Do low blood flows to the brain (and elsewhere) connect ME/CFS, POTS and Long COVID at a fundamental level?
A recent long-COVID paper, “Post-Covid-19 Tachycardia Syndrome: A distinct phenotype of Post-acute Covid-19 Syndrome“, was given some prominence by Medscape. The authors focused on the presence of postural orthostatic tachycardia syndrome (POTS) in long COVID. POTS is a condition characterized by rapid heartbeats upon standing which has almost identical symptoms to ME/CFS – an important data point to keep in mind.
The Gist
- A recent review paper asserted that postural orthostatic tachycardia syndrome (POTS) is found in a significant percentage (25-50%) of long-COVID patients, and proposed a new name for them “Post-COVID-19 Tachycardia Syndrome”.
- The authors proposed that the Post-COVID-19 Tachycardia Syndrome found in long COVID is itself made up of various subsets.
- They also listed a variety of factors that may be causing the syndrome including some emotional ones (depression, anxiety) and physiological ones (organ damage, inflammation-induced blood vessel damage, altered renin-angiotensin-aldosterone system, hypercoagulation). Except for the organ damage, all these have been found in ME/CFS at one point or the other.
- Perhaps importantly, the authors noted that they could find no symptoms which differentiated long-COVID patients with tachycardia from long COVID patients without tachycardia. That’s an intriguing finding as the symptoms found in POTS are similar to those found in ME/CFS.
- ME/CFS patients with POTS were thought to be distinct from ME//CFS patients without POTS until 2020 when a study found that both groups were characterized by dramatically reduced blood flows to the brain.
- That finding suggested that the core problem in both groups is reduced blood flows. While the high heart rates in POTS do make things worse, the main problem in POTS may be reduced blood flows to their brains (and conceivably other organs).
- POTS may have become characterized by high heart rates during standing because that was easy to measure. Measuring blood flows is more difficult, and the proper techniques have only been used in the past couple of years.
- Hopefully, the same team (Visser, Van Campen, and Rowe) which found the low brain blood flows in ME/CFS are looking at long COVID, and long-COVID researchers are making the connection as well.
- Finding reduced blood flows to the brains in high percentages of long-COVID patients could be a game-changer that focuses the immense resources provided to long-COVID research on some crucial factors – blood flows, blood volume, the RAA system, the mitochondria, etc.
I believe that’s potentially a very important finding – but not for the reasons the authors present. I believe the POTS connection opens the door to a blockbuster ME/CFS finding which could if it’s also present in long COVID, could cast a new light on that condition and reorient research in a direction that could benefit long COVID, ME/CFS, POTS, and other diseases.
You can have blockbuster findings which don’t make a difference if they’re not followed up on. One thing the long COVID funding presents is the opportunity to follow up on major findings with alacrity.
The Paper
Even without the authors mentioning ME/CFS once in their paper, it’s clear they’re that they’re referring to a quite similar condition. Besides the similar mode of onset and symptom similarity, virtually everyone believes numerous subsets exist in ME/CFS. The same is true in long COVID.
Post-acute Covid-19 syndrome should not be considered a single clinical syndrome but rather a uniting term characterized by different sub-syndromes and phenotypes. The authors
Even within the subset of long COVID patients with tachycardia, this appears to be true, as the authors propose that three conditions make up the new long COVID syndrome (Post-COVID-19 Tachycardia Syndrome); POTS, sinus tachycardia, and inappropriate sinus tachycardia. Given that four different types of POTS (neuropathic, hyperadrenergic, hypovolemic, secondary) exist, it makes sense that several types of POTS may be showing up in long COVID.
Why they’re showing up is another story. The authors, who do not appear to be POTS experts believe many factors, including some rather squirrely ones (deconditioning, anxiety) as well as others (sinus tachycardia, hypoxia, sinus node dysfunction, myocarditis/heart failure, persistent fever) may be causing the tachycardia they see so often in long COVID.
They also propose that tachycardia /Post-Covid-19 Tachycardia Syndrome could be caused by damage to the heart, lungs, or other organs, via inflammation caused by blood vessel damage, by hypercoagulability, by dysfunction of the renin-angiotensin-aldosterone (RAA) system, fever, pain, anxiety, depression, neuroinflammation, and low blood volume.
Let’s hope that long-COVID patients don’t have to go down the deconditioning or anxiety rabbit holes. If deconditioning does not actively contribute to the functional problems in ME/CFS, it’s not likely to be a problem in long COVID. Neither anxiety nor depression has proved to be a fundamental feature of ME/CFS or POTS either. Heart failure could be a problem in long-COVID patients with heart damage, but those people should be able to be quickly screened out.
As Lenny Jason’ found that fever declines pretty rapidly in long COVID it should not be a major problem either.
It’s intriguing that aside from the organ damage, the physiological factors they cite (inflammation-induced blood vessel damage, hypercoagulability, altered RAA system) have all popped up one time or the other in ME/CFS.
A Crucial Connection?
Still, why is a paper on POTS and long COVID potentially big news for ME/CFS? It’s simply because of the POTS connections found in both diseases. Just as the paper asserts that a substantial subset of people with long COVID have tachycardia/POTS, we know that a significant subset of people with ME/CFS also have POTS.
Something recently happened, though, which made us look at ME/CFS patients with POTS differently. Prior to 2020, there were people with ME/CFS and POTS, and people with ME/CFS without POTS, and the two groups seemed utterly distinct.
(That’s despite the fact, in retrospect, that if you looked closely enough, you could find many people with ME/CFS who did not have POTS (or another form of orthostatic intolerance), but who did not do well while standing. I, for instance, apparently passed a tilt test with flying colors despite being wiped out by it.)
We now know that ME/CFS patients with POTS and without POTS are connected in a fundamental way: both groups feature dramatically reduced blood flows to their brains. It’s the numbers that make this potentially such a big deal. While perhaps 20% of ME/CFS patients have POTS, almost 100% of them appear to have reduced blood flows to the brain. That kind of consistency is very unusual in this disease and it’s a sign that a core finding may have been found.
Those low brain blood flows may also be why the symptoms found in POTS are so similar to those in ME/CFS. They may be why, as the authors of the POTS/Long COVID study note, they could find no symptoms that differentiated long-COVID patients with POTS from long-COVID patients without POTS. The reason they couldn’t differentiate the groups using symptoms may be because those two groups of patients are essentially the same – except that one has increased heart rates when standing.
We may have been mistaking a clinical finding – increased heart rates – for a cause. It’s perhaps notable, in that regard, that some people with increased heart rates upon standing don’t have any symptoms. The heart rate issue may have come to the fore first in POTS because it was easy to measure. Blood flows to the brain, on the other hand, are more difficult to measure accurately. It’s only in the past couple of years that the right kind of extracranial doppler echography technique has been able to do that. (Unlike transcranial doppler which measures velocity but not total flow extracranial doppler echography uses vessel diameter and velocity to come up with total flows.)
Those high heart rates, while present, may be something of a sideshow that have been hiding the main act in POTS -that not enough blood is getting to the brain. This is not to downplay those high heart rates. They cause real problems. People with ME/CFS and POTS are more severely ill than people with ME/CFS without POTS. The heart rate problem we’ve been so focused on, though, may not be the real issue.
Of course, there’s no reason to believe that those blood flow problems stop with the brain and quite a few reasons to believe that they are found elsewhere. We know that some POTS patients, for instance, also have problems with blood flows to the abdomen and/or legs. Systrom’s studies suggest that problems with microcirculatory blood flows are present in ME/CFS. Some fibromyalgia studies suggest microcirculatory blood flows are present as well.
The low blood flow problem potentially links long COVID, POTS, and ME/CFS.FM together in a tight package. It provides plenty of room to study blood flows and blood volume, autoimmunity, mitochondrial problems, the RAA system, as well as the different disease permutations that have resulted. It would also potentially give a core problem that’s popped up in the little-studied ME/CFS and POTS fields access to a tremendous amount of funding.
So, while this research group should be acknowledged for bringing POTS to the long-COVID discussion, the big breakthrough may be the next step – when the brain blood flows are assessed in long COVID. I wouldn’t be surprised if the Visser, Van Campen, and Rowe team that brought us the stunning news that virtually everyone with ME/CFS has low brain blood flows, weren’t already looking at that.
Did they coin a new name for POTS when it is an effect of a specific virus?
Or are they just coining a name for a COVID symptom?
If just a new name, why?
Does it give them an advantage for grants to coin their own name?
Is it to separate their findings from a POTS diagnosis for post COVID patients who might otherwise been seen to have POTS?
Is it to ensure that they are not aligning with a “forgotten flavour” of disease. The flavour that no one with big big gov grants wants to “buy”?
Maybe, AFTER all COVID fall-out, people who develop symptoms akin to long COVID will be given a NEW diagnosis. One that will allow more expensive tests such as brain imaging etc. to be done/justified. The “new” name that could be coined might, in future, become …….post-COVID-like disease (PCLD)……
people worldwide, though they never understood CFS/ME may understand what post COVID is when so many many many are effected by it
I was not clear
maybe CFS/ME, after all COVID fall-out, will be given a new name in a few years
where, if someone is newly diagnosed with CFS/ME symptoms: maybe they will be known/ diagnosed as having PCLD. (Post-COVID-Like-Disease)
Is it to separate their findings from a POTS diagnosis for post COVID patients who might otherwise been seen to have POTS?
Yes, I think it’s, in part, an attempt to make clear that different kinds of tachycardia are found in long COVID -that it’s not all POTS.
Is it to ensure that they are not aligning with a “forgotten flavour” of disease. The flavour that no one with big big gov grants wants to “buy”?
I hope not but I don’t think so. I think the problem with POTS and dysautonomia is that the fields are still quite small but don’t have the same validation problems that diseases like ME/CFS have. I don’t mean that people with POTS are not diagnosed with depression sometimes but my guess is that’s mostly because the doctors aren’t thinking of things like POTS.
Maybe, AFTER all COVID fall-out, people who develop symptoms akin to long COVID will be given a NEW diagnosis. One that will allow more expensive tests such as brain imaging etc. to be done/justified. The “new” name that could be coined might, in future, become …….post-COVID-like disease (PCLD)……
Agreed. There is already PASC (post-acute coronavirus sequelae or whatever) and if subsets emerge I imagine we will get more names. And as they learn more about PASC eventually a new name will emerge.
thank you Cort
I am a nurse 18 months after contracting covid and now awaiting surgery for bowel abd gall bladder problems. I had none of these issues prior to covid. I have CFS and symptoms for all conditions mirror each other. I am sure covid triggered the issues if bowel and gallbladder as all body pain. It’s been hurendouus to get this far. I want to go back to work but CFS is challenging, life is better but uncertain. Stay strong
I’m curious about what long haul symptoms you had….I am experiencing POTS symptoms/Me/CFS…wondering if this protocol would help.
I have POTS/MCAS/EDS I did not have Covid-19. But because of the obvious association of my virally-mediated POTS and long-covid, I decided to followi the recommendations for Long-covid (LC) from the FLCCC https://covid19criticalcare.com/covid-19-protocols/i-recover-protocol/ I was already using the MCAS protocol since I have mast cell activation.
I started Ivermectin on Aug. 7 and I am now on Fluvoxamine. Both are helping me immensely. My neuropathy, POTS, bursitis, RLS and chronic pain are either much improved or resolved! This might be the silver lining of this pandemic. IVM in particular is a God-send!
How are you doing now ?
I think the link between these diseases may be the autoantibodies against B/Alpha adrenergic receptors (or other G protein coupled receptors).
I recently discovered, after 21 years of disease that my AABs against Alpha/B receptors are extremly high, and there is some early evidence in this way…
https://www.sciencedirect.com/science/article/pii/S2589909021000204?fbclid=IwAR3GJGnVEoX94UA772iqSk1tg5Bmo_hS7NS2WTOjlJiFtl_RrhmBl6Ukges&s=08
https://www.nature.com/articles/s41380-021-01148-4
https://pubmed.ncbi.nlm.nih.gov/26584137/
In a fascinating and in-depth presentation Carmen Scheibenbogen just spoke on that at the IACFS/ME conference. Lots of interesting stuff going on there.
Agree – I just found out I have these raised AABs (after 15 months of longcovid with POTS-type symptoms and now a ME/CFS diagnosis). Also see https://doi.org/10.3390/jcm10163675
Cort, have you seen this? https://www.pnas.org/content/118/34/e2024358118?fbclid=IwAR16Oi0FqKH7S7LYQDv8CkYOhI_4fBkAlLAaIdC5ETbmvl9s1jc4Nv2VmzU
I found this on the #MEAction Global Facebook page.
Yes! A blog is coming up. 🙂
Cort, thank you so much for your faithful reporting and helpful articles – we personally have had much benefit from them.
Our daughter (currently 9 years old) became very sick 1.5 years ago after a mild viral infection — and no one could figure out what was wrong even though we had exceptionally good access to a top Children’s hospital due to my familiarity with the system (infectious disease, cardiology, immunology, oncology, rheumatology, MRI, etc). She got sick to the point she was couch/bed bound in constant severe head pain, could hardly walk, weak, dizzy, no appetite, sleep issues, could no longer do schoolwork (which she loves!), etc.
It wasn’t until I finally came across POTS and ME/CFS that I figured out what was going on. It still took us months to find someone to willing help treat. (Childrens’ hospital at first only suggesting psychotherapy and meds for depression, CBT, and graded exercise! Yikes!
Thankfully one doctor was willing to read the ME/CFS pediatric primer that I desperately brought to the appointment and contact Peter Rowe MD for help in understanding.) All along I’ve realized that the tachycardia is only a helpful response from her body to try to get more blood out of her legs and up to her brain.
I was fortunate to find and read/watch a lot of Peter Rowe’s info and his thoughts about low blood volume in the brain. When our doctor consulted with him to try to figure out a treatment plan for our daughter – Dr. Rowe talked a lot about the blood volume/brain issue and this makes so much sense in our case.
It probably isn’t appropriate or helpful for me to say exactly how we have treated our daughter but by treating her in such a way as to address fluids, blood volume with a liter (4 cups) of WHO formula oral fluids daily – in addition to meds, she has had a dramatic improvement over several months of re-stabilizing.
She still gets PEM after a very active day but she is able to be active again like a normal child (with pacing), and completely back to being her curious, active, and cheerful self. This feels like a miracle!
We can MONITOR how she is doing by following her heart rate and resting heart rate, but I don’t think the higher heart rate it is the cause of her symptoms. However, it IS helpful to have that POTS designation (in addition to ME/CFS) – to say “she is struggling with a type of tachycardia” to outsiders who aren’t impressed with general chronic illness terms (tired, weak, dizzy, won’t eat, headaches, can’t do schoolwork).
Also oddly, when we aimed at addressing the fluids/blood volume, her other seemingly un-related dysautonomia issues have also resolved (constant low grade fever for over a year, flushing face/super pale face alternately, and others).
Yes – I think this is really a key finding and I hope there is more research in this area!
Congratulations SDS,
Do you make up the WHO organization formula yourself or do you use a packaged form? Would be willing to say which drugs helped your daughter?
For people interested in increasing their blood volume – here’s a blog on oral rehydration solutions – https://www.healthrising.org/blog/2020/09/15/saline-ors-oral-rehydration-pots-chronic-fatigue-syndrome/
Here’s a story of woman who’s panic was a result of low blood volume
https://www.healthrising.org/forums/resources/when-panic-isnt-dr-bell-on-maggies-me-cfs-and-fibromyalgia-story.237/
We buy Trioral brand from Amazon. She is taking Florinef 0.2 daily, and “low dose” Propranolol 10mg 3X daily. (We started doses very slow and have arrived at this. She weighs 58 pounds. (She also takes amitriptyline at bedtime as they were trying to treat the headache alone before we knew more of what was happening, it only helped a little bit on its own). Full disclosure, not knowing what helps the most. We also started quality aloe vera juice 1oz and probiotics for gut health and possibility it might help the hyper mobility that was developing before our eyes. She also takes methylated vitamins due to an MTHFR mutation. And vitamin D. There is a study that influenced me pushing for the WHO fluids. https://pubmed.ncbi.nlm.nih.gov/31405524/ Of these things we are doing – the Florinef, propranolol and the Trioral – if we miss any of them by themselves, symptoms begin to return. We have her drink extra WHO fluids when active. I do want to be clear, this does not completely get rid of the PEM (her resting heart rate goes up and she experiences fatigue, headache) – especially if she is active 2 or especially days in a row (like playground play or informal soccer or swimming) – but since April in starting the WHO fluids, she has gone from needing a disability stroller to get from parking lot to doctors office to being able to do these things regularly this summer. We are so thankful!
That’s amazing! Thanks for sharing that. I find the Trioral helpful. It’s one of the few things that I can helps.
Thought I’d share a new article which describes the latest research/theories on long haul Covid, especially in those with milder disease;
https://www.nationalgeographic.com/science/article/how-does-covid-19-affect-the-brain-a-troubling-picture-emerges
This article also mentions blood flow, but there is evidence of neuroinflammation too–and more. Although the article doesn’t make comparisons with ME/CFS, it might as well have, as the findings sound very similar. Seems as if they are still quite lost on how to deal with these symptoms and researchers are collecting anecdotal treatments to try to find things that are effective.
I also find it interesting that a large number of people with Ehlers-Danlos also have fatigue, POTS and fibromyalgia-like symptoms. Although a substantial number of EDS patients are being treated at Stanford’s CFS Clinic, I’m not sure how many have had a definite onset (viral perhaps?) of their fatigue rather than it just being a symptom of EDS.
Are there people with EDS, like myself, who had fatigue problems before getting the sickness which caused my most severe fatigue and diagnosis of ME/CFS? I remember getting various flus and each time I had a very long recovery period–and worsening energy issues–until finally I became where I am today. Does the body get broken to the point it cannot repair itself?
Like yourself, Cort, I also have dysautonomia symptoms, yet when tested, POTS did not show up. I do have near constant tachycardia and have had it since childhood. You might be comforted to know, that POTS symptoms can come and go, and it can be difficult to catch it with a single test. You many well have POTS, but it decided not to show in front of your doctor! Neurocardiology doesn’t know everything…
Right! A test that is not done long enough can miss POTS. Tests done at different times of the day may not pick it up as readily as well.
I had the test done during an ME/CFS twin study decades ago and while it seemed well done that was decades ago. My twin had no problem at all during the test; I, on the other hand, felt horrible.
Cort, I’m interested in trying Trioral but I have a sugar intolerance so I’m wondering if the glucose in it would be a problem.
It’s a really mild sweetness. I rarely eat sweets so when I do I really notice how sweet things are. It seems really mild to me.
After a year of extreme stress….I developed nightly tachycardia off and on during the night. This has been going on for over a year and other than trying to reset my heart beats thru some exercises involving the Vagus nerve…..this still continues during sleep. Needless to say, it is creating its share of anxiety and dreading sleep. Three separate cardiologist tell me not to worry and have suggested Beta Blockers, which I have been unable to tolerate. I try other methods of relaxation. Knowing that this is an offshoot of dysautonaumia, I don’t know what to try next. Any suggestions would be appreciated. I know the vagus nerve is involved, but beyond that my PCP has no suggestions. Also, my body temp has dropped to 94.5 to 96/5 over the last several months. Again, any input , direction, etc. wuld be appreciated. Thx. I have had CFS well over 50 years.
I’ve been wondering: Had the doctors that came up with POTS been from an endocrinology background, would they have recognized it as a sugar production and utilization problem? Hypoglycemia?
And no need to create a separate entity, a whole ‘new’ disorder…
Would they have seen the connection between the different systems in the body?
When blood glucose levels get to below about 54 mg/DL, measurable cognitive deficits show up, word finding and simple math problem solving difficulties – Sound familiar?
Your PEMs, your brain fogs…
Post on McGregor’s blood glucose findings in ME/CFS
“Emerging Insights #1: McGregor’s Grand Conception of ME/CFS”
they found that a very small percentage had normal glucose response after a meal, a bigger chunk went up after a meal but came back down quicker than normal, and a third group it flatlined, pretty much the same before and after a meal.
– Now, what if they measured levels upon activity, upon being upright, etc?
– Has anyone measured their blood glucose levels during a crash? after? how long does it take to bring them back up again?
If not all have outright measurable hypoglycemia, perhaps looking at brain glucose and ketone levels?
“Two patients with Neuroglycopenia”
– note the mitral valve prolapse – part of the hEDS diagnostic criteria
– note the dismissal of the patient as a liar, for denying insulin ingestion, and said patient not returning to the hospital
“Recurrent/moderate hypoglycemia induces hippocampal dendritic injury, microglial activation, and cognitive impairment in diabetic rats”
– has anyone looked at brain glucose at ketone levels in ME/CFS, POTS, hEDS, etc?
From “Mechanisms of hypoglycemia and exercise-associated autonomic dysfunction”:
“It is now known that a single episode of hypoglycemia can blunt the body’s normal counterregu- latory defenses against subsequent hypoglycemia or exercise. Similarly, a single bout of exercise can also blunt counterregulatory responses against subsequent hypoglycemia. Both neuroendocrine and autonomic nervous system responses are reduced by prior hypoglycemia and/or exercise. Work from several laboratories has identified multiple physiologic mechanisms involved in the pathogenesis of this hypoglycemia and exercise-associated counterregulatory failure.”
[ The comment was able to post by taking links to the papers out. You can look them up by the titles if interested ]
When I was a kid and experiencing weakness and near fainting episodes, I thought it may have been dehydration as they tended to happen when outside in the heat or sun. Knowing that water would only further deplete minerals, I would reach for potassium-rich fruits, etc.
Later on, when they become more intense and different seasons/time of day, I suspected hypoglycemic attacks. I made sure to be well fed, and to always carry something sweet on me.
Then it got worse, and I was constantly eating, constantly nibbling and packing so many calories in a day, and still wasting away. Until that no longer worked because the level of deterioration was having me crash any time I would be a few minutes upright. That was the descent into the ME/CFS hell.
How I got myself out of that, is by getting my body to make more CO2. How? You can read Ray Peat’s articles to find out.
Also, CO2 for hyperPOTS was noted here https://www.healthrising.org/blog/2018/08/19/stagnant-hypoxia-where-chronic-fatigue-syndrome-and-hyperadrenergic-pots-meet/
– – – – – – – – – – –
There is also orthostatic hypotension and orthostatic hypertension. Few doctors seem to be aware of the second one…
{ Oops… forgot to include that the weakness/near fainting spells only recently were labeled as POTS and orthostatic hypotension, which later became orthostatic hypertension }
ME/CFS and “Long Covid” are both a reactivation of Epstein Barr virus.
Once EBV is in the memory B cells, you’ve got it.
That means there must be a common underlying cause for it. Maybe an immunological predisposition.
A bit off-topic, On July 26th, the Biden Administration released guidance that stated long Covid could qualify as a disability under federal law, and would thus be covered under the Americans with Disabilities Act.
” could ” ? Or Would ?
Do you know anyone who has recieved disability for long covid ?
Following up on ME/CFS status with ADA, I found this:
Is Chronic Fatigue Syndrome a “disability” covered by the Americans With Disabilities Act (ADA)? “Yes” answered the Fifth Circuit Court of Appeals in its recent decision in EEOC v. Chevron Phillips. The court ruled that the employee presented sufficient evidence that her Chronic Fatigue Syndrome posed a substantial limitation for her in the major life activities of caring for herself, thinking and sleeping.
Has anyone tried to test homeostasis in any of these patients? Any virus will attack your weakest spot, then maybe any hormonal issues caused by a long haul of covid virus. After hormone tests, then possibly find out which or if any of the organs are causing certain deficiencies in vitamins, enzymes, or any endocrine glands. The balance in the bodies homeostasis is probably out of whack and needs corrected and whatever might be compromising the immune system to be weakened. After balance is figured out, I’m sure the gut needs repaired as well as good sporic probiotics that are capable of making it through our acidic stomach acids. Lots of water, fiber, and protease enzymes. The first focus is to dissolve the biofilm that some viruses secrete and turn off the immune cells. Moving of the lymp fluids. Take soil-based probiotics and magnesium malate. Certain essential oils might be helpful and depression could stem from homeostasis being unbalanced and I don’t think psycho meds should be the answer in a treatment against a virus. That could just be caused by the imbalance in hormonal changes of the body. Caprylic acid is also told to braeak through the biofilm of the bug. This is all so similar to how a certain yeast would effects our homeostasis and is usually never corrected or a concern for most doctors, which I find unusual. Some virus thrive off of sugar or hormones such as estrogen. Symptoms of depression could arise specifically because the gut microbiome needs restored.
What is interesting in my case is that when I first developed ME symptoms (still no official diagnosis, but symptoms certainly apply including severe PEM and crashes), i had very bad POTS symptoms also. this was about 3 years ago after severe viral infection of some kind and then shingles. I had very obvious issues with pulse rate going up over 30 points when standing, dizziness, light headed. I could not stand for more than a minute at a time without getting weak. I had to fill up on fluids and salt and it helped, but I was basically in bed for about 4 months. Somehow, the POTS symptoms eased up over time and was able to resume some normal activities, even working at home. I still have ME symptoms and am unable to exercise at all. I have crashes and periods of severe pain and fatigue, but the POTS has not returned. Not sure why I had this or why it resolved, but glad it did. I think the POTS to me was much more disabling than the ME symptoms even though both are very difficult.
I read the transcript for Chenney’s 2013 presentation.
Here is a gem, I just had to copy the extent of this section:
“So I ordered three of the patients who scored the lowest on this and I had them echoed in three different centers around the nation where they lived. The echoes all hit my desk at the same time, and they all said the same thing. They said, “Normal wall thickness. Normal chamber size. Normal valve function. Normal everything. Except, Type 1 Diastolic Dysfunction.”
They all said the same thing, that last sentence. Type 1 Diastolic Dysfunction. But everything else was normal.
And so I was shocked, because I didn’t know what that meant. And I was embarrassed, because I went to Emory and am supposed to know everything about the heart.
So I called up a friend of mine that I went to school with and I said, “Why don’t I know what that means?”
He said, “That’s a new term. It didn’t exist when you and I went to school.”
I said, “This is a new term to me. This is something about the heart that no one knew existed?”
He said, “Yes, until about ten years ago, it did not exist.”
Well, it actually does exist, and it is a significant feature of chronic fatigue syndrome. Almost all of them have this.
So I said, “Would you tell me what it means?”
He said, “That is what the heart looks like when there is no energy in it at the cell level.”
I was shocked, and I asked if he would allow me to repeat what he just said back to him.
I said, “You mean that an energy defect at the cell level would manifest as diastolic dysfunction?”
He said, “Yes, absolutely.”
I said, “Would it drop the cardiac output?”
He said, “You betcha, especially when they stand up and you get gravity filling problems on top of energy filling problems.”
So I knew I was onto something, so I asked him, “So how do I measure this?”
He said, “You need to get a really good echo machine, one with tissue doppler capacities and sufficient power.”
I said, “Which would you recommend?”
He said, “Vivid 7 made by GE.”
So I called up GE and had them demo this big machine in my office. They brought it in in three different boxes, and they echoed six of my patients in a row. This was in early 2005.
After they finished, the echo stenographer turned to me and said, “We have never seen this before. They all have diastolic dysfunction and they’re relatively young.”
I said, “That’s interesting, but why do you seem so surprised?”
He said, “Oh, we’ve never seen this before in such young people. Could you tell me what they have?”
And I said, “They have chronic fatigue syndrome.”
And he said, “What’s that?”
So clearly, no one had even looked at this.
So I decided to get this machine, and I’ve been doing echocardiography ever since. And it’s been quite a journey because there’s not been a lot of help in the cardiology community.
They see diastolic dysfunction as an old person’s disease. Or it’s related to underlying conditions like diabetes or hypertension. And none of my patients have any of that. They’re not old, they’re not diabetic and they’re not hypertensive.
So it doesn’t really click with cardiologists that there might be such a thing as a pure energy deficit. Otherwise the heart is completely normal.
That’s a good thing, because with a normal heart, you can compensate for diastolic dysfunction. And it turns out that the major compensation mechanism is to squeeze your ventricles as hard as you can. And so you see high ejection fractions in these people. We call it cavitation. The ventricle squeezes really, really hard.
And that creates several complications that we’ll get into. But it’s not just that they have diastolic dysfunction. It’s that they have maintained systolic function and they use the systolic function to compensate.
As a result, if you squeeze hard enough, you can fire the C fibres, causing neuromediated hypotension. And you’ll pass out and hit the floor. That was reported at Johns Hopkins back in the 1990’s, that a certain percentage of these patients have NMH, POTS or difficulty standing, which they blamed on autonomic dysfunction.
It has absolutely nothing to do with autonomic dysfunction. They have diastolic dysfunction. And it’s not good for them to stand up. Partly because they have good systolic function.”
The sympathetic system is activating for a reason – to make up for the problems with not enough energy in the heart. Epinephrine and nor-epinephrine activate mechanisms to increase blood flow. Ties in with nitric oxide and histamine too, in that these have vaso-dilating effects.
Of course overtime, after decades of living with this, we are going to see problems.
I went from ‘normal’ POTS to hyperPOTS, etc. I am sure there are many other kinds of heart problems.
That florinef is used to treat some with POTS – it is a glucocorticoid. Have those individuals had a proper assessment of their adrenal function; not just the standard test, stress response tests as well? thyroid?
Would a cardiologist be trained to recognize endocrinological dysfunction?
[transcript from here https://paradigmchange.me/wp/cheney/ ]
Also, my heart report had mild tricuspid regurgitation. The doctor didn’t even bother telling me, I had to get a copy and read it myself.
Of course they don’t think it is a big deal – until it is and you need surgery…
I read an old paper looking at mitral valve prolapse in hEDS. Those that didn’t have it, had tricuspid regurgitation and another condition that escapes me at the moment. The author, which I believe was no other than Dr Graham, didn’t think those were ‘serious’ enough and since labeled as congenital heart problems, and hence they focused on the MVP and this is what made it into the diagnostic criteria. This is to say, that every single person with the joint hypermobility in the study had something going on with their hearts.
To be clear: I don’t think the heart problems in hEDS/HSD are coming from defective collagen. It’s all the energy dysfunction that leads to deterioration in collagen structures, or the functioning of the heart, and how the body makes up for this, and where it starts to fail that’s where your weakness is.
It seems notable that just about every drug used to treat POTS has a study of some size showing that it helped at least somebody with CFS – pyridostigmine (Mestinon), desmopressin, midodrine, fludrocortisone, and ivabradine.
I seem to have developed POTS after a period of overexertion about four years into post-EBV CFS, and I’m wondering if it wasn’t a blessing in disguise, because it sent me down the path of trying to treat my CFS by treating my POTS. I think there may be something here.
Good point and good luck!