ME/CFS,FM: Use of Anti-Platelets, Fibrinolytics, Anticoagulents, Vasodilators and Other Medicines/Supplements with Favorable Effects on Blood Vessels.

[SNT Gatchaman]

Don’t his findings run counter to the idea that long Covid patients have low venous O2?

Hmm, really interesting. LC patients won't typically be attempting peak exercise of course, but this finding that they are higher at rest does run counter to what I was suggesting.

The studied LC patients were —

We consecutively enrolled all patients who had recovered from COVID-19 and were referred to the Brigham and Women’s Hospital Dyspnea Clinic (Boston, MA) and the Yale New Haven Hospital Pulmonary Vascular Disease Clinic (New Haven, CT) between February and June 2021 for unexplained exercise intolerance.

So presumably between 12-16 months disease duration for those that got COVID first, with some in the study a bit less.

At rest: higher (normal) SvO2
Exercise: very much higher SvO2

Normal controls can extract a lot more O2 during peak exercise. If LC patients can't, then the key factor in the equation during peak exercise might be the reduced diffusion capacity. Maybe RBCs can't offload oxygen due to the interposed clot between them and endothelium, but they are moving through relatively well during high output state. Alternatively, they have already formed micro-circulation AV collaterals and under high-demand states are bypassing much of the capillary bed.

If we find that low SvO2 occurs at the beginning, maybe it's only generally in the first 6-12 months, before micro-circulation changes bring it back to normal or high. This could vary depending on the number of patient crashes, placing additional stress on the micro-circulation.

 

[Consul]

Gatchaman i think low extraction could also be because of mitochondria dysfunction or poor autoregulation of blood flow.

 

[SNT Gatchaman]

Gatchaman i think low extraction could also be because of mitochondria dysfunction or poor autoregulation of blood flow.

Very true.

 

[Aguirre-Chang]

The severity must be taken into account, Saturation will be normal in mild cases, and very affected in severe cases, who cannot leave their home due to dyspnea and fatigue.
In Dr Jaeger's 18 case report,
case 12 is a 72-year-old mechanic,
that he was hospitalized for persistent hypoxemia of less than 90% (this measured with a finger pulse oximeter).
In him, the oxygene saturation in venous blood before HELP Apheresis was 25.3%.
And immediately after the 1st apheresis, it rose to 44.2%.
They point out that the blood that came out is almost black, which indicates the presence of clots.
In several cases it was pointed out that clots remained in the filters and catheters, it was something evident, without the need for analysis or microscope.
There are some patients with CFS who mention to me that years before they have indicated that they find their blood thick, or that they have identified elevated fibrin.
The SvO2, Lactate and D-Dimer analyzes are not complex, the results come out in hours.

 

[Shanti1]

I think the SvO2 levels in ME were discussed in the apheresis thread - maybe @Shanti1 shared some studies? I can't recall exactly sorry.

The two studies I posted of SvO2 in pwME showed normal SvO2 at rest and SvO2 higher than controls during exercise (poor oxygen extraction). This could be due to mitochondrial dysfunction, altered capillary blood flow, microclots, or poor oxygen release from altered RBC deformability.

Unexplained exertional intolerance associated with impaired systemic oxygen extraction
https://link.springer.com/article/10.1007/s00421-019-04222-6

Insights from Invasive Cardiopulmonary Exercise Testing of Patients with ME/CFS (Joseph et al., 2021)
https://forums.phoenixrising.me/thr...patients-with-me-cfs-joseph-et-al-2021.82907/

 

[Aguirre-Chang]

Poor oxygen extraction,
I understand it to be due to Hypoperfusion.

It happens that clots with high fibrin content create like a wall or barrier, which limits the passage of oxygen from the blood to the tissues and cells.

Hypoperfusion causes cellular hypoxia,
and this forces the mitochondria to resort to the anaerobic pathway to generate ATP,
a path that is very inefficient,
so the energy it generates lasts very little.

And there is an important difference between Chronic COVID and CFS / ME:
it is lung compromise.

Pulmonary hypoperfusion occurs in moderate cases of COVID,
and can cause dyspnea even when speaking.

This Hypoperfusion implies that less oxygen is passing from the alveoli to the blood.

So, unlike CFS/ME patients,
in Chronic COVID or Long COVID,
there is no good oxygenation of the blood at the pulmonary level.

 

[Aguirre-Chang]

CFS/ME, FM: "THERAPEUTIC TESTS" TO ASSIST THE DIAGNOSIS OF PERSISTENT CLOTS IN DISEASES PRESENTING CHRONIC FATIGUE AND BRAIN FOG.

For patients with Chronic Fatigue Syndrome, Persistent Symptoms of COVID, Fibromyalgia, Chronic Lyme, Herpesvirus, EBV, Bartonella, Babesia, Enterovirus, Coxsackievirus, HPV, Parvovirus, Anaplasmosis, Gulf War Disease, Alzheimer's and, other Diseases that present Chronic Fatigue and/or Brain Fog.

In this link a "Therapeutic Test" is described that helps to diagnose Persistent Clots.
https://www.researchgate.net/public...ASES_PRESENTING_CHRONIC_FATIGUE_AND_BRAIN_FOG

It is indicated that D-Dimer and/or SvO2 analysis be performed, then you should take 1 Antiplatelet and 1 Fibrinolytic/Anticoagulant for 6 days.
And the response is evaluated on the 7th day.

If the analysis is not possible, you can see the response to the treatment, if there is improvement of 30% or more, it is a Positive result for Persistent Clots.

I have included a Table with the doses for patients weighing between 55 to 95 kilos.

In Table 3 the doses for people weighing between 45 to 55 kilos.

https://www.researchgate.net/public...AGNOSIS_OF_PERSISTENT_CLOTS_AND_HYPOPERFUSION

 

[Aguirre-Chang]

NewPublication
on Use of Anticoagulants in Long COVID:

COMBINED TRIPLE TREATMENT
OF FIBRIN AMYLOID MICROCLOTS AND PLATELET PATHOLOGY
IN INDIVIDUALS WITH LONG COVID/PASC
CAN RESOLVE THEIR PERSISTENT SYMPTOMS
https://doi.org/10.21203/rs.3.rs-1205453/v1

Before starting treatment with Anticoagulants, the Risk of Hemorrhage should be evaluated for each patient.

If the Platelet Count is below 200,000 it is not advisable to take anticoagulants.

It should be taken into account that many supplements, plants and herbs have effects on blood clotting, reducing it. For example, you have Garlic, Ginger, Onion, Vitamin E, Omega 3, etc.

Therefore, if Aspirin, Apixiban and / or other anticoagulants are to be taken, it must be taken into account that the anticoagulant effects will add up and that increases the risk of bleeding.

 

[Learner1]

It should be noted that many supplements, plants, and herbs have clotting effects. For example you have Garlic, Ginger, Onion, Vitamin E, Omega 3, etc

I think we need to be careful of making such broad brush statements that are not true....


Garlic is on your anticoagulant list above.

Vitamin is anticoagulant
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC41118/
So are omega 3s
https://www.ebmconsult.com/articles...a-platelet-inhibition-bleeding-risk-mechanism

Ginger is another anti-inflammatory spice that may stop blood clotting. It contains a natural acid called salicylate. Aspirin (acetylsalicylic acid) is a synthetic derivative of salicylate and a potent blood thinner.

Conclusion: This study showed that red onion aqueous extract in different concentrations inhibits clot formation and increases prothrombin time.

https://pubmed.ncbi.nlm.nih.gov/22531131/

 

[aquariusgirl]

very interested in Pretorius protocol. David Berg told me I had a big fibrinogen problem back in 2011.. high T/AT complexes on ISAC panel.

Serious family history of strokes...so don't take this stuff lightly.

@Aguirre-Chang .. do u have any leads on any physicians in the USA who would help with this?

 

[aquariusgirl]

Problem is most Cfs docs are ID docs, and isn't this stuff.. blood thinning outside their wheelhouse. are they gonna want to assume responsbiliity for this??

 

[Aguirre-Chang]

Garlic is on your anticoagulant list above.

Vitamin is anticoagulant
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC41118/
So are omega 3s
https://www.ebmconsult.com/articles...a-platelet-inhibition-bleeding-risk-mechanism

Ginger is another anti-inflammatory spice that may stop blood clotting. It contains a natural acid called salicylate. Aspirin (acetylsalicylic acid) is a synthetic derivative of salicylate and a potent blood thinner.

Conclusion: This study showed that red onion aqueous extract in different concentrations inhibits clot formation and increases prothrombin time.

https://pubmed.ncbi.nlm.nih.gov/22531131/

It was a mistake in the translation.
In the previous paragraph I mentioned the risk of bleeding, and that anticoagulants should not be used if platelets are low.

About Garlic, Ginger, Onion, Vitamin E, Omega 3,
should say:
… Have effects on clotting, reducing it.

That was the point. I already changed that part of the text.

As a doctor, we have seen cases in which ecchymosis and hemorrhages occur due to the use of medications and supplements at the same time with effects on the coagulation and fibrinolysis process.

 

[andyguitar]

Problem is most Cfs docs are ID docs, and isn't this stuff.. blood thinning outside their wheelhouse. are they gonna want to assume responsbiliity for this??

There must be some who are Medical Doctors.

 

[Learner1]

There must be some who are Medical Doctors.

Infections Disease doctors ARE medical doctors.

It was a mistake in the translation.
In the previous paragraph I mentioned the risk of bleeding, and that anticoagulants should not be used if platelets are low.

About Garlic, Ginger, Onion, Vitamin E, Omega 3,
should say:
… Have effects on clotting, reducing it.

That was the point. I already changed that part of the text.

Thank you for clarifying.

As a doctor, we have seen cases in which ecchymosis and hemorrhages occur due to the use of medications and supplements at the same time with effects on the coagulation and fibrinolysis process

As a patient, it would be extremely helpful if doctors were educated in the use of supplements, as well as drug-drug interactions and interactions with supplements. There are many cases where nutrients and botanicals have been found helpful in medicine:

https://asbmr.onlinelibrary.wiley.com/doi/full/10.1359/jbmr.2000.15.3.515

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7024754/

https://openheart.bmj.com/content/5/2/e000775

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7352314/#__ffn_sectitle

https://pubmed.ncbi.nlm.nih.gov/17569213/

https://www.nature.com/articles/aps20061

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7564301/

https://acsjournals.onlinelibrary.wiley.com/doi/full/10.1002/cncr.25945

Unless patients find a doctor knowledgeable about these supplements, they are left to research and try them on their own.

For those of us who are allergic to milk, corn and gluten allergens found as supposedly "inert," ingredients in most FDA approved drugs, many of which can't be compounded, in many cases, there are supplements, like Huperzine A, for POTS/dysautonomia, that provide helpful therapy. But, doctors regularly dismiss these, even though research supports their medical benefits.

It would be useful for all if we all could acknowledge there is a large toolbox of tools for treating illness that should be thoughtful selected from and combined wisely, with attentiveness to the medical goals and risks for each patient.

 

[Learner1]

I had a big fibrinogen problem back in 2011.. high T/AT complexes on ISAC panel.

Serious family history of strokes...so don't take this stuff lightly.

Resveratrol can help with fibrinogen. Mine has gone up and down 200 points depending on whether or not I was taking resveratrol.

https://dbcfspace.unisi.it/handle/20.500.12779/6875

It has some other benefits as well:

https://www.thrombosisresearch.com/article/S0049-3848(10)00458-5/pdf

Problem is most Cfs docs are ID docs, and isn't this stuff.. blood thinning outside their wheelhouse. are they gonna want to assume responsbiliity for this??

My ME/CFS specialist is on top of this as hypercoagulation is known in ME/CFS.

 

[Aguirre-Chang]

THE SARS-COV-2 VIRUS COLONIZES THROMBUS (CLOTS).

http://dx.doi.org/10.1186/s13054-021-03643-0

Using PCR analysis,
this study identified the SARS CoV-2 virus in the coronary thrombus of Symptomatic COVID patients.

84.9% of the Asymptomatic (without evident symptoms) also had Positive thrombus for SARS CoV-2,
which is a relevant finding.

These findings give further support to the theory of Persistent Bioclots, and to the application of HELP Apheresis.

In this study, it was also identified that the Viral Load of the thrombus correlated with its dimension.
It is recommended that patients with Long COVID have a PCR test taken as a sample of their centrifuged blood.

Not PCR from plasma, which is the acellular component (without cells) of blood,
but from cells, since it is an intracellular infection.

Instead of using a nose and throat swab, blood cells are used as the sample

 

[junkcrap50]

84.9% of the Asymptomatic (without evident symptoms) also had Positive thrombus for SARS CoV-2,
which is a relevant finding.

That's incredible. 85% of ASYMTOMATIC case??

In this study, it was also identified that the Viral Load of the thrombus correlated with its dimension.
It is recommended that patients with Long COVID have a PCR test taken as a sample of their centrifuged blood.

That's pretty interesting too about viral load within the thrombus. Why would centrifuged blood (I assume plasma) be better for PCR testing of long covid?

 

[Aguirre-Chang]

THE THROMBUS MICROBIOME:

Several publications have been made that support our theory of Persistent Bioclots in LongCOVID and a Subgroup of Chonic Fatigue Syndrome (CFS)

This article from the a Journal of NATURE Portfolio, detected Bacterial DNA in thrombus of patients with Myocardial Infarction.

https://www.nature.com/articles/s12276-020-00543-1

When SARS CoV-2 infection becomes chronic, latent infections that were contained or dormant in privileged anatomical locations (places where immunity does not adequately reach) are reactivated.

An alteration of the Microbiomes is produced in several places of the Organism.

In these cases, we indicate a 3-3-3 Treatment Scheme, with 3 medications for each of the 3 Therapeutic Lines of Action.

And if the symptoms are moderate to severe, other Schemes with more medications can be given.

 

[Aguirre-Chang]

That's incredible. 85% of ASYMTOMATIC case??


That's pretty interesting too about viral load within the thrombus. Why would centrifuged blood (I assume plasma) be better for PCR testing of long covid?

The virus is located inside the cells,
so if samples that include cells (cytological samples) are used,
the chances of detecting the virus increase considerably.

In the Pasteur Institute study described in the following link:

https://www.researchgate.net/public...ETECTABLE_WITH_MOLECULAR_TEST_PCR_USING_SWABS

100% of the PCRs that used the secretions obtained with swabs as samples were Negative.

And when Cytobrushes were used to obtain cells at the level of the olfactory epithelium, 100% were positive for SARS CoV-2 infection.

As for the blood.

Plasma is the acellular component (without cells),

so it will be difficult for the virus to be identified at this level.

What we propose is that samples of blood cells and platelets be taken, this can be obtained by centrifuging the blood.

This is how we have included it in the 1st Step of managing patients with Persistent Symptoms of COVID:

https://www.researchgate.net/public...c_COVID_or_Long_COVID_DIAGNOSIS_AND_TREATMENT

 

[aquariusgirl]

Forgive me if this is off topic.. but if we suspect high fibrinogen.. should we be avoid any lipid therapies like IV phosphatidyl choline until we have resolved the underlying hypercoagulation?

thank you