Blood clot drug totally ineffective as post-Covid treatment, research finds. Results from UK-wide trials on anticoagulant Apixaban

Trish

Trish

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Financial Times article:
Blood clot drug totally ineffective as post-Covid treatment, research finds
Results from UK-wide trials on anticoagulant Apixaban set to change protocols around the world

A drug to reduce blood clots, widely prescribed to Covid-19 patients after discharge from hospital, does not lessen their chances of readmission or improve survival, according to groundbreaking research which is set to change treatment protocols around the world. The results of the UK-wide trial, led by Addenbrooke’s Hospital and the University of Cambridge, were shared with the Financial Times. They found that prescribing the anticoagulant Apixaban did not help patients recovering from moderate and severe Covid and in a small number of cases caused serious harm.
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https://www.ft.com/content/db1e6c05-b8bb-429e-8cbd-8ea0dde58bf0
 
Dr Asad Khan says:
Not surprising. Apixaban will only affect the enzymatic pathway of clotting. Not the platelets which are key here.
Dr Resia Pretorius says:
Exactly@doctorasadkhan
targeting 1 of the 2 main clotting pathologies will probably not succeed. Hyperactivated platelets drive microclotting and visa versa. The endothelial layers need a chance to heal: BOTH hyperactivated platelets&microclots perpetuate endothelial pathology

Click to expand...
 
It looks like the drug was tried on hospitalised people with Covid, and success measured as survival after release from hospital and need to return to hospital. There was no significant difference in these between untreated and treated with this anticoagulant. So it's not looking at Long Covid and microclots, but at major clotting and other reasons for death or readmission to hospital.
 
From the commentary above, I take it that this morning's breathless headlines, like this one in the Guardian, are highly misleading:

Covid blood-thinner drug treatment dangerous and does not work – study
https://www.theguardian.com/world/2...g-treatment-dangerous-and-does-not-work-study
​
To breakdown the issues with this headline specifically:

[Covid blood-thinner drug treatment] ---> the blood-thinning drug included in the study does not actually address the hyperactivated platelets caused by COVID-19.
[dangerous] ---> what are the dangers, specifically? Are these dangers also found in other medications that DO address both hyperactivated platelets and microclots?
[and does not work] ---> do we have any studies on the efficacy of other anti-clotting medications that address both hyperactivated platelets and microclots?
 
ContraindiKate said:
From the commentary above, I take it that this morning's breathless headlines, like this one in the Guardian, are highly misleading:

Covid blood-thinner drug treatment dangerous and does not work – study
https://www.theguardian.com/world/2...g-treatment-dangerous-and-does-not-work-study
​
To breakdown the issues with this headline specifically:

[Covid blood-thinner drug treatment] ---> the blood-thinning drug included in the study does not actually address the hyperactivated platelets caused by COVID-19.
[dangerous] ---> what are the dangers, specifically? Are these dangers also found in other medications that DO address both hyperactivated platelets and microclots?
[and does not work] ---> do we have any studies on the efficacy of other anti-clotting medications that address both hyperactivated platelets and microclots?
Click to expand...

I think you are misinterpreting. The headline, article, and paper are about one particular drug, not blood thinners / blood clotting in general, or other potential mechanisms, such as platelet activation.
 
Dr Resia Pretorius has had the protocol including anti clotting and anti platelet since the beginning when they analysed the make up of the clots (https://europepmc.org/article/PPR/PPR436609).

(Clopidogrel 75mg/Aspirin 75mg) once a day, as well as a direct oral anticoagulant (DOAC) (Apixiban) 5 mg twice a day
Click to expand...

Its a bit surprising I think to not see some benefit from half this protocol on its own however.
 
Last edited:
Article now posted as preprint: https://www.medrxiv.org/content/10.1101/2022.12.07.22283175v1

Participants with a hospital admission related to confirmed COVID-19 and an expected date of discharge in the subsequent five days were randomised to either apixaban 2.5 mg twice daily or standard care (no anticoagulation) for 14 days.
Click to expand...

The apixaban arm was stopped on the recommendation of the oversight committees following an interim analysis due to no indication of benefit.
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So a half-therapeutic dose for a couple of weeks showed no benefit and this was framed as "Blood clot drug totally ineffective as post-Covid treatment". Wow.
 
I am hoping people here can help me understand more about the microclots, anticoagulants and ME...

I know people with ME who have been on anticoagulants for months to years and they've had no change in their ME (for better or worse). Not all of these people are on the same class of blood thinner.
In the microclot theory, at what point should improvements be noticed and to what degree?
 
Denise said:
I am hoping people here can help me understand more
Click to expand...

We don't have enough data yet. The "microclot" theory is unproven/not accepted. There is strong evidence of hypercoagulability in LC, and cardiovascular events are clearly significantly increased post COVID, even in those without symptoms of LC. There is some evidence that hypercoagulability is present in ME also.

If we were to accept this as true in LC and ME, how long does it stay true? The longest anyone can have had LC is not quite 3 years, versus 30-40+ years for ME in many cases. Does hypercoagulability become less of a feature, only present in the onset years? Is there survivorship bias when looking at long-term ME?

Regardless, I think your comment about people experiencing no change in ME suggests that hypercoagulability is not the fundamental cause. It may well be a downstream effect in some, many or even all. Treating it may be helpful in some, but we don't have the tools to guide this adequately.

However, your friends that have been on anticoagulants (presumably for reasons unrelated to ME) are unlikely to have been on both anti-platelet and anticoagulant treatments. As noted above those treating "microclots" have for the last 18 months proposed a two anti-platelet and direct oral anticoagulant regimen. Studies needed.

While I think hypercoagulability is going to be very important, we need to properly understand the interlinked immune dysregulation, immunometabolic and immunothrombosis aspects. I think the answer to this disease — when it comes — is going to be hard to put into just a couple of sentences.
 
SNT Gatchaman said:
We don't have enough data yet. The "microclot" theory is unproven/not accepted. There is strong evidence of hypercoagulability in LC, and cardiovascular events are clearly significantly increased post COVID, even in those without symptoms of LC. There is some evidence that hypercoagulability is present in ME also.

If we were to accept this as true in LC and ME, how long does it stay true? The longest anyone can have had LC is not quite 3 years, versus 30-40+ years for ME in many cases. Does hypercoagulability become less of a feature, only present in the onset years? Is there survivorship bias when looking at long-term ME?

Regardless, I think your comment about people experiencing no change in ME suggests that hypercoagulability is not the fundamental cause. It may well be a downstream effect in some, many or even all. Treating it may be helpful in some, but we don't have the tools to guide this adequately.

However, your friends that have been on anticoagulants (presumably for reasons unrelated to ME) are unlikely to have been on both anti-platelet and anticoagulant treatments. As noted above those treating "microclots" have for the last 18 months proposed a two anti-platelet and direct oral anticoagulant regimen. Studies needed.

While I think hypercoagulability is going to be very important, we need to properly understand the interlinked immune dysregulation, immunometabolic and immunothrombosis aspects. I think the answer to this disease — when it comes — is going to be hard to put into just a couple of sentences.
Click to expand...
Thank you very much
 
SNT Gatchaman said:
There is strong evidence of hypercoagulability in LC, and cardiovascular events are clearly significantly increased post COVID, even in those without symptoms of LC. There is some evidence that hypercoagulability is present in ME also.
Click to expand...

I think this may be misleading.

There is good evidence for an increase in clot-related events for several months after Covid. It is likely that a relatively high proportion of the people involved have residual ill-health due to lung damage just on the basis of clotting being a common comorbidity of being ill.

But I think it may be unhelpful to relate this to 'Long Covid' in the sense of suggesting that clotting events might be the cause of felling ill in any way like ME.

I think there may be a confusion a bit like the confusion between osteoporosis and back pain. Osteoporosis produces fractures that give episodes of acute pain chiefly in the thorax. It has nothing to do with the common chronic lumbar back pain that most people get. Osteoporosis is, in itself completely painless.

Similarly, whatever the cause of more frequent clots after Covid is it is very likely completely asymptomatic most of the time - maybe a rise in circulating fibrinogen or something.

So no, I don't think there is any evidence for any link between clotting and Long Covid in the sense that is of interest to people here. I am not aware of any reliable evidence for increased clotting in ME.
 
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