Orthostatic Intolerance after COVID-19 Infection; Wirth 2022

[Murph]

Medicina (Kaunas). 2022 Dec; 58(12): 1807.
Published online 2022 Dec 8. doi: 10.3390/medicina58121807

Orthostatic Intolerance after COVID-19 Infection: Is Disturbed Microcirculation of the Vasa Vasorum of Capacitance Vessels the Primary Defect?
Klaus J. Wirth and Matthias Löhn*

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Abstract
Following COVID-19 infection, a substantial proportion of patients suffer from persistent symptoms known as Long COVID. Among the main symptoms are fatigue, cognitive dysfunction, muscle weakness and orthostatic intolerance (OI). These symptoms also occur in myalgic encephalomyelitis/chronic fatigue (ME/CFS).

OI is highly prevalent in ME/CFS and develops early during or after acute COVID-19 infection. The causes for OI are unknown and autonomic dysfunction is hypothetically assumed to be the primary cause, presumably as a consequence of neuroinflammation.

Here, we propose an alternative, primary vascular mechanism as the underlying cause of OI in Long COVID. We assume that the capacitance vessel system, which plays a key role in physiologic orthostatic regulation, becomes dysfunctional due to a disturbance of the microvessels and the vasa vasorum, which supply large parts of the wall of those large vessels.

We assume that the known microcirculatory disturbance found after COVID-19 infection, resulting from endothelial dysfunction, microthrombus formation and rheological disturbances of blood cells (altered deformability), also affects the vasa vasorum to impair the function of the capacitance vessels. In an attempt to compensate for the vascular deficit, sympathetic activity overshoots to further worsen OI, resulting in a vicious circle that maintains OI. The resulting orthostatic stress, in turn, plays a key role in autonomic dysfunction and the pathophysiology of ME/CFS.

 

[Murph]

This is the latest in a series of 3 hypothesis papers to come from a group of researchers associated with Carmen Scheinbenbogen in Germany.


CONTEXT

These hypothesis papers

• An attempt to explain the neurological symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and
• Pathophysiology of skeletal muscle disturbances in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

have focused on finding a "parsimonious explanation" for the symptoms of me/cfs, and to cut a long story short, they zero in on blood flow.

This all ties in with Scheinbenbogen's findings of elevated levels of antibodies to the adrenergic and muscarinic receptors (the receivers that your nerves used to tell your blood vessels to expand and contract). That was first discovered by Japanese researchers about two decades ago, bu they didn't build on it, whereas Scheinbenbogen has piled on paper after paper.

THIS PAPER

In the paper this thread is about, Klaus Wirth (a frequent collaborator of Scheinbenbogen) argues you don't even need to assume autonomic nervous dysfunction is causing the major blood vessels to fail in long covid.
Big blood vessels feed small blood vessels, but are also fed by them. They need microvessels to operate, to bring them oxygen etc.

He says the after-effects of covid infection (clots, endothelial problems) could be enough to cause failure in the small blood vessels, and that could cause problems in the big blood vessels.

MY TAKE

I watched the movie Unrest years ago and one way it resonated with me is everyone they interview has their legs up. Even if we're up and sitting, few of us go for long with out feet on the floor. POTS and orthostatic intolerance are perceived as "comorbid" to ME/CFS but I'm ready to believe they're more central in many people. THis paper alone may not be especially important (hypotheses are cheap, it's data that matters), but I think this line of enquiry is extremely important.

 

[sunshine44]

Thank you for sharing this. I have been waiting for this kind of research to come out more. This is ABSOLUTELY one of my hugest issues. Something happened to my blood and my blood vessels. I have tried so many times to tell Drs something feels like it started happening to my blood in 2016/2017. I believe it started waaaayyyyy back (slowly) in my teen years with epstein barr and shingles. I noticed when i would bend over to garden and pick up beach glass, i wasn't recovering like everyone else. Fast forward to now being severe and being bedridden and sitting up for toilet is now akin to that.

Anyways, i really hope more research is put into this avenue. I concur, i think it is way more than a comorbid condition.

 

[marcjf]

I came across this paper a while ago. I think this hypothesis has a lot of merit based on what we know about Covid-19 (here is a good summary of the research:

). I personally feel the issue is more vascular in nature than related to the nervous system itself. That is why I feel it is misleading how we throw around the label "dysautonomia" everytime, we should instead be talking more about "endothelial dysfunction" instead. The autonomic nervous system is just trying to compensate for the faulty vessels.

But I am truly disappointed that it has been nearly 3 years since the pandemic started, and we are still into the hypothesis stage, as this is just an hypothesis paper. How can we not know for certain how Covid-19 leads to OI? I mistakenly assumed that we would be in the treatment stage by now.

My fear is that this is probably some permanent damage at this point.

 

[lenora]

This has been my experience: Long before they discovered (shall we say?) OI in certain people, I suffered from extremely low BP.....it was taken a number of times at the doctor's office in order to prove that it was OK. It never was.

I had an early menopause......and then my BP went into the stratosphere. I'm presently on 3 meds trying to get it within "normal" range....which isn't normal at all. Why these two disparities?

I was a high energy person with bouts of fatigue. I never thought much of it because it's the way I had always been. I slept well then, but definitely lost that ability after menopause.

It would be interesting to hear the experiences of others. There are many things that have changed in the body as I've aged.....one thing replaces another, etc. What are the answers? Yours, Lenora

 

[Oliver3]

I came across this paper a while ago. I think this hypothesis has a lot of merit based on what we know about Covid-19 (here is a good summary of the research:

). I personally feel the issue is more vascular in nature than related to the nervous system itself. That is why I feel it is misleading how we throw around the label "dysautonomia" everytime, we should instead be talking more about "endothelial dysfunction" instead. The autonomic nervous system is just trying to compensate for the faulty vessels.

But I am truly disappointed that it has been nearly 3 years since the pandemic started, and we are still into the hypothesis stage, as this is just an hypothesis paper. How can we not know for certain how Covid-19 leads to OI? I mistakenly assumed that we would be in the treatment stage by now.

My fear is that this is probably some permanent damage at this point.

It's ehlers danlos. Either acquired or genetic.
We need CRISPR and stem cells and any bridging therapies until then

 

[marcjf]

It's ehlers danlos. Either acquired or genetic.
We need CRISPR and stem cells and any bridging therapies until then

I come across EDS quite often ever since catching Covid, as there are many EDS/MCAS folks among us.
I questioned myself whether I have EDS many times. It is just that the I have none of the symptoms.

 

[Oliver3]

I come across EDS quite often ever since catching Covid, as there are many EDS/MCAS folks among us.
I questioned myself whether I have EDS many times. It is just that the I have none of the symptoms.

Yes, sane as me. I have a friend who has exactly the same symptoms as me but a few points on the Brighton scale.
Jen Brea believes the issue is in the tissue.
There's a weakness in us that starts off everything else.
I'm no scientist but I'd put my house on it.
I really believe the RCCCX theory is correct in the main.
The rest is beyond my pay grade.
Why it develops into this I don't know but tissue type is the starting block.
EDS science is not that well formed.
These are just my views, so obviously, probably mean nothing except from my intuition. Perhaps there's loads of reasons.but in everyone I know with CFS, there's some kind of tissue problem.
I've rarely if at all seen a thick skinned, strong boned strong veined sufferer of cfs