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.
- 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.
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.