Rapid Amyloidosis: The Kinetic Viewpoint: Sudden Death and Diabetes

Up to half of all patients with cardiac amyloidosis die suddenly

The amyloidogenic properties of the Spike Protein have been well established.

The prospective of S-protein amyloidogenesis in COVID-19 disease associated pathogenesis can be important in understanding the disease and long COVID-19.

Amyloidogenesis of SARS-CoV-2 Spike Protein
https://pubs.acs.org/doi/10.1021/jacs.2c03925

Now, when you have amyloids aggregating rapidly, which is what I believe is happening, they NUCLEATE. This is established through the kinetic viewpoint of nucleation.

Polymerization into larger structures involves a set of necessary but unfavorable steps in the reaction that bottleneck the formation of large aggregates. These steps are views as constituting formation of a critical nucleus.

Kinetic viewpoint: the rate of monomer addition to the aggregate exceeds the rate of monomer loss, after the nucleus size is surpassed but not before.

Mechanisms of amyloid fibril formation by proteins
https://www.icts.res.in/sites/default/files/1285914321Jayant%20Udgaonkar%202.pdf

Why is this extremely dangerous? Because, once nucleated, AMYLOID AGGREGATES SELF-PROPOGATE.

Proteins that aggregate in disparate neurodegenerative disorders share with prions the molecular properties of nucleation, templating, growth, multiplication and spread. Each of these phenomena presents potential therapeutic targets. For example, reducing the production or stimulating the removal of amyloidogenic proteins will lower the concentration of the protein and thereby impede nucleation and growth.

Self-propagation of pathogenic protein aggregates in neurodegenerative diseases
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963807/

But we are not just dealing with neurodegenerative aggregates. The proteins which can become amyloid are numerous – and INSULIN IS ONE OF THEM.

So, I believe the mechanism for those who die suddenly, without the presence of myocarditis, is amyloidosis. Also caused by the Spike Protein. A rapid death, or a delayed rapid death.

This also explains why it is so difficult to find.

Sudden death in patients with AL amyloidosis is usually attributed to pulseless electrical activity, followed by ventricular arrhythmias, but may result from thromboembolic complications or bradyarrhythmias and conduction system disease secondary to amyloid infiltration or autonomic dysfunction. Despite advances in therapeutic regimens the frequency of sudden death within ≤90 days of diagnosis remains at 25%-30%. All unexplained sudden death victims should undergo post-mortem expert examination to investigate whether a cardiac origin should be suspected [38]. Unfortunately, even when an autopsy is performed, a proportion of sudden deaths, ranging from 2 to 54%, remain unexplained: this broad range of values is likely due to heterogeneity of the autopsy protocols. Postmortem diagnosis of cardiac amyloidosis is rare and needs a rigid protocol of macroscopic and microscopic investigations. Elevated standards for autopsy, heart examination, and histologic sampling are needed.

Sudden death in lambda light chain AL cardiac amyloidosis: a review of literature and update for clinicians and pathologists
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7414507

This mechanism may also explain any large fibrous formations which have been observed.

Clearly this is insidious, and this phantom is now emerging from the microscopic shadows where it has hidden.