Covid and Vascular System, Endothelium, Blood Clots

Covid and Vascular System, Endothelium, Blood Clots

#vascular
COVID-19 raises the stakes for heart attacks, strokes, and even death long after infection, new study finds
COVID-19 raises the stakes for heart attacks, strokes, and even death long after infection, new study finds
“COVID-19 raises the stakes for heart attacks, strokes, and even death long after infection, new study finds”
COVID-19 raises the stakes for heart attacks, strokes, and even death long after infection, new study finds
·fortune.com·
COVID-19 raises the stakes for heart attacks, strokes, and even death long after infection, new study finds
COVID-19 raises the stakes for heart attacks, strokes, and even death long after infection, new study finds
COVID-19 raises the stakes for heart attacks, strokes, and even death long after infection, new study finds
“COVID-19 raises the stakes for heart attacks, strokes, and even death long after infection, new study finds”
COVID-19 raises the stakes for heart attacks, strokes, and even death long after infection, new study finds
·fortune.com·
COVID-19 raises the stakes for heart attacks, strokes, and even death long after infection, new study finds
The Cardiac pathophysiology of Covid-19
The Cardiac pathophysiology of Covid-19

“Findings emphasize that Covid-19’s myocardial pathology predominantly arises from fibrin thrombi within the coronary MICROVASCULAR network, especially in the abluminal spaces.

➡️This pathological process leads to myocardial fibre injury, necrosis, and ischemic changes( = fibrosis), contributing to both the acute symptoms and long-term sequelae (Long Covid).”

·x.com·
The Cardiac pathophysiology of Covid-19
The uptick in avascular necrosis (AVN) cases of the hip after COVID-19 is a serious development that's got the medical community buzzing.
The uptick in avascular necrosis (AVN) cases of the hip after COVID-19 is a serious development that's got the medical community buzzing.

Uptick in post-acute Covid avascular necrosis.

Just like what happened in SARS1 survivors, which was well-documented but our government chose to ignore and pretend Covid is a cold.

·x.com·
The uptick in avascular necrosis (AVN) cases of the hip after COVID-19 is a serious development that's got the medical community buzzing.
Remodeling of intracellular architecture during SARS-CoV-2 infection of human endothelium
Remodeling of intracellular architecture during SARS-CoV-2 infection of human endothelium

Covid, and even asymptomatic covid is an endothelial disease.

Polish study Study on endothelial cells shows SARS-CoV-2 disrupts cell elasticity, causing vascular damage even without full replication.

“Clinical data indicate that COVID-19 causes cardiovascular complications, regardless of the severity of the disease. In this work, we have shown that SARS-CoV-2 infection causes vascular dysfunction due to the modification of endothelial cell elasticity.”

·nature.com·
Remodeling of intracellular architecture during SARS-CoV-2 infection of human endothelium
Endothelial inflammation in COVID-19
Endothelial inflammation in COVID-19

The vascular endothelium, which normally maintains blood flow and resists clotting and inflammation, can become overactive during COVID-19.

This overactivation can lead to multiorgan complications and long-term effects associated with Long Covid.

“Disrupted endothelial function underlies the multiorgan complications of COVID-19”

Disrupted endothelial function underlies the multiorgan complications of COVID-19
·science.org·
Endothelial inflammation in COVID-19
SARS-CoV-2 infection of human pluripotent stem cell-derived vascular cells reveals smooth muscle cells as key mediators of vascular pathology during infection
SARS-CoV-2 infection of human pluripotent stem cell-derived vascular cells reveals smooth muscle cells as key mediators of vascular pathology during infection

Using stem-cell-derived vascular cells, researchers found SARS-CoV-2 infects smooth muscle cells (SMCs), not endothelial cells.

Infected SMCs cause inflammation and clotting factors, explaining vascular issues seen in severe COVID-19 cases.

·biorxiv.org·
SARS-CoV-2 infection of human pluripotent stem cell-derived vascular cells reveals smooth muscle cells as key mediators of vascular pathology during infection
COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type | Arteriosclerosis, Thrombosis, and Vascular Biology
COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type | Arteriosclerosis, Thrombosis, and Vascular Biology
“COVID-19 at all levels of severity was associated with significantly higher risk of MI, stroke, or all-cause mortality over 1003 days of follow-up."
·ahajournals.org·
COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type | Arteriosclerosis, Thrombosis, and Vascular Biology
Persistent endothelial dysfunction in post-COVID-19 syndrome and its associations with symptom severity and chronic inflammation
Persistent endothelial dysfunction in post-COVID-19 syndrome and its associations with symptom severity and chronic inflammation

Long Covid patients exhibited persistent endothelial dysfunction.

This was indicated by lower venular flicker-induced dilation (vFID), narrower central retinal artery equivalent (CRAE), and lower arteriolar-venular ratio (AVR).

“Our results demonstrate that prolonged endothelial dysfunction is a hallmark of PCS, and impairments of the microcirculation seem to explain ongoing symptoms in patients.”

·link.springer.com·
Persistent endothelial dysfunction in post-COVID-19 syndrome and its associations with symptom severity and chronic inflammation
Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis
Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis
“Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis”
Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis
·medrxiv.org·
Increased levels of inflammatory molecules in blood of Long COVID patients point to thrombotic endotheliitis
How Long COVID Research Could Change the Way We Think About Blood Microclots
How Long COVID Research Could Change the Way We Think About Blood Microclots
“This observation seemingly confirmed a biomolecular link between the immediate symptoms experienced by acute COVID patients and the lingering symptoms of those with long COVID”
This observation seemingly confirmed a biomolecular link between the immediate symptoms experienced by acute COVID patients and the lingering symptoms of those with long COVID
·technologynetworks.com·
How Long COVID Research Could Change the Way We Think About Blood Microclots
The acute phase of was and is misunderstood by the majority of doctors.
The acute phase of was and is misunderstood by the majority of doctors.

“Medical images show us that the severe lung disease of #COVID-19 is the opposite of influenza - it occupies a different anatomical compartment in the lungs. All of this means there is no reason to expect that the later phases of COVID-19 should be anything like influenza.”

·x.com·
The acute phase of was and is misunderstood by the majority of doctors.
Unraveling Covid’s Pernicious Role in Brain Fog and Clotting
Unraveling Covid’s Pernicious Role in Brain Fog and Clotting

“Navigating social distancing requirements that complicated lab work, Akassoglou and her collaborators conducted a series of experiments in mice to explore the pernicious role of the coronavirus’s spike protein.

They discovered that beyond serving as the virus’s “key” to enter cells, spike binds with a blood clotting factor called fibrinogen, creating structurally abnormal, inflammation-promoting clumps of fibrin — the insoluble material that forms the mesh-like structures essential for wound healing.

High levels of these abnormal clots not only push the body’s clotting system into overdrive, increasing clot formation and inflammation, but also suppress natural killer cells — the immune system’s virus-clearing soldiers.”

Navigating social distancing requirements that complicated lab work, Akassoglou and her collaborators conducted a series of experiments in mice to explore the pernicious role of the coronavirus’s spike protein. They discovered that beyond serving as the virus’s “key” to enter cells, spike binds with a blood clotting factor called fibrinogen, creating structurally abnormal, inflammation-promoting clumps of fibrin — the insoluble material that forms the mesh-like structures essential for wound healing. High levels of these abnormal clots not only push the body’s clotting system into overdrive, increasing clot formation and inflammation, but also suppress natural killer cells — the immune system’s virus-clearing soldiers.
·bloomberg.com·
Unraveling Covid’s Pernicious Role in Brain Fog and Clotting
Table 3 Adjusted hazard ratios (95% CI) comparing the incidence of arterial thrombotic events after versus before or without a COVID-19 diagnosis, in the pre-vaccination, vaccinated and unvaccinated cohorts, overall and according to COVID-19 severity
Table 3 Adjusted hazard ratios (95% CI) comparing the incidence of arterial thrombotic events after versus before or without a COVID-19 diagnosis, in the pre-vaccination, vaccinated and unvaccinated cohorts, overall and according to COVID-19 severity
“Adjusted hazard ratios (95% CI) comparing the incidence of arterial thrombotic events after versus before or without a COVID-19 diagnosis, in the pre-vaccination, vaccinated and unvaccinated cohorts, overall and according to COVID-19 severity”
Adjusted hazard ratios (95% CI) comparing the incidence of arterial thrombotic events after versus before or without a COVID-19 diagnosis, in the pre-vaccination, vaccinated and unvaccinated cohorts, overall and according to COVID-19 severity
·nature.com·
Table 3 Adjusted hazard ratios (95% CI) comparing the incidence of arterial thrombotic events after versus before or without a COVID-19 diagnosis, in the pre-vaccination, vaccinated and unvaccinated cohorts, overall and according to COVID-19 severity
SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels
SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels

Autopsy study in patients with COVID shows that: SARS-CoV-2 infects, replicates and persists in Macrophages within the coronary vasculature Since CARDIAC MACROPHAGES have a half-life of 8.8years they would act as VIRAL RESERVOIRS in Atherosclerotic plaques

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels
·nature.com·
SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels
The Main protease (Mpro) from SARS-CoV-2 triggers plasma clotting in vitro by activating coagulation factors VII and FXII
The Main protease (Mpro) from SARS-CoV-2 triggers plasma clotting in vitro by activating coagulation factors VII and FXII
“Although the connection between COVID-19 and coagulopathy has been clear since the early days of SARS-CoV-2 pandemic, the underlying molecular mechanisms remain unclear. Available data support that the burst of cytokines and bradykinin, observed in some COVID-19 patients, sustains systemic inflammation and the hypercoagulant state, thus increasing thrombotic risk. Here we show that the SARS-CoV-2 main protease (Mpro) can play a direct role in the activation of the coagulation cascade.”
Although the connection between COVID-19 and coagulopathy has been clear since the early days of SARS-CoV-2 pandemic, the underlying molecular mechanisms remain unclear. Available data support that the burst of cytokines and bradykinin, observed in some COVID-19 patients, sustains systemic inflammation and the hypercoagulant state, thus increasing thrombotic risk. Here we show that the SARS-CoV-2 main protease (Mpro) can play a direct role in the activation of the coagulation cascade.
·biorxiv.org·
The Main protease (Mpro) from SARS-CoV-2 triggers plasma clotting in vitro by activating coagulation factors VII and FXII
NEW PREPRINT! Another study about ABNORMAL BLOOD CLOTTING related to SARS-CoV-2, but unlike the others I've covered, this isn't related to the spike protein.
NEW PREPRINT! Another study about ABNORMAL BLOOD CLOTTING related to SARS-CoV-2, but unlike the others I've covered, this isn't related to the spike protein.

“NEW PREPRINT! Another study about ABNORMAL BLOOD CLOTTING related to SARS-CoV-2, but unlike the others I've covered, this isn't related to the spike protein.

Turns out that Mpro, a viral protease [pro-tee-ace], can START the cascade.

a thread written for everyone:

Here's the takeaway: The Main protease (Mpro) of SARS-CoV-2—an enzyme that cuts up viral polyproteins—can also cleave a few host coagulation factors in a way that ACTIVATES them and BEGINS the blood clot cascade.”

·x.com·
NEW PREPRINT! Another study about ABNORMAL BLOOD CLOTTING related to SARS-CoV-2, but unlike the others I've covered, this isn't related to the spike protein.
The Significance of Endothelial Dysfunction in Long COVID-19 for the Possible Future Pandemic of Chronic Kidney Disease and Cardiovascular Disease
The Significance of Endothelial Dysfunction in Long COVID-19 for the Possible Future Pandemic of Chronic Kidney Disease and Cardiovascular Disease
Japan study: 65 million+ participants shows role of endothelial dysfunction in #longCOVID and leading to a potential chronic kidney disease and cardiovascular damage/disease.
·mdpi.com·
The Significance of Endothelial Dysfunction in Long COVID-19 for the Possible Future Pandemic of Chronic Kidney Disease and Cardiovascular Disease
Alterations in plasma proteome during acute COVID-19 and recovery - Molecular Medicine
Alterations in plasma proteome during acute COVID-19 and recovery - Molecular Medicine
“In-depth targeted proteome investigation evidenced substantial changes in plasma protein composition of patients during and recovering from COVID-19, evidencing a wide range of functional pathways induced by SARS-CoV-2 infection. In addition, we show that a subset of acute phase proteins, clotting cascade regulators and lipoproteins could have clinical value as potential predictors of long-term cardiovascular events in COVID-19 convalescents.”
In-depth targeted proteome investigation evidenced substantial changes in plasma protein composition of patients during and recovering from COVID-19, evidencing a wide range of functional pathways induced by SARS-CoV-2 infection. In addition, we show that a subset of acute phase proteins, clotting cascade regulators and lipoproteins could have clinical value as potential predictors of long-term cardiovascular events in COVID-19 convalescents.
·molmed.biomedcentral.com·
Alterations in plasma proteome during acute COVID-19 and recovery - Molecular Medicine
No Amount of Hand-Washing Can Make COVID-19 a Seasonal Virus - WHN
No Amount of Hand-Washing Can Make COVID-19 a Seasonal Virus - WHN
“With regard to COVID, terms such as “seasonal”, “like a cold”, and “like the flu” can be selected by writers to paint a portrait that lulls the reader into a false sense of security, drawing comparisons between a virus that has been around for less than five years to other viruses or conditions with respect to which the audience has grown familiar with. Moreover, even stock photos selected for certain news articles can subtly influence your response to the content expressed in that piece. A selected photo of a person gently cradling a tissue paper over their nose, instead of a person waiting for treatment in the ER, may give off the impression that they are harmlessly recovering from a tear-jerking soap opera instead of from a viral illness. In fact, we want to believe that COVID-19 is as gentle as a cold, as this outcome is far more pleasing, so this skewed presentation of the risk is far more palatable than what is expressed in the scientific literature.”
·whn.global·
No Amount of Hand-Washing Can Make COVID-19 a Seasonal Virus - WHN
No Amount of Hand-Washing Can Make COVID-19 a Seasonal Virus
No Amount of Hand-Washing Can Make COVID-19 a Seasonal Virus

No Amount of Hand-Washing Can Make COVID-19 a Seasonal Virus

"The selection of words modulates the message...terms such as “seasonal”, “like a cold”, and “like the flu” can be selected by writers to...lull the reader into a false sense of security... COVID-19 is not primarily a respiratory infection. This virus can cause a systemic disease with far-reaching effects on the body, particularly blood vessels. Once SARS-CoV-2 enters the body, the virus can affect the ...blood vessels, causing inflammation and damage.

·x.com·
No Amount of Hand-Washing Can Make COVID-19 a Seasonal Virus