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(Definition: Microangiopathy (also known as microvascular disease, small vessel disease (SVD) or microvascular dysfunction) is a disease of the microvessels, small blood vessels in the microcirculation.
Small vessel diseases (SVDs) affect primarily organs that receive significant portions of cardiac output such as the brain, the kidney, and the retina. Thus, SVDs are a major etiologic cause in debilitating conditions such as renal failure, blindness, strokes from brain clots, and dementia.)
Executive Summary:
…repeated exposure to the Spike Protein causes small blood vessels to be scarred and damaged resulting in fibrosis.
It is being so injured that it is repairing repairs. Layer upon layer of non-functioning fibrous tissue.
Why is this so important? Perhaps the most urgent reason:
Microvasculature collagen I deposition was only evident in fatal COVID-19, long COVID, and in the mice exposed to the S1 subunit for 1.5 months.
Please reread that carefully. Several times, if need be. The deposition of collagen was evident not only in those who died or had Long COVID, but ALSO IN THOSE MICE WHO WERE EXPOSED TO THE SPIKE PROTEIN FOR 1.5 MONTHS.
What does this tell us?
This tells us that the Spike Protein may damage us EVEN IF IT DOES NOT CAUSE APPARENT DISEASE. Therefore, you could seem to be completely healthy, without experiencing a case of severe COVID or Long COVID, yet the Spike Protein, if present (repeatedly being injected/produced), may be slowly erasing your microvasculature. This could result in a whole host of deleterious conditions, including sudden cardiac death. And have we seen sudden cardiac death, unfortunately.
Of course, the list goes on, and virtually every major organ could have its functionality severely impaired over time. Yet without the appearance of any major symptoms while the devastation grows.
It was precisely this disease process that I predicted the Spike Protein would induce in the microvasculature.
Article:
Five years ago, I wrote a post wherein I warned that repeated exposure to the Spike Protein would result in a systemic microangiopathy resulting in fibrosis.
The microvasculature is being lacerated and scarred. It is being so injured that it is repairing repairs. Layer upon layer of non-functioning fibrous tissue. This unfortunately hearkens back to my hypothesis that the Spike Protein of SARS-CoV-2 is turning us into masses of living cartilage.
COVID-19 LOOKS LIKE RADIATION POISONING: NOT JUST A VASCULAR DISEASE BUT A DISEASE OF SYSTEMIC MICROANGIOPATHY FOLLOWED BY SYSTEMIC FIBROSIS
Walter M Chesnut
1) MY MOST IMPORTANT FINDING TO DATE – WHY COVID-19 LOOKS LIKE RADIATION POISONING COVID-19: NOT JUST A VASCULAR DISEASE BUT A DISEASE OF SYSTEMIC MICROANGIOPATHY FOLLOWED BY SYSTEMIC FIBROSIS, ALMOST CERTAINLY INDUCED BY THE TISSUE-DAMAGING EFFECTS OF THE SPIKE
The date of that post? 9:16 PM · Nov 29, 2021!!!
Just last week a major study was published confirming this exact hypothesis of mine. And due to the exact same mechanism – repeated exposure to the Spike Protein.
The question of whether the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein persists in angiotensin converting-enzyme 2–positive (ACE2+) endothelia in the central nervous system (CNS)/other sites and induces a prolonged microvasculature injury syndrome was addressed. People who died of COVID-19, with age-matched controls, and people with long COVID with symptoms persisting from 1 to 5 years, with controls of people who had recovered from COVID-19, were studied. Also compared were wild-type mice injected with the spike protein euthanized at day 5 versus 1.5 months. The ACE2+ microvasculature density in the CNS increased 19-fold in the mice exposed to spike protein for 1.5 months. Human fatal COVID-19 cases exhibited an ACE2+ CNS density of 13.2/3.9 versus 2.1/0.9 for the controls. Long COVID cases showed an ACE2 microvasculature density of 11.9/3.0 versus 3.5/0.9 for the people who recovered from COVID. Viral spike microvasculature density in the CNS was similar in the fatal COVID-19 cases (6.9/2.1) and mice (7.0/4.0) and in the skin of long COVID cases (6.0/1.9) and less in people who recovered from COVID-19 (0.9/0.3). Microvasculature collagen I deposition was only evident in fatal COVID-19, long COVID, and in the mice exposed to the S1 subunit for 1.5 months. Thus, SARS-CoV-2 spike (S1) protein can persist for months to years with an associated microvasculature pro-inflammatory state and a restrictive fibrosing microangiopathy, and exposure to high-dose S1 markedly increases ACE2 endothelial density.
Effects of Prolonged SARS-CoV-2 Spike Protein Exposure in Long COVID and a Mouse Model of the Disease
https://ajp.amjpathol.org/article/S0002-9440(26)00296-8/abstract
Why is this so important? Perhaps the most urgent reason:
Microvasculature collagen I deposition was only evident in fatal COVID-19, long COVID, and in the mice exposed to the S1 subunit for 1.5 months.
Please reread that carefully. Several times, if need be. The deposition of collagen was evident not only in those who died or had Long COVID, but ALSO IN THOSE MICE WHO WERE EXPOSED TO THE SPIKE PROTEIN FOR 1.5 MONTHS.
What does this tell us?
This tells us that the Spike Protein may damage us EVEN IF IT DOES NOT CAUSE APPARENT DISEASE. Precisely as I predicted it may. Therefore, you could seem to be completely healthy, without experiencing a case of severe COVID or Long COVID, yet the Spike Protein, if present (repeatedly being injected/produced), may be slowly erasing your microvasculature. This could result in a whole host of deleterious conditions, including sudden cardiac death. And have we seen sudden cardiac death, unfortunately.
The coronary vascular system has a unique structure and function that is adaptive to myocardial demand. It is composed of a continuous network of vessels receding in size from epicardial arteries to the microvascular circulation. Failure to meet myocardial demand results in ischemia, angina, and adverse myocardial outcomes. It is evident that 50 % of patients with angina have a non-obstructive coronary disease and 66 % of these patients have coronary microvascular dysfunction (CMD). The impact of CMD on the atria and ventricles is exhibited through its association with atrial fibrillation and distortion of ventricular repolarization. Ultimately, this influence increases the risk of mortality, morbidity, and sudden cardiac arrest. CMD serves as an independent risk for atrial fibrillation, increases ventricular electrical inhomogeneity, and contributes to the progression of cardiac disease. The underlying pathogenesis may be attributed to oxidative stress evident through reactive oxygen species, impaired vasoactive function, and structural disorders such as fibrotic changes. Myocardial ischemia, brought about by a demand-supply mismatch in CMD, may create a milieu for ventricular arrythmia and sudden cardiac arrest through distortion of ventricular repolarization parameters such as QT dispersion and corrected QT dispersion.
Coronary microvascular dysfunction, arrythmias, and sudden cardiac death: A literature review
https://pmc.ncbi.nlm.nih.gov/articles/PMC10998042/
Of course, the list goes on, and virtually every major organ could have its functionality severely impaired over time. Yet without the appearance of any major symptoms while the devastation grows.
We need to have studies on the microvasculature of the general population by COVID infection history, COVID vaccination history and to see if Spike is circulating in those who have neither had COVID nor a COVID vaccine. And yes, this is extremely important and urgent. Clearly, I wish my warnings had been heeded half a decade ago. We will fight on.
Finish reading: https://wmcresearch.substack.com/p/confirmation-of-my-finding-from-five