May 26, 2021
The cases of Myocarditis being observed post COVID and post Spike Protein therapy are most likely due to the Spike Protein attaching to the surface of cardiomyocytes.
The Spike Protein is homologous to Hepcidin. In certain cardiac pathologies characterized with inflammatory infiltrate, local hepcidin can be overexpressed, but the source of this hepcidin is not cardiomyocytes. In Friedreich’s ataxia (FA) heart dysfunction is accompanied with chronic myocarditis. Inflammatory infiltrate in FA shows higher levels of hepcidin expression compared with cardiomyocytes.
This may also explain the instances of arrythmia being observed. Studies have shown that hepcidin in cardiomyocytes tends to accumulate near intercalate discs, especially in hypoxic conditions, which is interesting, as these intercellular contacts in the heart are crucial for propagating electrical impulses without resistance.
As the Spike Protein is "phantom" Hepcidin, it "confuses" the cells. There is a pattern of increased hepcidin expression in organs under stress, and this is the case with heart as well. In the early phase of myocardial infarction (MI) and in myocarditis, cardiac hepcidin expression is increased significantly.
Referenced/Related Papers
COVID-19 and iron dysregulation: distant sequence similarity between hepcidin and the novel coronavirus spike glycoprotein
https://biologydirect.biomedcentral.com/articles/10.1186/s13062-020-00275-2
Balance of cardiac and systemic hepcidin and its role in heart physiology and pathology