“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.
“‘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.”
“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.”
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!
"The COVID-19 thrombus has unique and distinct characteristics."
Thrombosis in acute and #LongCovid
Latest paper from Dr Robin Kerr & me: #LongCovid is primarily a Spike protein Induced Thrombotic Vasculitis https://researchsquare.com/article/rs-2939263/v1 Here we proposed that long covid is primarily a spike protein-induced thrombotic vasculitis, & we use Robin as a supporting case study 🧵 #TeamClots
"I hope to god I'm wrong. I've never wanted to be more wrong in my life.... Worst case scenario... we are going to see a tsunami of cardiovascular disease over the next few decades." #LongCOVID
Patient Anecdote thread on Twitter: Today I travelled 4000miles to get tested for Microclots to test the theory that this is causing my #longcovid symptoms. Turns out I have them. This testing needs to be made accessible to all those suffering around the world so they can be treated (1)
Detailed analysis thread on Twitter: 1/🧵 Micro Clots & Endothelial Dysfunction in Long COVID
Plus new Epidemiology in @JAMA_current some say proves #LongCOVID is a hoax⁉️
Truth is…endothelial dysfunction plus inflammation can lead to life-altering brain & body dz.
Let’s explore data
“One core question is: Do these microclots actually represent a root cause, or are they in response to something else that's ongoing?” says Michael VanElzakker PhD, co-founder of PolyBio Research Foundation, which is focused on studying viral reservoir:
Tiny, Menacing Microclots May Explain Long COVID’s Symptoms
