Intramyocardial Inflammation after COVID-19 Vaccination
Finally some evidence !
The paper we are about to discuss has more meaningful findings than the authors themselves are aware of, and the paper itself is highly important.
Intramyocardial Inflammation after COVID-19 Vaccination: An Endomyocardial Biopsy-Proven Case Series
Myocarditis in response to COVID-19 vaccination has been reported since early 2021. In particular, young male individuals have been identified to exhibit an increased risk of myocardial inflammation following the administration of mRNA-based vaccines. Even though the first epidemiological analyses and numerous case reports investigated potential relationships, endomyocardial biopsy (EMB)-proven cases are limited. Here, we present a comprehensive histopathological analysis of EMBs from 15 patients with reduced ejection fraction (LVEF = 30 (14–39)%) and the clinical suspicion of myocarditis following vaccination with Comirnaty® (Pfizer-BioNTech) (n = 11), Vaxzevria® (AstraZeneca) (n = 2) and Janssen® (Johnson & Johnson) (n = 2). Immunohistochemical EMB analyses reveal myocardial inflammation in 14 of 15 patients, with the histopathological diagnosis of active myocarditis according to the Dallas criteria (n = 2), severe giant cell myocarditis (n = 2) and inflammatory cardiomyopathy (n = 10). Importantly, infectious causes have been excluded in all patients. The SARS-CoV-2 spike protein has been detected sparsely on cardiomyocytes of nine patients, and differential analysis of inflammatory markers such as CD4+ and CD8+ T cells suggests that the inflammatory response triggered by the vaccine may be of autoimmunological origin. Although a definitive causal relationship between COVID-19 vaccination and the occurrence of myocardial inflammation cannot be demonstrated in this study, data suggest a temporal connection. The expression of SARS-CoV-2 spike protein within the heart and the dominance of CD4+ lymphocytic infiltrates indicate an autoimmunological response to the vaccination.
First a clarification, reduced ejection fraction means your heart muscles are not functioning properly and pumping less blood than it should. 2 patients had myocarditis and 11 inflammatory cardiomyopathy. They are similar for the layperson, but from a medical perspective and treatment, they are slightly different.
Spike Protein was sparsely (meaning low levels of) detected in cardiomyocytes, meaning they didn’t find enough Spike Protein to explain direct causation. In line with the piece below.
By measuring different inflammatory markers in CD4 and CD8 cells, they found out it is most autoimmune mediated. And most by CD4+ cells. Infiltration means abnormal accumulation of something, in this case, CD4+ lymphocytes.
They went further to discard any other type of viral infection, as SARS-CoV-2, Parvovirus B19 (B19V), Enterovirus, Adenovirus, Human Herpesvirus 6, and Epstein–Barr virus.
Moreover, except the cases with active myocarditis (patients 1 and 2), giant cell myocarditis (patients 3 and 14), and one case of DCMi (patient 9), CD4+-T-cell-to-CD8+-T-cell ratio was ≥1, suggesting a predominantly autoimmunological origin of the observed inflammation
To me, this was the most remarkable finding of this paper. The skewing in the ratio in CD4/CD8 was the first clue and has been the basis of the PAID hypothesis since the very start of it, and there was a massive production of CD4+ lymphocytes and this was driving many of the inflammatory, and autoimmune reactions we were witnessing, among all the other mechanisms I covered.
You can read the first part here.
What this means, finally we are starting to get the evidence we were aware of but couldn’t directly test, the skew in the ratio is real, it is more present than most are willing to accept.
Because viral infections have been ruled out as the cause for myocarditis/myocardial inflammation, autoimmunological mechanisms might be an explanation. Cross-reactivity of spike protein antibodies with myocardial contractile proteins, mRNA immune reactivity and hormonal involvement, have been discussed as potential mechanisms by which COVID-19 mRNA vaccines induce hyperimmunity [20]. In the present cohort, the SARS-CoV-2 spike protein was found to be expressed on cardiomyocytes in 9 of 15 patients. Thus, vaccine-encoded spike protein seems to reach the heart, where it might trigger an inflammatory response, resulting in the development of myocarditis or DCMi.
Interestingly, except for five cases (AMC = 2, GCMC = 2 and DCMi = 1), the number of CD4+ T lymphocytes was either equal or higher than those of CD8+ T cells. In acute myocarditis, a shift of CD4-to-CD8 ratio towards CD8+ T cells is known [22], explaining the elevated CD8+ cells in AMC and GCMC patients. However, as CD4+ T cells are considered to be the major driver of autoimmune myocarditis [20], our data support the idea that vaccine-induced myocardial inflammation is a consequence of excessive CD4+ T-cell infiltration, and thus, a potential driver of autoimmunological myocardial damage.
As per a recent paper and piece I wrote, we know the mRNA floats around the entire body, meaning the Spike Protein can be expressed literally anywhere that is suitable, and once again protein mimicry plays a role. This isn’t the first paper looking at the mechanism behind myocarditis from the mRNA vaccines, but this is the first with this mechanism.
The biggest problem with being immune-mediated means that upon rechallenge (meaning when the person gets either injected with mRNA again or is infected), it has a chance of the body, fixated in the immune response from the vaccine, by the same mechanism described here, inducing another round of heart damage, even at subclinical levels, in fact, I would argue it most likely will be at subclinical levels and some of the young and fit will just drop dead from mysterious sudden death.
Bear in mind this isn’t exactly, or solely the mere expression of the Spike Protein in the heart, this has much more to do with the actual design of the vaccine and how they chose to elicit an immune response, overcompensating to one side of your immune system so they would create a flood of antibodies and sell it as “95% effective”, the Spike protein and its properties add fuel to the raging fire.
The following piece bears more clues to the mechanisms and is in line with the PAID hypothesis. It covers both sides of this paper, myocarditis, and lymphs, to be specific, Lymphadenopathy, the immune dysregulation aspect of it. Lymphadenopathy is underwhelming reported among the vaccinated, so we have very little data on forms, types of cells, and duration.
And would share another piece, because I got a feeling it will become relatively important within months.
They have been ignoring safety signals since the start, and still doing it to this day.
Given the current dynamics at play with the new variants (more transmissible, high replication rate) I think it will burden the cardiovascular system of many of the younger vaccinated crowd to the extent it will be even more perceptible. And as I wrote today on Twitter, this entire fucking thing was entirely avoidable.
I wish everyone a nice Sunday, I might send another short e-mail in a few hours or sometime tomorrow.
Thanks for the Link to the paper!
GREAT WORK!
Excellent walk through of this paper and linkages to your previous posts. And bravo to Europe for much bolder scholarship than the US is currently tolerating about the evidence of vax injury. I've always been curious about Pfizer's "Golden Child" status. Even the MSM has gone after J&J (called it ineffective and dangerous), Oxford/AZ, and Moderna, but no one is allowed to say that Pfizer is causing the same problems and injuries. Which was always clear from VAERS. Why?
Can HCW's use the CD4+T Cell values and CD8 ratios for predictive screening? One thing I would really like to see is data on differential outcomes (if any) from docs that utilized early intervention strategies vs. ones that follow the mainstream COVID standard of (non) care. There is a need not just to point out the injuries, and mechanisms of injury, but also, as you said "avoidability." Lots of prima facie evidence that early intervention matters, but need detailed clinical evidence. Increasingly relevant as these variant waves continue