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

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FIRST EVIDENCE PUBLISHED OF PERSISTENT CLOTS IN PATIENTS WITH CHRONIC COVID OR LONG COVID (see image).

http://www.sun.ac.za/english/Lists/news/DispForm.aspx?ID=8621

THIS IS A STUDY ALREADY PEER-REVIEWED.

These findings support the 6 steps to follow described in the “MANAGEMENT OF THE PATIENT WITH PERSISTENT SYMPTOMS OF COVID”:

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

And they support our Treatment Schemes that include Fibrinolytics, Anticoagulants and Antiplatelets.
Our indication is that all patients with Chronic Fatigue Syndrome (CFS) and/or Persistent COVID Symptoms should undergo a: VENOUS BLOOD GAS MEASUREMENT test, which is useful to know: VENOUS OXYGEN SATURATION (SvO2 or SatvO2). This will be reduced if there is a lower oxygen supply, the most frequent cause of this in Chronic COVID and CFS, the presence of persistent Bioclots.

As an aid to the diagnosis of persistent clots, the patient must also perform a D-dimer analysis (which may be within normal parameters or slightly elevated) and then the patient must follow the "Therapeutic Test" for the diagnosis of Infection. Persistent Viral. As this Test includes an antiplatelet such as Aspirin, and a diet high in Lysine, if at the end of this Test an increase in D-dimer is identified, this would indicate the presence of persistent Bioclots.

If there is dyspnea or a lot of fatigue, it is recommended to include in this Test 500 mg L-Lysine, which is sold without a prescription, as a nutritional supplement.

The drugs and doses of the "Therapeutic Test" are detailed in the document at the following link:
https://www.researchgate.net/public...SSIST_DIAGNOSIS_OF_PERSISTENT_VIRAL_INFECTION

Persistent Clots and hypercoagubility cause tissue Hypoperfusion and a decrease in Venous Oxygen Saturation (SvO2), and this causes the symptoms of Chronic Fatigue and Mental Fog:
https://www.researchgate.net/public...ED_WITH_HYPOPERFUSION_AND_PERSISTENT_BIOCLOTS

In women of childbearing age, the presence of persistent clots can cause decreased, absence or delay menstruation:
https://www.researchgate.net/public...IATED_WITH_THE_PRESENCE_OF_CLOTS_IN_THE_BLOOD

These persistent clots serve as a refuge and protection function for viruses and other intracellular microorganisms, in a similar way to how biofilms or biofilms do, which is why we have called them Bioclots:
https://www.researchgate.net/public...CROORGANISMS_USE_CLOTS_AS_A_REFUGE_TO_PERSIST

In a document from the end of 2020, we explained how several microorganisms that cause persistent intracellular infections use platelets and clots to persist, and we point out that the use of antiplatelets, fibrinolytics and anticoagulants is supported:
https://www.researchgate.net/public..._INCLUDING_SARS_CoV-2_INFECTION_AND_NEOPLASMS
 

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  • Investigations should be directed at the intravascular level and not overemphasize the role of the immune response.

  • The persistent presence of hypercoagulability and blood clots causes tissue hypoperfusion, affecting the normal functioning of the muscles when they are subjected to greater demands.

  • The patient has fatigue, weakness and/or muscle pain associated with exertion, because due to hypoperfusion he does not receive the required supply of oxygen and nutrients to be able to perform greater physical activity.

  • At the brain level, tissue hypoperfusion would be the main cause of the so-called “Brain fog” or "mental fog", characterized by a decrease in cognitive functions, with a lower capacity for concentration and attention, decreased memory and other neurological disorders.
 

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  • The Hypoperfusion and Hypometabolism that occurs in CFS is associated with dysfunctions of the cells of the vascular walls (endothelial cells and pericytes) and of the blood cells (red, white blood cells, and platelets).

  • In recent years, several studies have been published in which it is evidenced that in Chronic Fatigue Syndrome (CFS) there is persistent endothelial cell dysfunction, a decrease in blood flow and perfusion has also been identified in tissues (tissue hypoperfusion).

  • Based on published evidence, and our experience in treating patients with CFS and Chronic or Persistent COVID, we propose to consider CFS as a Vascular Disease.

  • As there is no obvious organic damage, the usual tests tend to be within normal parameters, or only show a slight alteration.

  • To identify Hypoperfusion and Hypometabolism, regular tomography is not very useful, since the tissues are not damaged. One of the following exams is required:
  • - PET Scan or PET/CT Scanner: which is the acronym for Positron Emission Tomography.
  • - SPECT/TC: which is the acronym for Single Photon Emission Computed Tomography.

  • Both PET and SPECT/CT can be performed on the brain, heart, lungs, and other organs.

  • A simpler and lower cost test than PET Scan and SPECT/CT is the: Venous Oxygen Saturation (SvO2 or SatvO2) analysis, for which a: Venous Blood Gas Measurement must be requested. When there is tissue hypoperfusion, the supply of oxygen to the tissues by the blood is decreased, so that SvO2 will be low.

  • POSSIBLE TRIGGERING CAUSES.
  • As possible external triggers, the following should be considered:
  • - Persistent infections in cells of the vascular wall (endothelial cells and pericytes) and blood cells, by Viruses (Herpesvirus, Enterovirus, Coxsackievirus, HPV, others), Intracellular Bacteria (Borrelia, Bartonella, others), Rickettsia, Parasites, etc.
  • - Viral antigens, particles or fragments.
  • - Antibodies.
  • - Toxins and Others.
  • - Trauma and others Injuries.
  • Summary graphic is attached (available in PDF version in link and with more details).
 

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Shanti1

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@Aguirre-Chang A warm welcome to Phoenix Rising. Your intro posts and this post are timely as we have had some interesting discussions lately on the role of endothelial dysfunction, activated clotting, and low RBC deformity in people with ME/CFS. I personally feel this is a player in my case (secondary to EBV infection). I hope you don't mind if I ask you a few questions:

1. May I be so bold as to ask if you are THEE Aguirre Chang noted as the author on many of the papers you link to?

Depending on the answer to #1, you may or may not have input on these questions:

2. The COVID micro-clots seem to be unique in nature as they have high alpha-2antiplasmin, which renders them resistant to breakdown by serine peptidase enzymes (this would include the body's own fibrinolytic enzymes but also nattokinase, serratiopeptidase, and others are serine peptidase enzymes). It seems this resistance is confirmed by the spike-protein mixing with the clot material. Do you think that non-COVID-induced ME/CFS has resistant clots like this or more so just hypercoagulation of the "normal" variety?

3. For evaluation of hypoperfusion by PET/CT, what tracer is used (SPECT scans aren't always readily available)

4. For SvO2, I'm definitely interested in this test, would it need to be done in a hospital or large clinic setting where they have the equipment on-site for immediate measurement? It s a peripheral draw?

5. Do you know if HELP Apheresis helps non-COVID ME/CFS?

I have more questions, but I want to look through all of the info you posted, it may answer some of them.

Thank you!
 
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2. The COVID micro-clots seem to be unique in nature as they have high alpha-2antiplasmin, which renders them resistant to breakdown by serine peptidase enzymes (this would include the body's own fibrinolytic enzymes but also nattokinase, serratiopeptidase, and others are serine peptidase enzymes). It seems this resistance is confirmed by the spike-protein mixing with the clot material. Do you think that non-COVID-induced ME/CFS has resistant clots like this or more so just hypercoagulation of the "normal" variety?
got any references for this topic?
 

Shanti1

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got any references for this topic?
Yes, see this post from the Apheresis thread:

On another note, the clots found in long-COVID are distinctly different from clots found in other pathologies.
Dr. Etherisius Pretorius authored the paper, Persistent clotting protein pathology in Long Covid/Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased level of antiplasmin, which first brought the micro-clot issue in long-COVID into the public eye.

Both in the paper, and here in this video where she presents her work, she explains that micro-clots in COVID-19 patients are resistant to normal enzymatic breakdown, unlike clots in other conditions. She further explains in the video that the reason for the resistance to fibrinolysis (enzymatic breakdown) is the incorporation of the COVID-spike protein into the clot and how it alters the clot behavior. She also discusses how COVID microclots have a different composition from normal clots, even apart from the spike protein.
 
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Yes, see this post from the Apheresis thread:
thanks, I'll keep wading thru the studies....

I don' t have COVID, so I can perhaps continue my going after biofilms and microclots with some proteolytic enzymes. I"m also using the concept- drink some water (I actually don't drink much, my bladder hates it). And some CTM teas that help moisten the lung (that biofilm)

(Need to order a new batch of enzymes, maybe Dr. Wongs).
 
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@Aguirre-Chang A warm welcome to Phoenix Rising. Your intro posts and this post are timely as we have had some interesting discussions lately on the role of endothelial dysfunction, activated clotting, and low RBC deformity in people with ME/CFS. I personally feel this is a player in my case (secondary to EBV infection). I hope you don't mind if I ask you a few questions:

Hello, I answer the questions:
1. Yes, I am Gustavo Aguirre-Chang, with Dr. Aurora Trujillo we have been documenting our findings since last year.

2. Clots rich in Fibrin and the use of platelets are frequent by microorganisms that cause persistent intracellular infections. In the initial post we have put the links to several of the documents in which this is described. There is one from December 2020 entitled: THE USE OF PLATELETS AND CLOTS FOR PERSISTENT INTRACELLULAR INFECTIONS INCLUDING SARS CoV-2 INFECTION AND NEOPLASMS.
https://www.researchgate.net/public..._INCLUDING_SARS_CoV-2_INFECTION_AND_NEOPLASMS
And this year we have written about Bioclots.

Alpha-2 antiplasmin is elevated in most of these diseases, and its elevation is correlated with an inhibition or arrest of the body's fibrinolysis system.

3 and 4. PET and SPECT are complex and high-cost examinations, therefore, to support that, Fatigue and Chronic Pain, are due to Hypoperfusion and Hypoxia of the tissues, the practical thing is that a blood test of: MEASUREMENT OF VENOUS BLOOD GASES.

That it is not a complex test, nor expensive, a blood sample is taken in a similar way that, for blood count or cholesterol analyzes, fasting is not necessary.

If in the result, the VENOUS OXYGEN SATURATION is decreased, the symptoms are due to Hypoxia, Hypoperfusion and Endothelial Dysfunction, which implies that not enough Oxygen and Nutrients are reaching the cells and tissues of the organism, limiting their functioning and causing the effort intolerance.

5- Yes, HELP Apheresis is indicated in cases that do not respond to Schemes 3 x 3, 3-6-6 and 3-6-9 (which I will describe in a next post). If there is not a great improvement with the use of Medications and Supplements, it is necessary to resort to the mechanical eradication of Bioclots through HELP Apheresis.
 
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Screenshot_20211028-165713_Health.jpg
You might find this interesting then Dr Aguirre-Chang .
Not sure if you will be able to see this picture but it is my heart rate track for earlier today, average was 96, minimum around 65, maximum 150 to 160. I did no real exercise, just slow walking short distances and pushing a 60 kg motorbike a little. I don't have anxiety and my usual resting heart rate seems to vary between around 60 to 100, depending on how tired I am.

Since getting this heart rate monitor I have tried to capture my sometimes unusually high heart rates but I found that to begin with, when I exercised such as walking hundreds of meters or doing landscape gardening work, my heart rate averaged a very stable 110 to 120, today is the first time I have seen it go past 140. I have had POTS and OI in the past but it hasn't been a consistent problem lately. Yesterday morning I became very tired after exertion and spent most of the day resting, and this morning I felt like perhaps I had caught a virus or something because just waking up felt 'extreme' as if my body wasn't happy about something.
 
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You might find this interesting then Dr Aguirre-Chang .
My personal Primary Care Physician wrote a whole book on his theories of what going on with Capillaries and Endothelial inflammation .


I wonder if something in this book, would be useful to this entire ME related issue.

Hazing Aging is the name and I think he keeps doing new editions. Dr. Robert Buckingham.

https://www.amazon.com/Hazing-Aging-Capillary-Endothelia-Inflammation/dp/1491766727

I have not had a chance to discuss all this with him yet, but I really need to. (COVID stuck here).
 

Learner1

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@Aguirre-Chang Thank you for posting sand for your explanations. I have already done extensive testing and treatment and find some similarities to what you describe but I have some questions...
As an aid to the diagnosis of persistent clots, the patient must also perform a D-dimer analysis (which may be within normal parameters or slightly elevated) and then the patient must follow the "Therapeutic Test" for the diagnosis of Infection. Persistent Viral. As this Test includes an antiplatelet such as Aspirin, and a diet high in Lysine, if at the end of this Test an increase in D-dimer is identified, this would indicate the presence of persistent Bioclots
My d-dimer runs a little high. I have a Factor 2 (prothrombin) mutation and have already been treated for persistent infections (chlamydia and mycoplasma pneumonias, Epstein Barr, HHV6, cytomegalovirus and HSV1 as well as toxins. Therefore, does your theory apply? My fibrinogen is always near or over top of range - 390-500.
If there is dyspnea or a lot of fatigue, it is recommended to include in this Test 500 mg L-Lysine, which is sold without a prescription, as a nutritional supplement.
Ive been taking 1-3g lysine for 5 years, due to low value on tests and the herpes infections. Should I do this test? I've been on Valcyte for a total of over 26 months out of the past 5 years.
The patient has fatigue, weakness and/or muscle pain associated with exertion, because due to hypoperfusion he does not receive the required supply of oxygen and nutrients to be able to perform greater physical activity.
I can do a great deal of activity, walking over 10,000 steps a day, on average. However, increased pace or intensity, i.e. aerobic exercise for more than 3 minutes crashes me. I get a drained feeling in firearms and lower legs, dizziness and a need for eyes closed and total rest, but usually able to recover within 20 minutes and return to normal activity, other times, I have post-exertionsl malaise for days. Treadmill metabolic testing has shown very abnormal results - my mitochondria prefer to use glycolysis and only rarely fatty acid oxidation, so it has been hypothesized that I deplete muscle glycogen stores too quickly. I am never out of breath, and heart rate never exceeds 105 even at maximum effort.

I can believe muscles are not getting adequate oxygen, but think there's more going on, wouldn't you agree?
At the brain level, tissue hypoperfusion would be the main cause of the so-called “Brain fog” or "mental fog", characterized by a decrease in cognitive functions, with a lower capacity for concentration and attention, decreased memory and other neurological disorders.
Agree, but this is temporary. Seems to relate to oxidative stress.
it is evidenced that in Chronic Fatigue Syndrome (CFS) there is persistent endothelial cell dysfunction, a decrease in blood flow and perfusion has also been identified in tissues (tissue hypoperfusion).
I have been greatly helped by Kuvan, a firm of tetrahydrobiopterin (BH4) which repeatably increases my exercise capacity, I believe, due to increased nitric oxide production and decreased peroxynitrite production which damaged membranes. I've also been helped by lipid replenishment which repairs these membranes.
  • To identify Hypoperfusion and Hypometabolism, regular tomography is not very useful, since the tissues are not damaged. One of the following exams is required:
  • - PET Scan or PET/CT Scanner: which is the acronym for Positron Emission Tomography.
  • - SPECT/TC: which is the acronym for Single Photon Emission Computed Tomography
A PET scan has a huge amount of radiation and is virtually impossible for patients without suspected cancer to get. SPRCT also has radiation?? And is difficult to get.
A simpler and lower cost test than PET Scan and SPECT/CT is the: Venous Oxygen Saturation (SvO2 or SatvO2) analysis, for which a: Venous Blood Gas Measurement must be requested. When there is tissue hypoperfusion, the supply of oxygen to the tissues by the blood is decreased, so that SvO2 will be low.
the practical thing is that a blood test of: MEASUREMENT OF VENOUS BLOOD GASES
ok, what exactly does the doctor order, at what type of lab? E.g. can I order it at LabCorp or Quest Diagnostics, 2 major US labs or do I need to go to a hospital or reseaarch institution?

I will say that my autonomic neurologist explained that I had hypoparathyroidism in my brain when I fainted on a tilt table test... Does this count? (We think this is caused by adrenergic and muscarinic antibodies, however...)
  • POSSIBLE TRIGGERING CAUSES.
  • As possible external triggers, the following should be considered:
  • - Persistent infections in cells of the vascular wall (endothelial cells and pericytes) and blood cells, by Viruses (Herpesvirus, Enterovirus, Coxsackievirus, HPV, others), Intracellular Bacteria (Borrelia, Bartonella, others), Rickettsia, Parasites, etc.
  • - Viral antigens, particles or fragments.
  • - Antibodies.
  • - Toxins and Others.
  • - Trauma and others Injuries.
So, I've been extensively tested and treated for bacterial and viral infections, toxins, autoimmunity, and neck trauma. I'm a lot better, but not cured and d-dimer and fibrinogen still run high, but again, I have Factor 2.

If in the result, the VENOUS OXYGEN SATURATION is decreased, the symptoms are due to Hypoxia, Hypoperfusion and Endothelial Dysfunction, which implies that not enough Oxygen and Nutrients are reaching the cells and tissues of the organism, limiting their functioning and causing the effort intolerance
What about NO status, peroxynitrite damage to cell membranes, lipid replenishment, and gut malabsorption due to leaky gut? There are other studies that show these things in ME/CFS patients, hence my curiosity about this.

Thank you very much!😃
 

Shanti1

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ok, what exactly does the doctor order, at what type of lab? E.g. can I order it at LabCorp or Quest Diagnostics, 2 major US labs or do I need to go to a hospital or reseaarch institution?
I checked with Quest and LabCorp and the test is not available through them, presumably because the sample won't keep. You might find this post I just made on another thread useful:

The Low Down on Venous Oxygen Saturation (SvO2):)

I spoke with a friend of mine today who is an ER doc and learned the following:
  • SvO2 is typically done on ICU patients either through the pulmonary artery (SmVO2) or a PICC line placed in the vena cava or subclavian vein (ScVO2). The pulmonary artery placement is the most accurate but, more often, it is taken from the PICC line because ICU patients have them already placed and pulmonary artery placement is very invasive. SvO2 is monitored daily in these patients.
  • SmVO2 and ScVO2 range is 60-70% and 70-80% respectively
  • Peripheral draws for venous oxygen saturation (SpVO2) are rarely done (but they can be) because they are not as accurate as SmVO2 and ScVO2
  • Tourniquet use in a SpVO2 draw would not be expected to interfere with the SpVO2 reading unless the tourniquet was left on for an unusually long period (more than 3-4mins)
  • A peripheral SpVO2 will typically read lower than a SmVO2 or ScVO2, however, any reading below 55% on SpVO2 is highly predictive of a low ScVO2
  • If you want to measure your SpVO2, you would want to see a doctor as an outpatient who works in a hospital complex where they can do the draw and process the specimen immediately
Here is a paper on how well peripheral venous oxygen saturation (SpVo2) correlates with the more commonly used ScVO2 drawn from a PICC line:
Relationship between Central and Peripheral Venous Oxygen Saturation and Lactate Levels: A Prospective Study
https://pubmed.ncbi.nlm.nih.gov/27210904/


Low SvO2 is an indication of low tissue perfusion, either due to capillary compromise or something like low blood pressure or heart failure.