If you recall, months ago I noticed the resemblance of reactions to the Spike Protein to Graft vs Host disease. I have now discovered the mechanism for this similarity.

It has been determined that the Spike Protein damages hematopoietic stem/progenitor cells in the mechanism of pyroptosis in Nlrp3 inflammasome-dependent manner. This leads to the release of cytosol components to extracellular space and final cell lysis.

When hematopoietic stem cells are lysed, they release angiopathic molecule filamentous actin.

THIS IS EXACTLY WHAT HAPPENS AFTER HEMATOPOIETIC STEM CELL TRANSPLANT!

Endothelial injury after hematopoietic stem cell transplant is an important initiating factor for early transplant toxicities of thrombotic microangiopathy and acute graft versus host disease. We hypothesized that release of the angiopathic molecule filamentous actin from hematopoietic cells lysed during conditioning prior to stem cell transplant would be associated with clinical outcomes.

Cell lysis leads to the release of toxic intracellular molecules into the circulation, including filamentous actin (F-actin) and nucleotides such as ATP, that are usually present in low concentrations outside the cell. Actin is the most abundant protein in the human body and exists in two forms- monomeric or globular actin (G-actin) and a polymeric form, F-actin. F-actin is known to be angiopathic.

This can lead to transplant-associated thrombotic microangiopathy (TA-TMA). What are differential diagnoses for TA-TMA? THROMBOTIC THROMBOCYTOPENIC PURPURA and THROMBOTIC MICROANGIOPATHY!

Endothelial injury plays a significant role in a host of potentially lethal syndromes, including HSCT-associated thrombotic microangiopathy (HSCT-TMA), and can occur prior to, during, and after HSCT.

This raises the levels of catecholamines, which, I believe, are largely responsible for much of the sudden cardiac deaths we are observing, as has been noted by Cadegiani.

I believe this is related to the small vessel disease discussed above. Which, is intimately related to Diabetic Cardiovascular Disorders for parallel reasons.

Metabolic and hormonal factors, autonomic neuropathy and, microangiopathic alterations are the main ethiopathologic factors. The most important mechanisms of diabetic cardiomyopathy are metabolic  disturbances (depletion of glucose transporter 4, increased free fatty acids, carnitine deficiency, changes  in calcium homeostasis), myocardial fibrosis (association with increases in angiotensin II, IGF-I, and inflammatory cytokines), small vessel disease (microangiopathy, impaired coronary flow reserve, and endothelial dysfunction), cardiac autonomic neuropathy (denervation and alterations in myocardial catecholamine levels), and insulin resistance (hyperinsulinemia and reduced insulin sensitivity) (Fang et al., 2004).