“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).”
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.
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.”
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”
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.
“‘I couldn't believe what I saw; these amyloid signals were everywhere. And I got back to the control sample and did the same, and I saw little bits, but not much.’
Pretorius had become one of the first in the world to discover that COVID-19 could induce widespread clotting in the blood of patients.”
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.”
“About 20% of my young patients are showing evidence of increased clotting as part of the baseline lab panels.
Never used to see this.”
“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.”
“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.”
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
“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.”
Great analysis thread:
“SIGNIFICANT NEW STUDY PUBLISHED TODAY IN NATURE!
Fibrin ‘binds to the SARS-CoV-2 spike protein,’ forming clots that ‘drive systemic thromboinflammation and neuropathology,’ and it happens ‘independently of active infection.’
Simplified breakdown of the paper below!
