, but my favorite one is the Iontophoresis (https://www.perimed-instruments.com/content/periiont-for-laser-doppler-flowmetry/),which can be used, at least in theory to, to figure out what drugs can help mitigate it. They used a long time ago in low-flow POTS patients, and found out there is impaired NO vasodilation (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4511487/). Attaching a picture showing POTS patients compared to controls. Unfortunately, it seems to have hit a dead-end as a diagnostic tool.
Is the enhanced acetylcholine response a compensation for a sub-par NO response? If I recall correctly, NO and acetylcholine affect different muscle types. So would an altered acetylcholine/NO balance differentially affect muscle types, possibly disrupting the balance of mechanical forces within the body, and mechanically stressing other anatomy? Could the consequences of that be an non-invasively measurable mechanical change (albeit subtle) to the patient's body?