I haven't seen anything comparing the two yet, but I would be interested in seeing that.
I'll note that in general, I have seen studies indicating that the risk of both MIS-C (linked in GP) and long-covid[1][2] are decreased when comparing vaccinated/unvaccinated post active infection. I've also seen reports that those unvaccinated who experience long-covid sometimes see reduced / cleared symptoms after subsequent vaccination.[3] We also know that antibody titer levels seem to be correlated with a reduction in infection, which is why when those begin to fall off we see more breakthrough infections. And finally we know that building long term T and B cells tends to see a quicker, more effective immune response, both of which should be created post-vaccination.
Given that, I would speculate that vaccination is likely to reduce overall proliferation of cell infection (including directly infecting cardiac tissue via the ACE2 receptors) via having more free-floating antibodies in your system, and is likely to reduce the overall immune-mediated inflammatory response to the virus as it can respond more quickly before the virus has had a chance to proliferate as much. Both of these (reduced inflammation, reduced cell infection) should reduce the risk of myocarditis as a result of infection. And I would speculate that that tracks with other observed reduction of symptoms of infection (MIS-C, long-covid).
Again, speculation on my part; I would definitely want to see studies to confirm or refute that.
I'll note that in general, I have seen studies indicating that the risk of both MIS-C (linked in GP) and long-covid[1][2] are decreased when comparing vaccinated/unvaccinated post active infection. I've also seen reports that those unvaccinated who experience long-covid sometimes see reduced / cleared symptoms after subsequent vaccination.[3] We also know that antibody titer levels seem to be correlated with a reduction in infection, which is why when those begin to fall off we see more breakthrough infections. And finally we know that building long term T and B cells tends to see a quicker, more effective immune response, both of which should be created post-vaccination.
Given that, I would speculate that vaccination is likely to reduce overall proliferation of cell infection (including directly infecting cardiac tissue via the ACE2 receptors) via having more free-floating antibodies in your system, and is likely to reduce the overall immune-mediated inflammatory response to the virus as it can respond more quickly before the virus has had a chance to proliferate as much. Both of these (reduced inflammation, reduced cell infection) should reduce the risk of myocarditis as a result of infection. And I would speculate that that tracks with other observed reduction of symptoms of infection (MIS-C, long-covid).
Again, speculation on my part; I would definitely want to see studies to confirm or refute that.
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[1]: https://www.thelancet.com/journals/laninf/article/PIIS1473-3...
[2]: https://www.medrxiv.org/content/10.1101/2022.01.05.22268800v...
[3]: https://www.yalemedicine.org/news/vaccines-long-covid