“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).”

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.

“About 20% of my young patients are showing evidence of increased clotting as part of the baseline lab panels.

Never used to see this.”

“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.”

“COVID-19, caused by the SARS-CoV-2 virus is an acquired thrombophila with a high incidence of thrombosis.

“Thrombosis…can involve most organs and organ systems.”

Thread by @DickZoutman on Thread Reader App

From 2021: "Blood clot risk from coronavirus infection outweighs risk from vaccine: study

This is the largest study to date, covering almost 30 million people."