Covid Vaccine Myocarditis Implications
Why is there an increased risk of infection in the vaccinated and what are the key implications?
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This recent Swiss study has serious implications for longer term heart health.
Quote from the paper:
"First, our findings confirmed the study hypothesis. mRNA-1273 booster vaccination associated elevation of markers of myocardial injury occurred in about one out of 35 persons (2.8%), a greater incidence than estimated in meta-analyses of hospitalized cases with myocarditis (estimated incidence 0.0035%) after the second vaccination." Buergin, Natacha, et al. "Sex‐specific differences in myocardial injury incidence after COVID‐19 mRNA‐1273 Booster Vaccination." European Journal of Heart Failure.
Course Agenda (Subject to adjustment)
Introduction
Why is this important now?
Definition of myocarditis
Overview of the heart
Myocarditis signs and symptoms
What is troponin, and relevance to cardiac injury
Review of the Swiss paper
Comparison to other papers that only focus on significant myocarditis cases
Look at the investigations in the Big-10 study
Combination of increased risk of Covid infection in the boosted population with vaccine damage
Special focus on College and University vaccine mandates
Conclusion and closing remarks
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Thanks for sharing this important information Dr McMillan much appreciated
It is well established that CD4+ T cells are the main effector cells in myocarditis, and frequent self-antigen of CD4+ T is alpha-myosin heavy chain (α-MyHC). Predominance of myocarditis in young males after C-19 vaccination can be explained by autoreactive, negative selection impaired CD4+ T cells released by thymus glands that are not familiar to the α-MyHC during their early development. The risk of young males is higher because prolonged exposure to testosterone (during puberty and young age) increases newly expressed α-MyHC proteins on heart muscle and therefore increases potential self-antigen expression on the heart.
But what is antigen of those autoreactive, negative selection impaired CD4+ T cells in adult women after mRNA booster vaccination – has to be determine. My guess is that it is not viral S protein, but α-MyHC or other endogenously produced protein, where actually the problem starts - both self-antigen and newly generated self-proteins lacking MHC-II molecules can't be distinguished by those negative selection impaired CD4+ T cells.
I guess the risk of myocarditis after C-19 vaccination might be reduced by administering vaccine in anterolateral thigh muscle, instead of deltoid muscle.