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

[tyson oberle]

CHRONIC COVID (or LONG COVID or PACS) IT IS A VASCULAR DISEASE.

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

View attachment 45505

To identify Hypoperfusion and Hyperlactacidemia, regular tomography or X-rays are not more useful.
Since the tissues are not damaged, or they only present macroscopically not visible lesions.

Routine blood tests are also usually normal or slightly abnormal.

What is required are specific blood tests to identify hypoperfusion, persistent clots, and cellular hypoxia.

We indicate the following 3 analyzes are carried out, which are not complex or high-cost (on average the cost is 20 to 40 US dollars each):

1) MEASUREMENT OF VENOUS BLOOD GASES.
If Venous Oxygen Saturation (SvO2) is low, it is assumed that the supply of oxygen to the tissues is decreased, and it is highly probable that there is Hypoperfusion.

2) D-DIMER.
If it is elevated, it would indicate as a first option that there are persistent clots.
If it is within the normal range, clots cannot be ruled out, since D-Dimer is a product of fibrin degradation, so if there is no breakdown or lysis of clots (as can occur in COVID Chronic) the D-dimer would not be elevated.

3) LACTATE (also known as Lactic Acid).
If it is elevated, it would indicate that there is cellular hypoxia.

Taking a blood sample to perform these 3 tests is similar to the procedure performed for routine blood tests such as hemogram or cholesterol, that is, the sample is generally taken from a vein in one of the patient's arms.
The amount of blood required is not much, and the patient does not need to be fasting.

Besides these 3 tests, do you think that if a person has ice cold hands and feet that that would likely indicate microclots as well?

 

[Learner1]

Besides these 3 tests, do you think that if a person has ice cold hands and feet that that would likely indicate microclots as well?

You might find this helpful. In addition, iron or B12 deficiency can be causes.

"Why Are My Feet Always Cold? 5 Causes of Chronically Cold Feet" https://www.webmd.com/a-to-z-guides/cold-feet-reasons

 

[tyson oberle]

both iron deficiency and iron overload can favor blood clots, so it's important to check iron status

Can you explain how iron deficiency or iron overload favors blood clots? Thanks

 

[Learner1]

Can you explain how iron deficiency or iron overload favors blood clots? Thanks

"Iron deficiency linked to blood clots | Nursing Times" https://www.nursingtimes.net/clinic...-deficiency-linked-to-blood-clots-15-12-2011/

"Higher iron levels may protect arteries but raise clot risk" https://www.medicalnewstoday.com/articles/325788

 

[GlassCannonLife]

@Aguirre-Chang any reason you don't also recommend to try rutin along with the other supplements? I believe it has been shown to have thrombolytic activity.

 

[mariovitali]

@Aguirre-Chang

Thank you for your work and for joining the forum.

I have been using machine learning methods in order to generate potential research targets for ME/CFS. One of the methods identified transglutaminase as -potentially- an important factor.

From the paper : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8381139/

Furthermore, plasminogen activator inhibitor-1 (PAI-1) and α2AP, maintain a delicate homeostasis in the normal physiologic state [68]. α2AP is covalently cross-linked to fibrin in the thrombus by activated factor XIII, a transglutaminase [69, 70] which is a major source of the resistance of in vitro plasma clots to plasmin-mediated fibrinolysis [66]

Since transglutaminase exists in food, could avoiding transglutaminase from diet has a positive effect in the pathology you observed?

https://www.webmd.com/diet/is-transglutaminase-safe#1


Finally, could Vitamin K metabolism and problems to generate heparan sulfate could be attributing factors to the pathology you observed?


https://academic.oup.com/bjaed/article/13/3/87/278964

 

[Aguirre-Chang]

https://www.facebook.com/groups/659008718403141/posts/724862671817745/

We are working in the same direction as Dr Jaeger and her group, whom we have been selflessly supporting.

She supports our theory of Bioclots (clots that serve a similar function as biofilms).

Much progress has been made in the last year in understanding Chronic COVID (Long COVID), and other diseases that feature Chronic Fatigue and Brain Fog.

In summary:

the main triggering cause is a persistent intracellular microorganism,
which infects the cells of the vascular and blood walls,
causing endothelial dysfunction
with the consequent Hypoperfusion.

It is generated at the vascular level, a favorable environment for the persistence and reactivation of viruses and other microorganisms.

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

Pathogenesis and Physiopathology are already clear to us,
we are focusing on effective treatments,
and especially for cases that present a low response to the initial Treatment Schemes.

Dr Jaeger's first case report has been under review for about 6 months, there is still more time to be published.

 

[Aguirre-Chang]

Besides these 3 tests, do you think that if a person has ice cold hands and feet that that would likely indicate microclots as well?

Yes, the cold in the hands and feet indicates that there is low blood flow and hypoperfusion,
it can be accompanied by numbness or tingling, this can increase after lying in bed,
which is why several present it when they wake up.
In some cases there may be pale skin, or cyanosis, and changes in the nails may also occur.

 

[Rufous McKinney]

I'd say its possible to have not cold hands and feet while having good oxygen at the fingertip and yet the oxygen isn't reaching where it needs to go or is not being retrieved.

 

[Aguirre-Chang]

I'd say its possible to have not cold hands and feet while having good oxygen at the fingertip and yet the oxygen isn't reaching where it needs to go or is not being retrieved.

Blood has a temperature between 37.6 to 38 degrees
(slightly higher than what we measure with a thermometer).

Blood is the source of heat from inside the hands and feet.

If the blood flow goes down, the heat source goes down.
If the blood flow becomes too low, it can already cause ischemic lesions in the fingers.

 

[Consul]

So could someone tell me what would be a good idea to check in a blood test in relation to the micro clot theory, e.g venous o2 saturation? More?

 

[Aguirre-Chang]

POTS, ORTHOSTATIC HYPOTENSION

AND OTHER SYMPTOMS OF DYSAUTONOMIA

ARE ASSOCIATED WITH ENDOTHELIAL DYSFUNCTION,

REDUCED BLOOD FLOW AND PERSISTENT CLOTS.

This has been evidenced in patients with
Persistent Symptoms of COVID (Chronic COVID or Long COVID),
and Chronic Fatigue Syndrome (CFS).

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

According to the available published studies,
and the experience in the effective treatment of patients with Persistent Symptoms of COVID (Chronic COVID or Long COVID),
it is observed that the symptoms related to Dysautonomia improve significantly and resolve at the same time as the other symptoms,
which suggests that all these symptoms have the same etiology,
which is a persistent endothelitis with endothelial dysfunction and that in many cases it is accompanied by a state of greater blood density,
decreased blood flow and the presence of persistent clots.

 

[Consul]

Was at the doctor today and had a test thing put on my finger, probably some laser technology, it showed 96% o2 saturation. I was sort of hoping for a result that indicate blood clots but its ok i can live with it.

 

[SNT Gatchaman]

Was at the doctor today and had a test thing put on my finger, probably some laser technology, it showed 96% o2 saturation. I was sort of hoping for a result that indicate blood clots but its ok i can live with it.

That is using pulse oxymetry, measuring Sp02. From Wikipedia: "Peripheral oxygen saturation (SpO2) readings are typically within 2% accuracy (within 4% accuracy in the worst 5% of cases) of the more desirable (and invasive) reading of arterial oxygen saturation (SaO2) from arterial blood gas analysis."

The newly interesting value to know is the venous oxygen saturation (SvO2). This is a very big clue as to what is causing the symptoms of Long Covid, and quite possibly (at least early-onset) ME.

Following my first crash, I was seen in hospital and despite an SpO2 of 98%, my SvO2 was 22%. This is extraordinarily low - so far outside the normal physiological range, that it was probably thought spurious. Particularly as all other blood tests and vital signs were normal. (I was discharged as "probably a viral illness").

For reference, in the ICU situation, with patients in severe sepsis or profoundly low cardiac output states, patients can be stratified into predicted survival groups, based on measurements of central venous oxygen saturation (ScvO2). Lower ScvO2 is associated with poorer outcome. In one paper's studied groups, only 1% of patients had an ScvO2 < 50%.

The in-hospital mortality of our septic patients was 27%. A total of 73 patients arrived in the ICU from general wards (49%). The mean ScvO2 value was normal: 74.0 ± 10.2%. Only eight (6%) patients had a ScvO2 < 60%, and one (1%) < 50%.

For their severe sepsis patients: "in our study of the 14 patients with a ScvO2 < 50%, the in-hospital mortality was 57%".

It seems astonishing that we can be surviving with such a physiological derangement. Perhaps this is because it is apparently an isolated measurable abnormality.

Please note, this is not a blood test you can do via the GP.

 

[Aguirre-Chang]

DIAGNOSIS AND TREATMENT OF LONG COVID OR CHRONIC COVID
https://www.researchgate.net/public...c_COVID_or_Long_COVID_DIAGNOSIS_AND_TREATMENT

It is already very clear that it is a Vascular Disease that causes Hypoperfusion due to Endothelial Dysfunction.

With what has been achieved, the Treatment Schemes for CFS and other diseases associated with Chronic Fatigue and Brain Fog will be developed.

One must seek to eliminate viral persistence (or its components).

In the link, the First Treatment Scheme to be applied is included, with the details of the doses.

If total recovery is not achieved with the First Scheme,
3 or more medications (or supplements) should be indicated both against Viral Load,
as against platelet hyperactivity and for the breakdown of clots that have a high fibrin content.

If symptoms persist, other causes should be investigated,

such as Dysbiosis or SIBO,

the presence of other microorganisms,
such as viruses of the Herpesvirus family (HSV, VZV, EBV, CMV, VHH), HPV, Enterovirus, Coxsackievirus, Bartonela, Borrelia, Rikettsias, Babesia, Mycoplasma, Candida, etc.

There may also be a depletion of vitamins, minerals, hormones, and other substances.

The most basic analyzes to perform are:
1) Venous blood gases.
2) D-dimer (which is usually normal if you are not taking drugs to break down clots).
3) Lactate (which is also known in laboratories as lactic acid).

The sample for these tests is taken from one of the patient's arms, similar to the sample taken for a routine test, such as cholesterol.

In this case, for the 3 tests mentioned, the patient is not required to be fasting.

If the symptoms of Hypoperfusion are moderate to severe,
if possible a Viscoelastic Test (TEG, ROTEM, Quantra, Sonoclot, iCoagLab, ClotPro or other) should be included.

The immune component should not be overstated, since the inflammatory response will cease once the persistent infection is eradicated.

In the most persistent cases, if the bioclots cannot be broken down with medications and supplements, they must be removed mechanically,
that is, they must be extracted from the patient's bloodstream
(see step 6: HELP Apheresis or procedure with similar effect).

To avoid reactivation of the infection, a Treatment Scheme with medications and/or supplements must be followed in parallel,
which must be taken up to several days after the symptoms have resolved.

 

[Wishful]

This is a very big clue as to what is causing the symptoms of Long Covid, and quite possibly (at least early-onset) ME.

I don't see it as a big clue unless SvO2 is low in all those patients. If it's not, it might just be an indication that some patients have reduced heart function as a result of the disease. It might not even be a direct result, since it could be fairly far downstream of the core dysfunction.

Have there been any studies of SvO2 in ME patients?

 

[SNT Gatchaman]

I don't see it as a big clue unless SvO2 is low in all those patients. If it's not, it might just be an indication that some patients have reduced heart function as a result of the disease. It might not even be a direct result, since it could be fairly far downstream of the core dysfunction

Yes we need to see that it is occurring in essentially all long COVID / early-onset ME. Personally, I don't think cardiac function is so effected — only in terms of (mild?) diastolic dysfunction due to the effective low venous volumes and right-sided pressures of the POTS manifestation.

Have there been any studies of SvO2 in ME patients?

The Systrom team's invasive CPET studies looked at this, but they did not find low SvO2 at all. I think the opportunity to capture early-onset ME patients and study them has not been possible (too many years to diagnosis or no ME diagnosis at all). Now with COVID we can see large numbers of Long COVID patients (who will be ME) in the first year or two.

I don't believe there has been any published data on low SvO2 yet. So far, we have Dr Asad Khan's Twitter post (33%) and my own (22%) in support. Data is being captured now to get scientific validity and I think it has to be very likely they will confirm this finding.

If so, the marked change from early-onset to established ME seems very important in understanding the pathophysiology. My theory is that changes are induced in the micro-circulation (short AV shunts) that allow red cells to skip the more impaired regions of the capillary network. This may be the explanation for why every crash has the potential to make us worse and why both that and the longer ME goes on, the less spontaneous recovery there is observed.

Even if that were shown to be true however, it does not mean that the capillary bed is necessarily permanently altered / damaged. I think it's dynamic and capable of reverting once the underlying problem is fixed. (I suggest this also on the basis that there are people who have had ME badly for many years, but who have recovered to normal).

 

[GlassCannonLife]

Yes we need to see that it is occurring in essentially all long COVID / early-onset ME. Personally, I don't think cardiac function is so effected — only in terms of (mild?) diastolic dysfunction due to the effective low venous volumes and right-sided pressures of the POTS manifestation.



The Systrom team's invasive CPET studies looked at this, but they did not find low SvO2 at all. I think the opportunity to capture early-onset ME patients and study them has not been possible (too many years to diagnosis or no ME diagnosis at all). Now with COVID we can see large numbers of Long COVID patients (who will be ME) in the first year or two.

I don't believe there has been any published data on low SvO2 yet. So far, we have Dr Asad Khan's Twitter post (33%) and my own (22%) in support. Data is being captured now to get scientific validity and I think it has to be very likely they will confirm this finding.

If so, the marked change from early-onset to established ME seems very important in understanding the pathophysiology. My theory is that changes are induced in the micro-circulation (short AV shunts) that allow red cells to skip the more impaired regions of the capillary network. This may be the explanation for why every crash has the potential to make us worse and why both that and the longer ME goes on, the less spontaneous recovery there is observed.

Even if that were shown to be true however, it does not mean that the capillary bed is necessarily permanently altered / damaged. I think it's dynamic and capable of reverting once the underlying problem is fixed. (I suggest this also on the basis that there are people who have had ME badly for many years, but who have recovered to normal).

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

From memory they varied between studies and weren't chronically low (some were high).

 

[Consul]

https://www.sciencedirect.com/science/article/pii/S0012369221002567?via=ihub

The venous O2 saturation is included in table 2. They found more O2 remaining in me/cfs patients blood than controls after an exercise test.

 

[minimus]

David Systrom also recently published a research paper evaluating iCPET results of a small group of long Covid patients vs controls.

• At rest, long Covid patients had higher mean venous oxygen saturation (73%) than controls (66%), p value = 0.01.
• During peak exercise during iCPET, long Covid patients had markedly higher mean venous oxygen saturation (50%) than controls (22%), p value < 0.0001.

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