1/ 3-8 months after initial diagnosis of myocarditis in teenagers post jab, a large majority are still persistently showing abnormal markers (GLS and LGE) associated with a worse prognosis of present and future heart function. This is despite improvement in other cardiac markers.
2/ “The presence of LGE is an indicator of cardiac injury and fibrosis and has been strongly associated with worse prognosis in patients with classical acute myocarditis.”
3/“LGE is a predictor of all cause death, cardiovascular death, cardiac transplant, rehospitalization, recurrent acute myocarditis and requirement for mechanical circulatory support”
4/“Georgiopoulos et al found presence and extent of LGE to be a significant predictor of adverse cardiac outcomes in an 11 study meta-analysis”
5/ “Notably, in our cohort, though there was significant reduction in LGE at follow up, abnormal strain persisted for the majority of patients at follow up.” Note: Even though LGE improved, it is still abnormal.
6/“In a cohort of adolescents with COVID-19 mRNA vaccine-related myopericarditis, a large portion have persistent LGE abnormalities, raising concerns for potential longer-term effects.”
7/ “We plan to repeat CMR at 1 year post-vaccine for our cohort to assess for resolution or continued CMR changes.”
9/ Note:
LGE= Late Gadolinium Enhancement
GLS = Global Longitudinal Strain
10/ Once again, their statements are completely wrong. Jab-Induced myocarditis is not temporary and does not rapidly resolve to baseline. Add this to the growing list of duplicities.
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1/Remember this study from Denmark? It shows negative vaccine efficacy after the antibodies wane, which means an increased rate of infection if you’re jabbed. Data from other countries shows the same trend. Why? Is this evidence that the jab is impairing the immune system?
2/ Data from the UK shows higher rates of infection (rate per 100,000) with increased number of jabs.
1/ Repeated over-stimulation by the same antigen can reprogram T-cells (via TCR revision) to become autoantibody inducing cells, leading to autoimmune conditions, like Systemic Lupus Erythematosus (SLE) - as demonstrated in this mouse model.
2/ This mechanism for potentially causing unintended autoimmune disorders should not be overlooked when considering the safety of repeated doses of the same antigen, such as the proposed and developing regiment of the current mRNA jab program.
1/ Why do jabbed people still become infected and transmit the virus? As this recent Science paper shows, jabbed people are lacking IgA/IgG mucosal immunity. They also show that mucosal immunity is substantially gained only after a jabbed person has a natural infection.
2/ The authors conclude: “We also speculate that the extraordinarily high antibody titers observed in vaccinated individuals who develop breakthrough infections may lead to subsequent long-term protection in those individuals.”
3/ Translation: The only way a jabbed person can gain long lasting & sterilizing immunity that prevents further infection and transmission is to become naturally infected.
1/ Let’s take a look at the coordinated media blitz to explain away and normalize the rapid rise of heart attacks and blood clots. (If someone good at graphics would be willing to make a collage of these and post it in the comments, I would be thankful)
1/ Spike protein & *mRNA* persists for up to 2 months post jab in lymph nodes.
“The observed extended presence of vaccine mRNA and spike protein in vaccinee LN GCs for up to 2 months after vaccination was in contrast to rare foci of viral spike protein in COVID-19 patient LNs”.
2/ Normal mRNA is quite unstable and decays in a cell with a half life on the order of hours. We know that vaccine mRNA was stabilized using N1-methylpseudouridine, and by engineering the 5’-UTR, 3’-UTR and polyA tail. This engineering results in mRNA still present at 2 months.
3/ They also found circulating plasma levels of Spike protein in line with a COVID infection (174 pg/mL). After 2nd dose, Spike detection decreases, presumably due to circulating antibody/Spike immune complexes blocking detection by the assay.