The use of oral anticoagulation at the time of acute COVID-19 infection and subsequent development of [long-COVID], 2025, Frost+

There is stuff to unpick here.

This study is based on recorded clinical symptoms, presumably diagnosed by attending clinicians and reported by patients. Not laboratory level empiricism but nevertheless potentially informative.

What strikes me about this is people already taking OAC are likely to be more vulnerable to microthrombotic effects of LC/PASC since they are already having trouble with thrombosis risk requiring blood thinners. They may even already have a similar problem, undiagnosed, in relation to an immune response, possibly to another infection indicating a host generated predisposition to the kind of immune response causing LC/PASC.

By a mechanical analysis I would not really expect there to be an advantage reducing incidence rate of LC/PASC from taking OAC during infection. If anything I would expect potential increase in viral infectivity in those taking blood thinners and thereby initial severity simply due to easier diffusion of virus particles in thinner blood plasma increasing the rate at which they find their target receptor and infect host cells. However I have read of papers stating initial severity is not correlated with likelihood of developing LC/PASC.

It stands to reason, if LC/PASC involves microthrombosis you would expect less severe microthrombotic symptoms in patients taking OACs.


I am interested in this personally because I am having a long drawn out struggle with a migraine causing condition for which I am taking fibrinolytics bromelain and nattokinase because they do appear to reduce symptom severity.

 

I believe the main study showing that severity and LC risk are correlated is one of the Al-Aly veteran's center studies. Several others since then have shown that there's no strong correlation. There might be others I'm not remembering right now. As it stands, it seems like severity of illness is not a strong predictor of LC on its own. It also depends on how disease severity is defined--higher viral titres often do correlate with more respiratory stress, reduced oxygenation, use of ventilator, etc. but it's not a perfect correlation.

I also noticed a benefit from nattokinase. Small benefit for me but it did seem to help with lessening intensity of post-activity muscle pain, stiffness, and feverish feelings. My hairdresser also noted that I had much more growth in baby hairs at the first appointment after I started the supplement, which tends to be a sign of improved circulation.

Interestingly enough, I don't think I've ever had COVID. It's possible I've had a completely asymptomatic infection, but I was limited in how much I could be out of the house anyways since the pandemic started and always am very cautious about masks, avoiding crowded unventilated places, etc.

I actually had blood clotting issues before the pandemic ever started in 2019 when I got my wisdom teeth taken out. My ME/CFS did not start from a clear viral trigger, though I can't completely rule out another non-COVID asymptomatic infection. It makes me wonder whether differences in coagulation are generally related to ME/CFS pathology, and whether COVID is just one way of potentially triggering a long-term coagulation issue.

 

When I went searching for recent reviews, they all seemed to agree that acute severity increases LC risk. I didn't read them in detail, though.

 

It's very much up for debate--I did a deep dive on it about a month ago when I was searching for citations on that claim for a LC publication. There's evidence on both sides to some extent, the main issue is extreme inconsistency in how it's assessed.

For example, the studies I looked at varied on whether or not age was accounted for as a covariate (since age was strongly associated with severe disease to begin with), whether LC was defined by long-term physical and cognitive deficit or simply the persistence of one or more symptoms after infection, and whether there was enough data from non-hospitalized LC cases to accurately judge prevalence from mild infection.

As one example, the research team I was part of put out this study showing no correlation with severity amongst hospitalized patients. Granted, all were hospitalized, so it is skewed in that way. Though we did have a good number of mild cases that didn't exhibit high respiratory distress and were discharged after just a few days with no or minimal treatments.

 

Interesting, thanks. That link isn't working for me though, but I think it's supposed to be this study:

Features of acute COVID-19 associated with post-acute sequelae of SARS-CoV-2 phenotypes: results from the IMPACC study (2024, Nature Communications)

 

Yes it is! Sorry, I must have copied it wrong trying to do it in my phone.