Acute Myocarditis Following COVID-19 mRNA Vaccination in Adults Aged 18 Years or Older

SWAlexander

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In this population-based cohort study of 2 392 924 individuals who received at least 1 dose of COVID-19 mRNA vaccines, acute myocarditis was rare, at an incidence of 5.8 cases per 1 million individuals after the second dose (1 case per 172 414 fully vaccinated individuals). The signal of increased myocarditis in young men warrants further investigation.
Article: https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2784800
 

Pyrrhus

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We know that SARS-CoV-2 infects the heart muscle tissue.

We also know that most SARS-CoV-2 infections produce no symptoms.

So, if someone receives the SARS-CoV-2 vaccine and suddenly experiences inflammation of the heart muscle tissue (myocarditis), the obvious explanation is that the person had a silent infection of the heart muscle tissue and the vaccine gave the immune system a boost to start attacking the silent virus in the heart muscle tissue.

So why blame the vaccine when it's much more logical to blame the virus?
 

SWAlexander

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We know that SARS-CoV-2 infects the heart muscle tissue.

We also know that most SARS-CoV-2 infections produce no symptoms.

So, if someone receives the SARS-CoV-2 vaccine and suddenly experiences inflammation of the heart muscle tissue (myocarditis), the obvious explanation is that the person had a silent infection of the heart muscle tissue and the vaccine gave the immune system a boost to start attacking the silent virus in the heart muscle tissue.

So why blame the vaccine when it's much more logical to blame the virus?
Exactly. But how does the patient know if there was never a diagnosis?
Then there are doctors like Khullar: "On Taking Long COVID Seriously" https://www.socialsciencespace.com/2021/10/on-taking-long-covid-seriously/
 
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Pyrrhus

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Thanks for sharing that hypothesis! That (Can et al.) mouse model is indeed interesting and a bit surprising, and it is also plausible that a vaccination could accidentally hit a vein instead of muscle tissue, but the type of myocarditis demonstrated in the mouse model might be different from the type of myocarditis seen in practice:

From your link:
Can, L et al. (reference) have described an important and novel murine model of COVID-19 mRNA vaccination with features of myocarditis and pericarditis, i.e., myopericarditis. This murine model has the potential to provide significant insights into the pathogenesis of myopericarditis after COVID-19 vaccination via intramuscular and intravenous routes.

For example, the authors demonstrate in their paper that the inflammation in the myocardium after intravenous injection of the vaccine consists primarily of CD68+ macrophages or histiocytes, but not CD3+ T-lymphocytes. In comparison, evaluation of tissue from two patients suspected to have post COVID-19 mRNA vaccination related myocarditis demonstrated T-cells and macrophages, admixed with eosinophils, B cells, and plasma cells However, the myocarditis in those cases were only temporally associated with the vaccine (5).
[...]
It is important to note that future applications of the murine model system will likely require further investigation into how well this model represents the rare complication of myopericarditis following COVID-19 mRNA vaccination in humans.

For example, it is often challenging to correlate the dose of a drug when adjusted to body weight between a small mouse and a much larger human. In this case, the mouse received 0.25 mcg per gram weight. The Pfizer mRNA vaccine dose in humans is 0.4 x 10-3 mcg per gram for a 70 kg person.

Additional investigation will also be needed to determine the effect of murine strain in the model system of myopericarditis. This is particularly true since Balb/c mice, used in the study by Can, L et al., have a propensity to develop cardiac calcinosis (6).
 

hapl808

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So, if someone receives the SARS-CoV-2 vaccine and suddenly experiences inflammation of the heart muscle tissue (myocarditis), the obvious explanation is that the person had a silent infection of the heart muscle tissue and the vaccine gave the immune system a boost to start attacking the silent virus in the heart muscle tissue.
That's an interesting theory. And so it's possible that any viral infection could get reactivated and cause a problem, but also possible that the boost in the immune system could suppress a chronic infection? That might explain why some people improve and some get worse. Would be nice to have a more developed pre- and post- vaccine protocol for people with autoimmune dysfunction or possible latent viral issues.
 

Pyrrhus

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I had thrombosis after the first vaccination.
Thrombotic Thrombocytopenia after ChAdOx1 nCov-19 Vaccination: https://www.nejm.org/doi/full/10.1056/NEJMoa2104840

@Cipher's link also mentions a mouse model trying to explain the thrombosis from that adenoviral-vector vaccine:
For example, in a preprint, Nicolai L. et al describe a murine model of an adenoviral vector vaccine for COVID-19 using the ChAdOx1 nCov-19 vaccine that has been linked to a rare thrombosis with thrombocytopenia syndrome. They demonstrate that intravenous injection of this vaccine leads low platelet counts, clot formation and platelet activating PF4-polyanion antibodies similar to thrombotic thrombocytopenia (4).

To me, it also seems likely that people who experience thrombosis from an adenoviral vector vaccine may have had prior exposure to a similar adenovirus. This has always been a theoretical concern in the development of adenoviral-vector-based vaccines.
 

Pyrrhus

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And so it's possible that any viral infection could get reactivated and cause a problem, but also possible that the boost in the immune system could suppress a chronic infection? That might explain why some people improve and some get worse.
That's also a very interesting idea indeed, albeit a far broader statement than the one I made.

Would be nice to have a more developed pre- and post- vaccine protocol for people with autoimmune dysfunction or possible latent viral issues.
Yeah, would be nice. But at this point, I would simply settle for a more solid understanding of the origins of autoimmunity itself and a more solid understanding of viral persistence in the general population...
 

SWAlexander

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That's also a very interesting idea indeed, albeit a far broader statement than the one I made.



Yeah, would be nice. But at this point, I would simply settle for a more solid understanding of the origins of autoimmunity itself and a more solid understanding of viral persistence in the general population...
I wonder if any Long COVID or ME/CFS patients had a Thymus exam?