The problems with POTS - ME/CFS Skeptic blog

I've written an overview of the problems with Postural Orthostatic Tachycardia Syndrome (POTS) criteria.
https://mecfsskeptic.com/the-problems-with-pots/

A brief summary of the arguments looks like this:

• A heart rate increase of 30 bpm (or 40 bpm in 12–19-year-olds) is far from abnormal. Many young and healthy people without OI symptoms also have this. This suggests that POT is not pathologic and not a good marker of underlying disease processes.
• Most people with OI do not have POT. Only a minority of patients with OI symptoms has tachycardia upon standing.
• The relationship between POT and OI is weak. Symptom severity often correlates poorly with the magnitude of postural tachycardia. Increasing the threshold to a value higher than 30 bpm is therefore unlikely to solve the problem.
• Low reproducibility: POT measurements vary and are influenced by many factors including water intake, time of day, deconditioning, etc.

Would be interested in hearing other people's thoughts on this and what the implications are for POTS criteria.

 

Here's the summary I've posted on Twitter:
https://twitter.com/user/status/1806689605422326098


1) A new blog post about the problems with Postural Orthostatic Tachycardia Syndrome (POTS) criteria.

It’s quite a long read, so I’ll try to summarize the main ideas in this thread.


2) ARGUMENT 1: heart rate increases upon standing > 30 bpm are far from abnormal. In this study of the general population, for example, more than half of healthy young adults had an increase higher than the POTS threshold.

https://pubmed.ncbi.nlm.nih.gov/31476713/


3) Other studies found similar results. In the one below the median heart rate increase was 28 bpm in 120 participants aged 14 to 76 years.

https://journals.physiology.org/doi/full/10.1152/japplphysiol.00292.2013


4) In a German study the mean HR increase after 2 minutes of standing was 29 bpm. “In comparison with the previously published diagnostic limits for POTS, the reference values based on our population appeared to be higher”

https://pubmed.ncbi.nlm.nih.gov/8924754/


5) We see the same results in adolescents: the 40 bpm threshold is not very abnormal either. In the study below 10% had an HR increase above 39 bpm, and 2.5% above 52.7 bpm.

https://www.jpeds.com/article/S0022-3476(11)00884-5/abstract


6) Another study examined 307 public high school students and found that the 97.5 percentile was not 40 but 48 bpm. An older study from Hawaii reported that “a healthy adolescent may have an orthostatic heart rate increase of 40 to 50 beats per minute.”

https://jamanetwork.com/journals/jamapediatrics/article-abstract/516241

https://journals.sagepub.com/doi/10.1177/0883073809359539


7) The reference data used to justify the 30-bpm threshold comes from POTS pioneers Dr. David Streeten and Dr. Philip Low in the 1980s and 1990s. However, they used shorter test durations (1-3 minutes) and did not adjust for age differences.


8) ARGUMENT 2: Most people with orthostatic intolerance (OI) do not have POT, whether you look at ME/CFS, Long Covid or patients referred to an autonomic clinic. in ME/CFS the majority of patients (62-92%) have OI symptoms while only a minority (ca. 20%) has POTS.


9) ARGUMENT 3: The correlation between POT and OI is weak. Symptom severity often correlates poorly with the magnitude of postural tachycardia.


10) One study of the general population, for example, found that: “there was no significant correlation between […] heart rate increment on HUT [Head-Up Tilt] and symptoms of orthostatic intolerance.”

https://pubmed.ncbi.nlm.nih.gov/23766503/


11) Another study noted: “One cannot predict which seemingly healthy adolescents will have high heart rate changes based on orthostatic symptoms.”

https://journals.sagepub.com/doi/10.1177/0883073809359539


12) Other studies divided OI patients into those that met the heart rate threshold of POTS and those that didn’t and found no significant difference: “There are […] no clinical differences between patients as a function of HR increase during standing”

https://pubmed.ncbi.nlm.nih.gov/31385108/


13) Some ME/CFS studies also report that “orthostatic tachycardia did not account for OI symptoms in CFS” or that “POT was not associated with OI to an appreciable extent.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6547462/

https://www.sciencedirect.com/science/article/pii/S2590086220300094


14) Because of the weak correlation, moving the threshold likely won’t help much.

One study found that moving it to 38 bpm would still mean that 27% of healthy controls would still exceed it while 20% of POTS patients would no longer meet it.

https://pubmed.ncbi.nlm.nih.gov/22931296/


15) ARGUMENT 4: Heart rate increases after standing are influenced by many factors including sleep, salt and fluid intake, and deconditioning. There is almost no data on reproducibility.


16) Some studies suggest that a single test is not reliable. An ME/CFS study found that of the 7 patients who had POTS on a good day, 4 (55%) did not have it on a bad day. Of the 17 patients who did not have POTS on a good day, 8 (47%) had it on a bad day

https://pubmed.ncbi.nlm.nih.gov/26374335/


17) For a more thorough discussion, see the blog.

Did you spot errors or find data that contradicts some of the statements in this blog? Feel free to contact me (mecfsskeptic@yahoo.com). Thanks in advance!

 

I have been having trouble keeping up with all the posts on the recent OI/POTs threads, so it's nice to have some things summarized in one article. Thanks

 

Thank you

 

This is an important point that I rarely see addressed. For instance, the Bateman Horne Center’s protocol for the NASA lean test calls for “limit[ing] extra fluid and sodium intake[, not wearing] compression socks, and alter[ing] the intake of medications that might influence the test” but at Cardiozorg, the Dutch ME/CFS clinic ran by Prof Visser and Dr van den Campen, patients are asked to eat normally and to drink a lot before the test.

Besides reproducibility between studies, in my experience, a tilt test does not necessarily reproduce POT as it happens in the conditions of daily life. I underwent one in 2021 for which I withheld water, salt and midodrine for 2 days prior and came in fasted — my HR doubled from 55 to 110 BPM over 5 minutes with a stable blood pressure, then I fainted. However, I had never fainted prior to the test and even though I had pre-syncopal symptoms / lipothymia, I could keep them at bay by consuming enough salt, water and food, as I normally would. Also, while I always wore robust medical grade compression thighs (French class 3 / 36 mmHg) at the time, orthostatic challenges in daily life made my HR shoot up higher than it did during the test — usually 120 BPM when I stood up for too long and 150 BPM when I walked outdoors, with a recorded maximum of 166 BPM. So there was a clear discrepancy.

 

@ME/CFS Skeptic , did you see this paper from 1986? It has been referenced in recent papers as describing what would now be called POTS.

https://www.acpjournals.org/doi/10....=ori:rid:crossref.org&rfr_dat=cr_pub 0pubmed

Judging by the title, the authors thought that the hypovolemia was the most important characteristic.

Who knows, if blood volume testing hadn’t become scarce in recent decades, hypovolemia might be in the diagnostic criteria, and POTS might have a different name.

(Note: We don’t know whether everyone with POTS has hypovolemia. Not enough studies, due to the usual lack of funding and the difficulty of getting blood volume testing until now.)

 

Thanks, but blood volume is also something that is strongly impacted by bed rest and deconditioning so I suspect it would be difficult to make this part of diagnostic criteria.