“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).”
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.
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.”
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
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.
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
Not only does a mild Covid infection cause vascular degeneration and arterial stiffness, but it also appears that both of these conditions are degenerative.
"The longer the period from COVID-19 infection the worse the vascular impairment...."
ENDOTHELIAL dysfunction in COVID-19 infections may lead to CARDIOVASCULAR COMPLICATIONS. "Cardiovascular-related proteomic changes in ECFCs exposed to the serum of COVID-19 patients" https://ijbs.com/v19p1664.htm *ECFC (endothelial colony forming cells)
Even mild Covid can increase your chance of blood clots after the initial infection. *all images available as editable, printable files, DM for info.
