Impaired Endothelial Function in Patients With Postural Tachycardia Syndrome, 2021, Abby H Chopoorian

https://pubmed.ncbi.nlm.nih.gov/33486983/


A research team led by finds endothelial dysfunction plays a key role in postural tachycardia syndrome, leading the way toward targeted treatment for this poorly understood condition.

https://discover.vumc.org/2021/04/endothelial-dysfunction-in-postural-tachycardia-syndrome/

 

So the bit of blood vessels that affects how/allows blood vessels respond to change in demand is implicated in a condition where it is thought that demand/response isn't being controlled correctly?

Is it just me?

Shouldn't they have confirmed this very likely scenario.....like 50 years ago?

 

An uneducated guess, but my understanding is this study is in the same ballpark, or maybe even the same row in the stadium? It's from 2005:



"Circulation. 2005 Oct 25; 112(17): 2611–2618.
Published online 2005 Oct 17. doi: 10.1161/CIRCULATIONAHA.104.526764
PMCID: PMC4511487
NIHMSID: NIHMS708540
PMID: 16230486
Decreased Microvascular Nitric Oxide–Dependent Vasodilation in Postural Tachycardia Syndrome
Marvin S. Medow, PhD, Christopher T. Minson, PhD, and Julian M. Stewart, MD, PhD......



Background
One variant of postural tachycardia syndrome (POTS), designated low-flow POTS, is associated with decreased peripheral blood flow related to impaired local vascular regulation."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4511487/


Seeing this study was published in 2005, and the leader for this thread was published in 2021 causes me to echo @Wonko, and the frustration that science is indeed very slow. How many people with POTS could be helped if there could a breakthrough in this area, instead of just resorting to extra hydration, salt and maybe steroids that work for a while, perhaps have side effects etc.? I find OI one of the top debilitating symptoms.

 

Thank you @Mij for posting this study. It is hopeful researchers are looking at this part of the chain.

 

I wonder if the lesser amount of dilation in patients correlated to higher blood pressure on standing. You'd think more blood trying to get through a less dilated blood vessel might do that. It's also not clear from the abstract if there were differences in vessel diameters in patients and controls prior to standing. It seems like you'd want to know if there were absolute baseline differences in vessel diameter between patients and controls before they were stressed by standing. The percentage differences between patients and controls after standing might be on top of greater constriction in patients prior to standing (in other words, it could be even worse than it looks). I'm not sure how easy it is to establish baseline blood vessel diameters, though. They might vary due to body size, gender and other variations.