> It has recently been reported that the incidence of myocarditis and pericarditis is increased in COVID-19 patients during the acute illness [12]. However; whether or not myocarditis and pericarditis after the recovery period are a part of the long COVID-19 syndrome is yet unknown. Herein, we studied the incidence of myocarditis and pericarditis in a large cohort of COVID-19 patients after recovering from the acute infection.
It's looking at myocarditis and pericarditis not in the acute phase, but post. And iirc there has been other papers showing there is an increased risk in a 12 month followup.
I was more just pointing out that this was in the recovery phase, not during the acute infection. I've seen people use this paper as evidence that a covid infection does not increase the risk of CV incidents.
And this seems to be an outlier anyway:
> In conclusion, either symptomatic or asymptomatic SARS-CoV-2 infection is associated with an increased risk for late CV outcomes and has a causal effect on all-cause mortality in a late post-COVID-19 period.
> In summary, using a national cohort of people with COVID-19, we show that risk and 12-month burden of incident cardiovascular disease are substantial and span several cardiovascular disease categories (ischemic and non-ischemic heart disease, dysrhythmias and others). The risks and burdens of cardiovascular disease were evident even among those whose acute COVID-19 did not necessitate hospitalization.
> The 12-month risk of incidental cardiovascular diseases is substantially higher in the COVID-19 survivors than the non-COVID-19 controls. Clinicians and patients with a history of COVID-19 should pay attention to their cardiovascular health in long term.
> First, we censored cohort participants at the time of receiving the first dose of any COVID-19 vaccine. Second, we adjusted for vaccination as a time-varying covariate.
I got OG Covid very early in 2020. I had something like a heart attack about six months later. It has not reoccurred. I suspect I had something kind of like a stroke a bit ago. The event was accompanied with very terrifying and specific neurological event. A loud noise that was only inside my head and unreal "sounding" that worked like a corkscrew from the right side of my head to the front while my vision dimmed. I legitimately thought I was about to die and was able to tell my partner so. It passed and I went to a doctor the following morning. More on that below. I've only noticed small motor function loss on my left side and some memory impairments. Since 2020 I have had what I call a "dinner plate in my chest". It goes away with some cardio exercise.
I can feel my vascular system radiating from the center of my chest up the sides of my neck and out through my shoulders. It's got a bit of a slow ache and upper body stiffness when it's flaring up. When it's bad, sometimes I wake up with numbness that radiates from my chest out to my finger tips on the top sides of my arms.
I have no problems taking deep breaths. The injury does not seem to be growing.
After the cardiac issue I had in 2020, my bloodwork showed signs that there was a possible event. My EKG was fine. This was days after. I have a constant dull to really shitty headache in the top front inside my head that has been persistent from the thing that seemed like a mini-stroke. I have never really had headaches without a serious hangover. I couldn't see my regular GP, still haven't been able to, but the doc I did see basically told me she thought it was vertigo and I needed to clean my ears. She checked my reflexes and some other things and said she could not recommend any further action without more events. I know what vertigo is. I've experienced it on accident and on purpose. I am not experiencing random vertigo. She did not seem to take anything I was saying seriously. She also told me she found it offensive that I was swearing while describing the experience and a gentleman would refrain from such language. I think she's a fucking moron, but she's functionally just as helpful as my curious, smart, and compassionate GP.
I'm 6' broad shouldered, and 210lbs. A bit chubby. I don't exercise a ton, but do some exercise, especially when the dinner plate flairs up. I don't smoke.
I've had a chest x-ray and it shows what looks like scarring in vascular structures radiating from my lungs. The forms kind of look on x-ray like the "ground glass nodules" that some people are experiencing. It's VERY hard to get a doctor that wants to do anything with me about this stuff. The fact that cardio makes things better and not worse is counter intuitive from traditional issues that look the same like Angina Pectoris. I've said since I recovered the first time (I've had it at least once more post vaccination but nothing was quite as near death as the first) that I felt cognitively and physically like I was 10 years older. I turn 40 next year. New research has been coming out showing that some people suffering from long COVID show aging of their CV systems of about 10 years.
It is going to take a long time to figure out what Long Covid is really doing to people. Some people that never showed symptoms get these things. Children are showing it too. The diagnostic criteria is really difficult and there is almost no treatment aside from some success with similar treatments used for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome[0]. I have found that most doctors don't want to touch it with a 200ft poll. The Red Cross says I should join an online support group[1]. A lot of the research is being done by scraping subreddits for people reporting symptoms because they vary so wildly and seem to have little correlation with the perceived severity of infection.
I suspect we may find a high correlation with exposure to heavy air born contamination. ...
I got Omicron in January '22 despite being double vaxx'd, and I felt totally fine until 3-4 mo. later when I started to get recurrent dizzy spells, major fatigue, and bouts of anxiety, which are all very unusual for me. Checkup / bloodwork showed nothing. I am 41 y.o. who exercise regularly, does not smoke, rarely drinks, etc.
So far I can still function and maintain a job, but it makes me wonder what's going on inside of me that 11 months later it's still causing these issues regularly. Our 4 y.o. son got it as well and although he was asymptomatic I am still very concerned about what the long-term effects on him may be.
I am not a doctor and this is not medical advice, but I read a paper saying that hyperbaric oxygen therapy helped some people, so I've been using Wim Hoff breathing as a poor man's version. It does seems to help with the fatigue but not the vertigo. Best of luck.
There's a balance with that sort of thing though. Thinner blood to alleviate the constriction, if kept constant can cause other problems. Definitely not the worst band aid in the world though.
My sister recommended Wim Hoff. I'll scope it out. I had been considering buying an o2 concentrator since 2020 and I do have some voice/breath training and have found some exercises related to that that aren't dissimilar from Wim Hoff show some reduction in symptoms.
Honestly, I feel very lucky to be as functional as I am. I do worry about how medical and political systems are responding to COVID and long COVID, but largely I think good care is going to come from the bottom up and not top down. I'm comfortable(ish) with a reality that I might just suddenly drop dead tomorrow, but this experience has given me a new appreciation for the health I have that I could not have fathomed before. Because I can alleviate symptoms with diet and directed exercise and it does appear to have a cumulative effect on their reduction, I think recovery is possible without intense intervention. I don't even mind being more spacey and a bit dumber. It suits me a bit and has changed the pace of my life in a way that once I embraced has been good.
My biggest worry is that if I suddenly die and how devastating that would be for people that depend on me, but I think without an infection of a new virus or several viruses I might live a shorter, but alright life. My chance of suddenly dying because I got light headed in an elevator now being slightly higher than my chance of being crushed by a vending machine.
There is no proven health benefit to using an oxygen concentrator for patients without lung disease (such as emphysema). The limiting factor in delivering oxygen to tissues is hemoglobin, not inhaled PPO2. Extended exposure to elevated PPO2 can cause oxidative damage to lungs and nerves, especially above about 0.5 bar, so you don't necessarily want to use it unless you need it.
This is solid info constructed in a form that includes so much that I needed. I did not have any designs, really, to go into this and experiment on myself, but you know... the wikis do pile up.
Thank so so much for this. Very useful information.
I had a vertigo issue crop up recently and was able to get it diagnosed (working in military aviation they take this stuff pretty seriously); I don't know that it will help but it's one avenue to look down:
One of my inner ear canal output signals dropped by about 75%. There is a diagnostic test they can do; more basic tests showed nothing but this more sensitive one showed it clear as day. No-one can tall me WHY the nerves are outputting a weaker signal and I couldn't tell you if it's related but it's something that doesn't get checked much.
Very interesting. My homunculus is very ears forward. A lot of my work and fun revolves around my relationship with sound. I did a hearing test last year. It was fine. I have not directly noticed any issues with my hearing, but I recognize that the types of things I might be experiencing might not be so much perceived as hearing but more as orientation, balance, or even be queues to memory that could be altered.
If you had the information available, I'd be very interested to know the names of the diagnostic tests you took. Analysis of how I'm hearing is something I'm uniquely able to analyze over time and compare to medically conducted tests. While I think I know how the second test might have worked, I don't know what I'd call such a test to look for it.
I think analysis of hearing on newly infected to post care of people with COVID and Long COVID could provide useful hints that most other methods might not be able to detect.
I had an 8 week dizzy spell in fall of 2020. Never had anything like it before, didn’t have any other symptoms. Went to ENT and ears were completely fine.
I have no idea if it was anxiety or Covid, but the dizziness was disorienting, at the worst I couldn’t walk , it felt like I was on a boat. During this time I had anxiety attacks almost non stop-triggered by the vertigo. As soon as I started to notice the vertigo I would begin to spiral because it was so unprecedented and disorienting. It just cleared up on its own after 8 weeks.
Part of the vertigo was dizzy spells every time I stood up.
I had ~ptsd from it for a full year, every time I stood up I would brace for the vertigo ,
Get an NAD+ booster like Niagen or liposomal NMN; Covid (even mild) seems to deplete a month worth of NAD+ reserves in a few days. You might want to combine it with megadoses of B1 that improve enzymatic affinity after major viral infections. NAC might be helpful as well.
Viruses can persist in tissues after infection even if they aren't circulating throughout the body. One weird example of this is when Ebola was going around. Some patients who survived it had antibodies that fought the infection to the point where it was undetectable, but the virus had retreated to the patients' eyes[1], where it continued to replicate in cells and cause eye disease[2].
Same thing can happen with EBV, where it is responsible for some flare up of symptoms post-infection, and chicken pox becoming symptomatic years after infection as shingles.
I wouldn't be surprised if long COVID symptoms are caused by latent COVID infections.
Very true, but we know almost nothing about what it's doing in the body in the short or long term other than some very dramatic lethal pathologies. If you aren't experiencing something like this in your life than it's easy to wait to know what evidence is there, but if you are... Well, just because scientists that I don't know haven't published a paper doesn't mean that exploration of an idea or possibility can't have a positive effect on my outcome. Sometimes that effect might be because I've looked at that possibility so much over time that it just isn't relevant to me, even though later it might come out that the effect or subsequent compounding effect were relevant. Anyway, while what you said could be true, it presents as an absolute that is only relevant to people who aren't studying this or are afflicted with it.
This statement is misleading. There are dozens of papers that show the corona virus alive and well in a large variety of tissues months and even years beyond the initial acute infection.
> Gastric specimens from 26 (32.5%) patients and 4 (100%) cholecystectomy [gallbladder removal] specimens showed positive cytoplasmic staining for the anti-SARS-CoV-2 nucleocapsid protein in surface mucosal epithelial cells.
> The median time between initial COVID-19 infection and surgery was 274 and 380 days in the positive and negative staining groups, respectively (p = 0.371). It's not clear whether these had any long lasting symptoms since infection.
> The inclusion criteria were a history of COVID-19 with one or more gastrointestinal symptoms [during the acute phase] and a negative PCR test result at the time of bariatric surgery.
There are literally dozens of these.
The problem is that most people don't get tissues resected from inside their body when their alive and most such tissues are not tested for the virus.
With regards to the general question of persistent corona viruses, just look at FIP in cats for another such example.
The linked paper does not support your claim. The presence of those nucleocapsid proteins doesn't necessarily mean that there was live virus. They didn't attempt to culture it.
The only confirmed cases of SARS-CoV-2 infections in humans lasting beyond a few weeks have been in immunocompromised patients. Their immune systems were able to somewhat suppress the virus, but not clear the infection. (There is a hypothesis that such patients were the sources for some of the variants because the extended infections gave the virus more time to evolve but that can't be conclusively proven.)
I knew about that feature of viruses, but hadn't consider it in this context. Not that even regular COVID tests are worth a shit. Better now than 2020, but still... About as useful as tests for gonorrhea/chlamydia. If you think you need the test, then the test is a formality. Dose for the potential risk... not that we have a treatment/dose in this situation.
Thinking about this now though gives me some ideas that could even be testable that could help. Thank you for sharing this.
I didn't have the neuro event or symptoms, but the dinner plate and cardio helping sounds awfully familiar.
As far as I know I did not contract COVID, however I was part of the early response team for isolation after travel for the US Military so was exposed on several occasions early on and could have been asymptomatic.
My first vaccine was a non-event; the second fostered a reaction so bad I almost went to the hospital. 103F fever, rigor (shivering so bad you lock up), etc. for about 8 hours, then the fever broke and I recovered fine.
I had an anxiety induced possible cardiac event about a year after that (March 22), but I went to the ER and there was no EKG evidence and no troponin. Was monitored for 12 hours to be sure.
I have had a weird vertigo issue crop up; I actually managed to have exactly what causes it diagnosed! One of the inner ear canals has dropped it's output signal about 75%; no evidence to why the nerves were damaged. I am slowly adjusting. I have no idea if it's related.
> I don't exercise a ton, but do some exercise, especially when the dinner plate flairs up.
In general, regular exercise helps strengthen the heart and reduce risks of CVD. If you're generally only exercising when you feel chest pressure and you do have CVD, your heart muscles aren't as strong and strenuous exercise can lead to problems. Going for a walk everyday would be better than exerting yourself irregularly, as the regular exercise will lower your risk of having problems when you do exercise.
Thank you for your concern. I do daily exercise. Sometimes more, sometimes less. I know a lot about fitness. I sit for a living. I live a high stress lifestyle (working on that too). I'm not the healthiest person in the world. I have several mental/physical/environmental factors that contribute to that to that. Yes exercise is crucial and very helpful in the short and the long term not just with this but all the other issues I had before and compounding because of this, yes doing more of it would be very helpful, yes I'm working on it. Do you even lift bro?
Sorry about your troubles. I agree with your hypothesis that COVID does more damage when given the right scaffold and that underlying conditions lay the groundwork for lasting damage. Have you considered your problems may be clot related?[0]
Not just considered, but seems likely. I have had a lot of trouble finding the key pair values with doctors to pursue any treatment down those lines. I also have ADHD and some other issues that make the diligent pursuit of treatment that is met without collaboration to be extremely difficult. I've found that the best way to NOT get treatment is to go into a doctors office with an idea of what might be wrong with me. I get the best results when I can compose myself enough to go in and complain about symptoms until they come up with something they think will help... which most of the time is 800mg ibuprophen or some weird pill that will reduce ear wax... but after a few visits they might say "GEE IT MIGHT BE BLOOD CLOTS".
Ugh. I'm just gonna do some deep breathing in cold baths, maybe DIY a hyperbaric chamber, get better at pullups, buy a rowing machine, and cut out sugar. Likely by the time that's effective the damage done will be compounded, but at least I won't be left in a holding pattern of how fucked US medicine is.
I'm just some random person on HN so please take this with giant heap of salt, but you've described problems in 2 of the 3 major organs in your arterial system (the third is your kidneys). FWIW, I'd encourage a Hematologist to look there.
Thank you. You might be able to tell the frustration and anxiety this stuff brings me going through it. I appreciate you talking with me about it and you're right. I should ask for a hematologist. Weird that no GP has suggested that, but seriously, you suggestion here might be the key to me living and extra 30 years. Might not, but it's one of the best key/pair value suggestions for treatment path I've heard in a discussion in some time.
DIY hyperbaric chambers can be extremely dangerous in terms of explosive decompression and fires. If you're considering building one then for the sake of yourself and your neighbors please don't try hacking one together out of plans your find online.
Holy shit, this is very similar to what my mom went through.
One day she heard a very loud bang that she described as sounding like it was coming from inside her head. Shortly after she started getting dizzy spells, specially when getting up in the morning and when lying down to sleep at night. Every once in a while her left arm would go numb and she would lose strength in it.
She went to many doctors and it was the same story, they thought it was vertigo. Thankfully she found a better one who requested a brain CT scan which showed that she actually had had a mild ischemic stroke on the right side of her brain.
I think we'll discover that the post-vax myocarditis and pericarditis were caused by pre-existing, latent COVID infections. This probably means that there's a large number of people walking around with completely asymptomatic infections until the body attacks it either because of a vaccination or it finally stumbles across it and generates an immune response.
A tag-along tangent to that: I'm curious as to the cases where there are adverse reactions to the vaccine, what is the probability/possibility that the individual's response would be comparable if exposed to the virus directly.
Unlikely. Your hypothesis wouldn't explain the significantly higher rate of vaccine induced myocarditis in young males compared to females. Infection rates are similar between the sexes so there must be something else going on.
The studies I've seen largely indicate that it's insignificantly higher, at most.
> vaccine induced
There are far too many confounding variables to declare with any sort of honesty that it's "vaccine induced" - even if you could prove correlation (remember: correlation != causation).
For example:
> young males
Gender disparities exist in youth athletics participation, and student athletes are well known to be disproportionately at risk of sudden death from undiagnosed myocarditis (see https://www.dukehealth.org/blog/preventing-sudden-cardiac-ar... as one information source which predates COVID and the vaccines thereof). Young males being more likely to participate in activities which can cause myocarditis or worsen existing myocarditis would readily explain the gender disparity, in a way that neither infection nor vaccination likely would.
That is nonsense bordering on medical misinformation. Multiple independent studies have established clear causality for vaccine induced myocarditis. The risk is low but it absolutely exists, and the relative difference between males and females can't possibly be explained away by sports participation rates. Come on.
Here is an autopsy report: A Case Report: Multifocal Necrotizing Encephalitis and Myocarditis after BNT162b2 mRNA Vaccination against COVID-19 [0].
Quoting the abstract: Surprisingly, only spike protein but no nucleocapsid protein could be detected within the foci of inflammation in both the brain and the heart, particularly in the endothelial cells of small blood vessels. Since no nucleocapsid protein could be detected, the presence of spike protein must be ascribed to vaccination rather than to viral infection.
Also quoting literally the first sentence of the abstract:
> The current report presents the case of a 76-year-old man with Parkinson’s disease (PD) who died three weeks after receiving his third COVID-19 vaccination.
If I had a nickel for every confounding variable implied by either "76-year-old" or "Parkinson's disease" (let alone both, let alone for a sample size of 1), the Powerball jackpot would look like pocket change.
I already had, and my point still stands. It makes no effort to control for said confounding variables. It's heavily reliant on family members' subjective evaluations of health deterioration (i.e. it makes no effort to differentiate between "the patient's health started to decline immediately after the second dose" v. "the patient's health had already started declining but family members only noticed it after the second dose"). Hell, it doesn't even specify whether the cardiac events actually happened after or before the first dose; it just says it was on the "same day", which would be a pretty quick onset of symptoms.
And that's just on the timeline of events. The autopsy itself only demonstrates the presence of spike proteins in the affected tissue; it does not demonstrate said presence to have caused the tissue to be affected, and it's just as likely that something else caused the inflammation (like, you know, the myriad health issues typical of elderly men) and kept the spike proteins around.
Glaringly, the immunohistochemical portion of the autopsy seems to focus solely on SARS-CoV-2, and from that combined with ANE not normally being associated with PD concludes that the ANE has some relation to the presence of SARS-CoV-2 spike proteins. Such an analysis entirely ignores that ANE's causes are already known to include many other viruses, not just SARS-CoV-2. Did he test for influenza A? Influenza B? Herpes virus 6? What about genetic factors?
Similar deal for myocarditis. Other viruses can cause it, like influenza (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7793451/). That the article is silent on that possibility is a rather glaring flaw in its analysis.
Variable after variable after variable after variable after variable, all entirely uncontrolled for, and I'm supposed to be convinced that this demonstrates a causal relationship?
How do you “control”, when it’s a (high quality) report of a single autopsy?
The idea would be to encourage other autopsies which look for similar pathology.
The key thing here is finding spike protein WITHOUT CAPSID protein in areas where the vaccine was not supposed to produce any protein (brain and heart). The foreign mRNA was supposed to stay at the injection site in the upper arm.
> How do you “control”, when it’s a (high quality) report of a single autopsy?
By testing for and ruling out the myriad causes of myocarditis and ANE with already-established causal links, as I described above.
> The idea would be to encourage other autopsies which look for similar pathology.
And if those other autopsies fail to even so much as mention other more-well-known causes of myocarditis and ANE (let alone make any effort to rule out said causes), then they, too, will consequently fail to demonstrate causation.
> The foreign mRNA was supposed to stay at the injection site in the upper arm.
Okay, and it's good to know that it doesn't. That still doesn't do anything to establish a causal relationship between spike protein production and tissue damage.
> Multiple independent studies have established clear causality for vaccine induced myocarditis.
Neither of your linked articles do any such thing. They demonstrate and conclude correlation alone, and - again - correlation != causation.
The first article you linked only assesses myocarditis diagnoses after vaccination (since that's how VAERS data works), i.e. it makes zero attempt to eliminate the possibility of myocarditis having been present before having even received the vaccine and then subsequently detected later. Again: athletes (including those of the youth variety) are already at disproportionately higher risk for myocarditis, with or without the vaccine.
The second article you linked (or rather, the actual study, rather than an editorialized summary thereof) is a meta-analysis of other studies, and itself documents some pretty glaring caveats - namely, inability to control for post-vaccination infection, missing data on first v. second dose, and lack of access to the text of some of the analyzed papers. The analyzed papers all seem to have the same problem as the first one you linked: they take myocarditis diagnoses and work backwards to whether or not the patient was vaccinated, and therefore make no effort to determine whether myocarditis preceded or succeeded vaccination in the affected individuals.
A more compelling test would be to check for myocarditis, then administer the vaccine, then check for myocarditis again (and repeat for subsequent doses). That still wouldn't prove causality, but it would at least actually establish (or fail to establish) that elevated myocarditis risk actually follows vaccination rather than already existing and only being detected after vaccination.
If you're going to accuse me of "nonsense bordering on medical misinformation", you are encouraged to refrain from doing the same.
That's not how it works. There is a clear casual relationship between certain COVID-19 vaccines and myocarditis. No one has proposed a viable alternative hypothesis.
For some issues in medicine we're never practically going to have the level of evidence that you seem to be insisting upon. For example, there has never been a study which proves that smoking causes lung cancer. But the correlation established through observational studies is so strong that causality is clear.
> There is a clear casual relationship between certain COVID-19 vaccines and myocarditis.
No, there is not. Yet again: correlation does not equal causation. If you know of a study that actually asserts causation (and not just correlation), link it.
> For example, there has never been a study which proves that smoking causes lung cancer.
Unlike either of the studies you linked, this one goes at great lengths to describe the myriad identified confounding variables (for which they can then be controlled) in the correlation between smoking and lung cancer, the exact mechanisms by which tobacco smoke causes lung cancer (and the exact carcinogens present in tobacco smoke), even the exact mutations in tumor-suppressing genes like p53. The studies linking mRNA vaccines to myocarditis don't come anywhere close to that level of examination.
> But the correlation established through observational studies is so strong that causality is clear.
And that is very unlike the situation with vaccines and myocarditis, wherein the correlation is nowhere near as strong and for which the causality is nowhere near as clear. That vast difference is why - unlike either of the articles you cited - the myriad articles on the relationship between smoking and lung cancer are able to assert causation, and indeed do so.
Until that changes, it is deeply irresponsible to prematurely declare the relationship between vaccines and myocarditis to be in any way "causal". It's a "maybe" at best.
How many uncontrolled-for confounding variables do I need to pull up before you're willing to admit how utterly irresponsible it is to declare from on high that the link between mRNA vaccines and myocarditis in young males is "causal"?
I can't help but think -- what if it is from people that work from home, don't exercise as much when they went to work, or are getting older post-covid
It was first observed in Israel iirc, that you can get myocarditis by exercising in the period after the shot. It is the same when you exercise while sick. That might explain why more men where affected too.
In that case the shot is highly unlikely to be a significant factor, seeing as how exercise-related myocarditis has been a thing since long before COVID was a thing. Demonstrating the vaccine to be a factor would require checking for myocarditis before and after vaccination, and also doing so for the control group. I don't know of any studies which do that, though; usually it's more the other way around: diagnosing myocarditis and correlating that with a past vaccination or infection.
> We did not observe an increased incidence of neither pericarditis nor myocarditis in adult patients recovering from COVID-19 infection.
you should be careful not to interpret this as evidence of absence. The previous sentence gives confidence intervals:
> Post COVID-19 infection was not associated with either myocarditis (aHR 1.08; 95% CI 0.45 to 2.56) or pericarditis (aHR 0.53; 95% CI 0.25 to 1.13).
Here a 95% CI from 0.45 to 2.56 means that the data is statistically consistent with myocarditis being 0.45 times as likely in people with COVID infection, or 2.56 times more likely.
The sample size here is simply not enough to be more precise, simply because myocarditis and pericarditis are so rare. (It's hard to be precise about the rate of something that happened in only nine COVID patients in the study!) Hence you should not interpret this as demonstrating no difference between people with and without prior COVID infection -- merely bounding the size of the difference that may exist, and saying it can't be more than roughly a factor of 2.5-3.
To be blunt, the authors are wrong to say in their Conclusion that "Our data suggest that there is no increase in the incidence of myocarditis and pericarditis in COVID-19 recovered patients compared to uninfected matched controls." Again, the confidence interval shows that a 2x increased incidence of myocarditis would be consistent with the data.
right, i was going to make a similar kind of critique (but probably less lucidly). the effect sizes are tiny and the confidence intervals overwhelm the supposed conclusions. seems to be motivated reasoning rather than impartial science.
covid may cause a rise in heart disease in unvaxed individuals relative to vaxed, but this study does nothing to support, and especially doesn't prove, that contention. one thing it does reveal is that the overall incidence rates for myo-/pericarditis are pretty small, vaxed or otherwise.
what would be more interesting is a comparative study of incidence relative to similar cardiopulmonary infections like the flu. that would tell us whether heart disease from covid is something to worry more about than our ambient worry over heart disease in general (which seems relatively mild compared to covid).
> Covid may cause a rise in heart disease in unvaxed individuals relative to vaxed, but this study does nothing to support, and especially doesn't prove, that contention.
The issue that comes to mind for me is there no explanation given on why the unvaccinated were unvaccinated. From what I remember, the jab was not recommended for those with compromised immune system or other similar less-than-healthy conditions.
Without such transparency, it feels like possible apple to orangers comparisons.
that could be a confounding factor, but it's hard to know for sure without really digging into their data and methods. they may have tried to correct for that. in any case, this study actually seems to suggest that while vaccination probably has a marginal benefit, the effect size is too small to really matter.
Right, the parent post was making the same point: the article claims to have shown a lack of statistical correlation, but all they did was show that their study lacked the ability to detect correlation. It is a subtle movement of a few words, but they are important
It can be interpreted in statistical terms. They could use the confidence interval instead to state that the study suggests infection reduces these adverse events by no more than half, nor increases their frequency by no more than triple.
You’ve only emphasized one side of the interval, which suggests some bias. Eg you haven’t written out that the other side implies you might have a smaller chance of these issues once you get covid. That said, it probably is reasonable to have as a prior that it’s unlikely that covid would lower your risk of these issues.
That feels an awkward way to word that claim, since both of those outcomes have mathematically zero chance of being true literally (interpreted as points), or less than 5% total chance of being true (interpreted as areas)
I think the converse statement would have been more strictly true statistically (e.g. that 0.45 is statistically consistent with the data), and more accurately descriptive of what a p-test actually means.
It would presumably be able to detect a massive increase, yes, if by "massive" you mean something like a 10x increase in rate. One could do a power calculation to determine its ability to detect different sizes of effect. Normally you'd do that when planning a study to determine the sample you need, but here they took every available patient in the medical records database they had access to, so they didn't really have a choice of sample size.
I beg to differ. I think you and the paper are committing another falacy: getting hung up on relative instead of absolute hazards.
Myocarditis and pericarditis (at least the reportable kind studied in the paper) are rare — all groups had incidence well under 0.01%. That’s 10 per 100k for those who prefer those units. The study enrolled almost 200k COVID patients and over 500k controls. This is a lot of power to bound the absolute risk, but it is indeed underpowered to get good bounds on the hazard ratio.
The paper would be substantially improved if it said “the absolute risk of myo/pericarditis in COVID patients is <10 per 100k with confidence 99.9%” or “the increased risk is <9 per 100k with confidence such-and-such” (I made up the numbers, but the analysis is easy.)
So yes, a 2x increased risk would be consistent with the data, but an actual substantial risk would not be consistent with the data.
Yes, I agree that it's important to put the absolute risk in context. The NEJM paper that started the concern about myocarditis put it this way:
> Vaccination was most strongly associated with an elevated risk of myocarditis (risk ratio, 3.24; 95% confidence interval [CI], 1.55 to 12.44; risk difference, 2.7 events per 100,000 persons; 95% CI, 1.0 to 4.6)
Giving the risk difference in terms of events per 100,000 people is useful. It's also trickier to interpret because the length of the follow-up period is important: if the vaccine changes the rate of events, then a study that observes patients for two years after vaccination will have (roughly) double the number of events of a study that follows patients for one year after vaccination. That's why people like relative risks in this setting.
Covid sometimes infects heart tissue and that infection can linger long after you’re asymptomatic. It is not at all surprising that a vaccination after such an infection can cause cardiac symptoms as your immune system is tuned up and starts attacking the infection in your heart. This is A) rather uncommon and B) hard to verify scientifically. Not to mention that this not happening is a morality issue for a lot of folks because vaccine good, suggestions of side effects bad.
If this were the cause, I would expect to see similar rates of myocarditis from the viral vector vaccines, but it's much lower. The MRNA vaccines work by causing cells to produce antigens, which are presented on the cell surface and induce the immune system to attack the cell. We know now as well that the lipid vehicle doesn't stay at the injection site but distributes through the body to varying degrees. No need to posit a secondary mechanism - it's more likely the vaccine is just carried to the heart in some cases, is absorbed, and induces immune attack like it does in other tissue.
The biodistribution of the viral vector vaccines is likely different and also dependant on what tissue the vector prefers to infect, so when it leaks out of the injection site you get side effects in other places (clotting and vascular effects) instead of the heart.
While I'm probably wasting my time here. I'm going to say what I think many aren't saying. We need to heavily study and reflect on the impact of vaccinations regardless of the outcome and IF "we made the right decision".
This means comparing outcomes between the vaccinated and unvaccinated.
While this study might be a step in the right direction, I feel there are too many in the medical, political and scientific spheres of influence that are shutting down such medical/scientific/humane study and debate. The silence is deafening.
If I don't hear such debate, my mind goes full tinfoil hat and thinks of concepts such as the Tenth Man Rule. It's good to have a civil discussion and disagreement on ANY subject. The data is out there. Where is that disagreement? Where are those studies? What were the impacts on heart conditions, strokes, neurological, SADS and other medical conditions?
The silence is truly deafening.
And to further increase my chances of getting censored - it's those same spheres of influence that likely created COVID in the first place and continue to allow institutions to dabble with genetic modification of these viruses. No one cares about the definition of "gain of function". We (humanity) dabbled with the code of life and messed up; we messed up big. Let's learn from this mistake and move on.
You seem to think that COVID was definitely man made, but we still don't have enough data to make any kind of assertion on that. Some recent finds lean more to a zoonotic source.
As for censorship, I don't think anyone is censoring truly good studies on this stuff right now. And I don't think there is that much central control of the entire medical and scientific community.
Take ivermectin, for example. Low power, poorly conducted studies trying to point to the benefits of Ivermectin to treat covid are still coming out. Doesn't seem like they are being censored.
If you're only hearing silence in the vaccination debate (which, mind you, has been raging since before the first SARS outbreak, let alone the current SARS 2: CoV Boogaloo), then you might want to get your ears checked ;)
There is no shortage of medical professionals with all sorts of opinions on whether or not to vaccinate for any manner of disease, COVID included. Sure, the overwhelming majority have reached a consensus in favor of vaccination doing more good than harm (for good reason), but the tiny minority with contrary opinions are not at all being censored (if anything, they're being anti-censored, e.g. by social media posts and your usual gaggle of conspiracy-theory-peddling news outlets).
> the overwhelming majority have reached a consensus in favor of vaccination doing more good than harm (for good reason)
Do you believe they have all the data needed to make that a final conclusion?
Or are most of those medical professionals simply following certain leaders and descission makers? Would that even count as (useful) consensus then?
> Do you believe they have all the data needed to make that a final conclusion?
There is no "final conclusion". There will always be more data. So far the data have rather strongly indicated greater benefit than harm, even among the reports asserting correlations between vaccines and adverse reactions, so it doesn't seem very surprising to see consensus on that among medical experts.
The consensus ain't always right, to be clear. Maybe the small minority of experts asserting more harm than good are onto something. The body of data supporting such assertions is far more lacking, so I wouldn't bet on it.
> Or are most of those medical professionals simply following certain leaders and descission makers?
It's usually the other way around: the "certain leaders and decisionmakers" in the pro-vaccination camp largely lead/decide based on how experts are informing them - and there's certainly no shortage of said experts.
It's a fair bit more varied in the anti-vaccination camp; some such leaders/decisionmakers do defer to experts (and it's simply a case of their pool of experts being in the anti-vaccination camp), but it seems like most instead assume they know better than the experts; they tend to be the sorts of folks who already reject scientific methodology for various reasons, and thus are not inclined to defer to experts informed by said methodology.
I appreciate the response. I agree with most of what you say.
I still think it's important to point out that in this situation, with
a) a lack of primary data
and especially
b) considering the political and societal implications for publicly disagreeing with the "accepted opinion"
consensus might just not be a great measure in this case.
I love the discussion on the statistical power of the findings and the appropriate interpretation of those numbers. However, there is a much larger problematic aspect to this paper that is subtle but critical and is being overlooked in this discussion. Once you understand this bias you will realize that the paper's reported findings are most certainly dramatically understated.
Put simply, not every single patient in the study was appropriately tested for myocarditis and/or pericarditis. The statistics provided by this retrospective cohort study depend on the outcome of patients traversing the healthcare system of the population in question. These statistics are really telling you the outcome of multiple probabilistic events (listed below). Once you think through each of these events, it quickly becomes apparent that all of the biases lead these conditions to be dramatically undercounted.
1. Patient sought healthcare
2. Patient reported symptoms doctor could identify as potential myocarditis and or pericarditis
3. Doctor recognized symptoms
4. Doctor ordered appropriate diagnostic testing
5. Radiologist recognized the condition.
Let's look at each of these.
1. Given this was a retrospective study, we know that (1) happened 100% of the time. No problem here.
2 and 3. A patient with myocarditis may have one or more of the symptoms below. Some of these symptoms, such as swelling in the lower extremities, are likely a dead give away. However, most are extremely common in COVID.
- Signs of a viral infection, such as body aches, joint pain, fever, headaches, vomiting, diarrhea or a sore throat.
- Rapid or abnormal heart rhythms (arrhythmias).
- Chest pain.
- Shortness of breath, both at rest and during physical activity.
- Swelling of your lower extremities (legs, ankles and feet).
- Fatigue.
I would wager that most patients who demonstrated one or more of these symptoms indicative for potential myocarditis/pericarditis were not actually tested for the disease. To get tested, a patient lacking extreme myocarditis would likely have to push and push hard to get the doctor to test. This *heavily* biases the results toward under counting.
4. Diagnosing COVID-caused myocarditis and pericarditis is hard. The typical standard of care, at least in the US, is an echocardiogram. This diagnostic ultrasound can indeed pick up some forms of the disease but multiple papers have shown that COVID-caused myocarditis and pericarditis can be invisible on an echocardiogram. The definitive scan is a specialized MRI machine capable of a particular scan sequence. This machine is hard to find even in major health centers (there are three of them total in the Washington DC area). The cost of an MRI is at least an order of magnitude more than an echocardiogram. The echo takes about 15 minutes whereas the cardiac MRI is about 90 minutes. Thus, it is highly unlikely that the doctors in question ordered the appropriate test that can actually detect the disease in question. This further biases the findings in the same direction.
Finally, the study looks at patients from March 2020 and January 2021. The fact that COVID myocarditis and pericarditis can typically only be resolved on a specialized cardiac MRI was not common knowledge for most of the study period.
Thus, the conclusions from this study are DRAMATICALLY underestimated.
89 comments
[ 1.8 ms ] story [ 139 ms ] thread> It has recently been reported that the incidence of myocarditis and pericarditis is increased in COVID-19 patients during the acute illness [12]. However; whether or not myocarditis and pericarditis after the recovery period are a part of the long COVID-19 syndrome is yet unknown. Herein, we studied the incidence of myocarditis and pericarditis in a large cohort of COVID-19 patients after recovering from the acute infection.
It's looking at myocarditis and pericarditis not in the acute phase, but post. And iirc there has been other papers showing there is an increased risk in a 12 month followup.
> We did not observe an increased incidence of neither pericarditis nor myocarditis in adult patients recovering from COVID-19 infection.
And this seems to be an outlier anyway:
> In conclusion, either symptomatic or asymptomatic SARS-CoV-2 infection is associated with an increased risk for late CV outcomes and has a causal effect on all-cause mortality in a late post-COVID-19 period.
https://www.ajconline.org/article/S0002-9149(22)00655-5/full...
> In summary, using a national cohort of people with COVID-19, we show that risk and 12-month burden of incident cardiovascular disease are substantial and span several cardiovascular disease categories (ischemic and non-ischemic heart disease, dysrhythmias and others). The risks and burdens of cardiovascular disease were evident even among those whose acute COVID-19 did not necessitate hospitalization.
https://www.nature.com/articles/s41591-022-01689-3
> The 12-month risk of incidental cardiovascular diseases is substantially higher in the COVID-19 survivors than the non-COVID-19 controls. Clinicians and patients with a history of COVID-19 should pay attention to their cardiovascular health in long term.
https://www.thelancet.com/journals/eclinm/article/PIIS2589-5...
What does this mean, specifically?
I can feel my vascular system radiating from the center of my chest up the sides of my neck and out through my shoulders. It's got a bit of a slow ache and upper body stiffness when it's flaring up. When it's bad, sometimes I wake up with numbness that radiates from my chest out to my finger tips on the top sides of my arms.
I have no problems taking deep breaths. The injury does not seem to be growing.
After the cardiac issue I had in 2020, my bloodwork showed signs that there was a possible event. My EKG was fine. This was days after. I have a constant dull to really shitty headache in the top front inside my head that has been persistent from the thing that seemed like a mini-stroke. I have never really had headaches without a serious hangover. I couldn't see my regular GP, still haven't been able to, but the doc I did see basically told me she thought it was vertigo and I needed to clean my ears. She checked my reflexes and some other things and said she could not recommend any further action without more events. I know what vertigo is. I've experienced it on accident and on purpose. I am not experiencing random vertigo. She did not seem to take anything I was saying seriously. She also told me she found it offensive that I was swearing while describing the experience and a gentleman would refrain from such language. I think she's a fucking moron, but she's functionally just as helpful as my curious, smart, and compassionate GP.
I'm 6' broad shouldered, and 210lbs. A bit chubby. I don't exercise a ton, but do some exercise, especially when the dinner plate flairs up. I don't smoke.
I've had a chest x-ray and it shows what looks like scarring in vascular structures radiating from my lungs. The forms kind of look on x-ray like the "ground glass nodules" that some people are experiencing. It's VERY hard to get a doctor that wants to do anything with me about this stuff. The fact that cardio makes things better and not worse is counter intuitive from traditional issues that look the same like Angina Pectoris. I've said since I recovered the first time (I've had it at least once more post vaccination but nothing was quite as near death as the first) that I felt cognitively and physically like I was 10 years older. I turn 40 next year. New research has been coming out showing that some people suffering from long COVID show aging of their CV systems of about 10 years.
It is going to take a long time to figure out what Long Covid is really doing to people. Some people that never showed symptoms get these things. Children are showing it too. The diagnostic criteria is really difficult and there is almost no treatment aside from some success with similar treatments used for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome[0]. I have found that most doctors don't want to touch it with a 200ft poll. The Red Cross says I should join an online support group[1]. A lot of the research is being done by scraping subreddits for people reporting symptoms because they vary so wildly and seem to have little correlation with the perceived severity of infection.
I suspect we may find a high correlation with exposure to heavy air born contamination. ...
I got Omicron in January '22 despite being double vaxx'd, and I felt totally fine until 3-4 mo. later when I started to get recurrent dizzy spells, major fatigue, and bouts of anxiety, which are all very unusual for me. Checkup / bloodwork showed nothing. I am 41 y.o. who exercise regularly, does not smoke, rarely drinks, etc.
So far I can still function and maintain a job, but it makes me wonder what's going on inside of me that 11 months later it's still causing these issues regularly. Our 4 y.o. son got it as well and although he was asymptomatic I am still very concerned about what the long-term effects on him may be.
I am not a doctor and this is not medical advice, but I read a paper saying that hyperbaric oxygen therapy helped some people, so I've been using Wim Hoff breathing as a poor man's version. It does seems to help with the fatigue but not the vertigo. Best of luck.
Wim Hoff Breathing: https://www.youtube.com/watch?v=tybOi4hjZFQ
Honestly, I feel very lucky to be as functional as I am. I do worry about how medical and political systems are responding to COVID and long COVID, but largely I think good care is going to come from the bottom up and not top down. I'm comfortable(ish) with a reality that I might just suddenly drop dead tomorrow, but this experience has given me a new appreciation for the health I have that I could not have fathomed before. Because I can alleviate symptoms with diet and directed exercise and it does appear to have a cumulative effect on their reduction, I think recovery is possible without intense intervention. I don't even mind being more spacey and a bit dumber. It suits me a bit and has changed the pace of my life in a way that once I embraced has been good.
My biggest worry is that if I suddenly die and how devastating that would be for people that depend on me, but I think without an infection of a new virus or several viruses I might live a shorter, but alright life. My chance of suddenly dying because I got light headed in an elevator now being slightly higher than my chance of being crushed by a vending machine.
Thank so so much for this. Very useful information.
One of my inner ear canal output signals dropped by about 75%. There is a diagnostic test they can do; more basic tests showed nothing but this more sensitive one showed it clear as day. No-one can tall me WHY the nerves are outputting a weaker signal and I couldn't tell you if it's related but it's something that doesn't get checked much.
If you had the information available, I'd be very interested to know the names of the diagnostic tests you took. Analysis of how I'm hearing is something I'm uniquely able to analyze over time and compare to medically conducted tests. While I think I know how the second test might have worked, I don't know what I'd call such a test to look for it.
I think analysis of hearing on newly infected to post care of people with COVID and Long COVID could provide useful hints that most other methods might not be able to detect.
It identified not just the issue but the actual specific structure that was giving me issues.
This has no impact on hearing, so wouldn't be caught by those tests.
I have no idea if it was anxiety or Covid, but the dizziness was disorienting, at the worst I couldn’t walk , it felt like I was on a boat. During this time I had anxiety attacks almost non stop-triggered by the vertigo. As soon as I started to notice the vertigo I would begin to spiral because it was so unprecedented and disorienting. It just cleared up on its own after 8 weeks.
Part of the vertigo was dizzy spells every time I stood up.
I had ~ptsd from it for a full year, every time I stood up I would brace for the vertigo ,
Hope you find some relief soon
[0]http://sanfordhealth.staywellhealthlibrary.com/Search/134,51...
Same thing can happen with EBV, where it is responsible for some flare up of symptoms post-infection, and chicken pox becoming symptomatic years after infection as shingles.
I wouldn't be surprised if long COVID symptoms are caused by latent COVID infections.
[1] https://www.sciencedaily.com/releases/2017/07/170717091954.h...
[2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5988239/
https://www.nationalgeographic.com/science/article/persistin...
Here is but one such paper - https://link.springer.com/article/10.1007/s11695-022-06338-9
> Gastric specimens from 26 (32.5%) patients and 4 (100%) cholecystectomy [gallbladder removal] specimens showed positive cytoplasmic staining for the anti-SARS-CoV-2 nucleocapsid protein in surface mucosal epithelial cells.
> The median time between initial COVID-19 infection and surgery was 274 and 380 days in the positive and negative staining groups, respectively (p = 0.371). It's not clear whether these had any long lasting symptoms since infection.
> The inclusion criteria were a history of COVID-19 with one or more gastrointestinal symptoms [during the acute phase] and a negative PCR test result at the time of bariatric surgery.
There are literally dozens of these.
The problem is that most people don't get tissues resected from inside their body when their alive and most such tissues are not tested for the virus.
With regards to the general question of persistent corona viruses, just look at FIP in cats for another such example.
The only confirmed cases of SARS-CoV-2 infections in humans lasting beyond a few weeks have been in immunocompromised patients. Their immune systems were able to somewhat suppress the virus, but not clear the infection. (There is a hypothesis that such patients were the sources for some of the variants because the extended infections gave the virus more time to evolve but that can't be conclusively proven.)
Thinking about this now though gives me some ideas that could even be testable that could help. Thank you for sharing this.
As far as I know I did not contract COVID, however I was part of the early response team for isolation after travel for the US Military so was exposed on several occasions early on and could have been asymptomatic.
My first vaccine was a non-event; the second fostered a reaction so bad I almost went to the hospital. 103F fever, rigor (shivering so bad you lock up), etc. for about 8 hours, then the fever broke and I recovered fine.
I had an anxiety induced possible cardiac event about a year after that (March 22), but I went to the ER and there was no EKG evidence and no troponin. Was monitored for 12 hours to be sure.
I have had a weird vertigo issue crop up; I actually managed to have exactly what causes it diagnosed! One of the inner ear canals has dropped it's output signal about 75%; no evidence to why the nerves were damaged. I am slowly adjusting. I have no idea if it's related.
Thank you for sharing more (probably this was your first post and I missed it) about your story and diagnosis. Seriously. Very helpful.
Happy to help!
In general, regular exercise helps strengthen the heart and reduce risks of CVD. If you're generally only exercising when you feel chest pressure and you do have CVD, your heart muscles aren't as strong and strenuous exercise can lead to problems. Going for a walk everyday would be better than exerting yourself irregularly, as the regular exercise will lower your risk of having problems when you do exercise.
[0]https://twitter.com/drclairetaylor/status/158936959572682342...
Ugh. I'm just gonna do some deep breathing in cold baths, maybe DIY a hyperbaric chamber, get better at pullups, buy a rowing machine, and cut out sugar. Likely by the time that's effective the damage done will be compounded, but at least I won't be left in a holding pattern of how fucked US medicine is.
One day she heard a very loud bang that she described as sounding like it was coming from inside her head. Shortly after she started getting dizzy spells, specially when getting up in the morning and when lying down to sleep at night. Every once in a while her left arm would go numb and she would lose strength in it.
She went to many doctors and it was the same story, they thought it was vertigo. Thankfully she found a better one who requested a brain CT scan which showed that she actually had had a mild ischemic stroke on the right side of her brain.
Hope you are feeling better now, take care!
There is no question mark in the article's title.
The studies I've seen largely indicate that it's insignificantly higher, at most.
> vaccine induced
There are far too many confounding variables to declare with any sort of honesty that it's "vaccine induced" - even if you could prove correlation (remember: correlation != causation).
For example:
> young males
Gender disparities exist in youth athletics participation, and student athletes are well known to be disproportionately at risk of sudden death from undiagnosed myocarditis (see https://www.dukehealth.org/blog/preventing-sudden-cardiac-ar... as one information source which predates COVID and the vaccines thereof). Young males being more likely to participate in activities which can cause myocarditis or worsen existing myocarditis would readily explain the gender disparity, in a way that neither infection nor vaccination likely would.
https://jamanetwork.com/journals/jama/fullarticle/2788346
https://www.news-medical.net/news/20221101/New-analysis-on-t...
Quoting the abstract: Surprisingly, only spike protein but no nucleocapsid protein could be detected within the foci of inflammation in both the brain and the heart, particularly in the endothelial cells of small blood vessels. Since no nucleocapsid protein could be detected, the presence of spike protein must be ascribed to vaccination rather than to viral infection.
[0] https://www.mdpi.com/2076-393X/10/10/1651
> The current report presents the case of a 76-year-old man with Parkinson’s disease (PD) who died three weeks after receiving his third COVID-19 vaccination.
If I had a nickel for every confounding variable implied by either "76-year-old" or "Parkinson's disease" (let alone both, let alone for a sample size of 1), the Powerball jackpot would look like pocket change.
And that's just on the timeline of events. The autopsy itself only demonstrates the presence of spike proteins in the affected tissue; it does not demonstrate said presence to have caused the tissue to be affected, and it's just as likely that something else caused the inflammation (like, you know, the myriad health issues typical of elderly men) and kept the spike proteins around.
Glaringly, the immunohistochemical portion of the autopsy seems to focus solely on SARS-CoV-2, and from that combined with ANE not normally being associated with PD concludes that the ANE has some relation to the presence of SARS-CoV-2 spike proteins. Such an analysis entirely ignores that ANE's causes are already known to include many other viruses, not just SARS-CoV-2. Did he test for influenza A? Influenza B? Herpes virus 6? What about genetic factors?
Similar deal for myocarditis. Other viruses can cause it, like influenza (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7793451/). That the article is silent on that possibility is a rather glaring flaw in its analysis.
Variable after variable after variable after variable after variable, all entirely uncontrolled for, and I'm supposed to be convinced that this demonstrates a causal relationship?
The idea would be to encourage other autopsies which look for similar pathology.
The key thing here is finding spike protein WITHOUT CAPSID protein in areas where the vaccine was not supposed to produce any protein (brain and heart). The foreign mRNA was supposed to stay at the injection site in the upper arm.
By testing for and ruling out the myriad causes of myocarditis and ANE with already-established causal links, as I described above.
> The idea would be to encourage other autopsies which look for similar pathology.
And if those other autopsies fail to even so much as mention other more-well-known causes of myocarditis and ANE (let alone make any effort to rule out said causes), then they, too, will consequently fail to demonstrate causation.
> The foreign mRNA was supposed to stay at the injection site in the upper arm.
Okay, and it's good to know that it doesn't. That still doesn't do anything to establish a causal relationship between spike protein production and tissue damage.
Neither of your linked articles do any such thing. They demonstrate and conclude correlation alone, and - again - correlation != causation.
The first article you linked only assesses myocarditis diagnoses after vaccination (since that's how VAERS data works), i.e. it makes zero attempt to eliminate the possibility of myocarditis having been present before having even received the vaccine and then subsequently detected later. Again: athletes (including those of the youth variety) are already at disproportionately higher risk for myocarditis, with or without the vaccine.
The second article you linked (or rather, the actual study, rather than an editorialized summary thereof) is a meta-analysis of other studies, and itself documents some pretty glaring caveats - namely, inability to control for post-vaccination infection, missing data on first v. second dose, and lack of access to the text of some of the analyzed papers. The analyzed papers all seem to have the same problem as the first one you linked: they take myocarditis diagnoses and work backwards to whether or not the patient was vaccinated, and therefore make no effort to determine whether myocarditis preceded or succeeded vaccination in the affected individuals.
A more compelling test would be to check for myocarditis, then administer the vaccine, then check for myocarditis again (and repeat for subsequent doses). That still wouldn't prove causality, but it would at least actually establish (or fail to establish) that elevated myocarditis risk actually follows vaccination rather than already existing and only being detected after vaccination.
If you're going to accuse me of "nonsense bordering on medical misinformation", you are encouraged to refrain from doing the same.
For some issues in medicine we're never practically going to have the level of evidence that you seem to be insisting upon. For example, there has never been a study which proves that smoking causes lung cancer. But the correlation established through observational studies is so strong that causality is clear.
That's exactly how it works.
> There is a clear casual relationship between certain COVID-19 vaccines and myocarditis.
No, there is not. Yet again: correlation does not equal causation. If you know of a study that actually asserts causation (and not just correlation), link it.
> For example, there has never been a study which proves that smoking causes lung cancer.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749017/
Unlike either of the studies you linked, this one goes at great lengths to describe the myriad identified confounding variables (for which they can then be controlled) in the correlation between smoking and lung cancer, the exact mechanisms by which tobacco smoke causes lung cancer (and the exact carcinogens present in tobacco smoke), even the exact mutations in tumor-suppressing genes like p53. The studies linking mRNA vaccines to myocarditis don't come anywhere close to that level of examination.
Similar deal with this one: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9603183/
Consequently:
> But the correlation established through observational studies is so strong that causality is clear.
And that is very unlike the situation with vaccines and myocarditis, wherein the correlation is nowhere near as strong and for which the causality is nowhere near as clear. That vast difference is why - unlike either of the articles you cited - the myriad articles on the relationship between smoking and lung cancer are able to assert causation, and indeed do so.
Until that changes, it is deeply irresponsible to prematurely declare the relationship between vaccines and myocarditis to be in any way "causal". It's a "maybe" at best.
----
Speaking of smoking and its deleterious effects: https://pubmed.ncbi.nlm.nih.gov/20555426/
And gender variance in high school student tobacco use - including of smoking tobacco - does exist: https://www.cdc.gov/tobacco/data_statistics/fact_sheets/yout...
How many uncontrolled-for confounding variables do I need to pull up before you're willing to admit how utterly irresponsible it is to declare from on high that the link between mRNA vaccines and myocarditis in young males is "causal"?
> We did not observe an increased incidence of neither pericarditis nor myocarditis in adult patients recovering from COVID-19 infection.
you should be careful not to interpret this as evidence of absence. The previous sentence gives confidence intervals:
> Post COVID-19 infection was not associated with either myocarditis (aHR 1.08; 95% CI 0.45 to 2.56) or pericarditis (aHR 0.53; 95% CI 0.25 to 1.13).
Here a 95% CI from 0.45 to 2.56 means that the data is statistically consistent with myocarditis being 0.45 times as likely in people with COVID infection, or 2.56 times more likely.
The sample size here is simply not enough to be more precise, simply because myocarditis and pericarditis are so rare. (It's hard to be precise about the rate of something that happened in only nine COVID patients in the study!) Hence you should not interpret this as demonstrating no difference between people with and without prior COVID infection -- merely bounding the size of the difference that may exist, and saying it can't be more than roughly a factor of 2.5-3.
To be blunt, the authors are wrong to say in their Conclusion that "Our data suggest that there is no increase in the incidence of myocarditis and pericarditis in COVID-19 recovered patients compared to uninfected matched controls." Again, the confidence interval shows that a 2x increased incidence of myocarditis would be consistent with the data.
This is a widespread misinterpretation of statistics and one that has been around for decades, so please excuse me for taking every opportunity to complain. (e.g. https://www.statisticsdonewrong.com/power.html#the-power-of-...)
covid may cause a rise in heart disease in unvaxed individuals relative to vaxed, but this study does nothing to support, and especially doesn't prove, that contention. one thing it does reveal is that the overall incidence rates for myo-/pericarditis are pretty small, vaxed or otherwise.
what would be more interesting is a comparative study of incidence relative to similar cardiopulmonary infections like the flu. that would tell us whether heart disease from covid is something to worry more about than our ambient worry over heart disease in general (which seems relatively mild compared to covid).
The issue that comes to mind for me is there no explanation given on why the unvaccinated were unvaccinated. From what I remember, the jab was not recommended for those with compromised immune system or other similar less-than-healthy conditions.
Without such transparency, it feels like possible apple to orangers comparisons.
Or maybe I'm misreading?
Descriptively, there is a trend, yes.
But it can not be interpreted in statistical (inferential) terms, I think.
It can be interpreted in statistical terms. They could use the confidence interval instead to state that the study suggests infection reduces these adverse events by no more than half, nor increases their frequency by no more than triple.
> the data is statistically consistent with myocarditis being 0.45 times as likely in people with COVID infection, or 2.56 times more likely.
I think the converse statement would have been more strictly true statistically (e.g. that 0.45 is statistically consistent with the data), and more accurately descriptive of what a p-test actually means.
From my limited understanding, 2.56x next to none is still pretty close to next to none.
Myocarditis and pericarditis (at least the reportable kind studied in the paper) are rare — all groups had incidence well under 0.01%. That’s 10 per 100k for those who prefer those units. The study enrolled almost 200k COVID patients and over 500k controls. This is a lot of power to bound the absolute risk, but it is indeed underpowered to get good bounds on the hazard ratio.
The paper would be substantially improved if it said “the absolute risk of myo/pericarditis in COVID patients is <10 per 100k with confidence 99.9%” or “the increased risk is <9 per 100k with confidence such-and-such” (I made up the numbers, but the analysis is easy.)
So yes, a 2x increased risk would be consistent with the data, but an actual substantial risk would not be consistent with the data.
> Vaccination was most strongly associated with an elevated risk of myocarditis (risk ratio, 3.24; 95% confidence interval [CI], 1.55 to 12.44; risk difference, 2.7 events per 100,000 persons; 95% CI, 1.0 to 4.6)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9025013/
Giving the risk difference in terms of events per 100,000 people is useful. It's also trickier to interpret because the length of the follow-up period is important: if the vaccine changes the rate of events, then a study that observes patients for two years after vaccination will have (roughly) double the number of events of a study that follows patients for one year after vaccination. That's why people like relative risks in this setting.
What does censored mean in this context?
https://en.wikipedia.org/wiki/Censoring_(statistics)
This means comparing outcomes between the vaccinated and unvaccinated.
While this study might be a step in the right direction, I feel there are too many in the medical, political and scientific spheres of influence that are shutting down such medical/scientific/humane study and debate. The silence is deafening.
If I don't hear such debate, my mind goes full tinfoil hat and thinks of concepts such as the Tenth Man Rule. It's good to have a civil discussion and disagreement on ANY subject. The data is out there. Where is that disagreement? Where are those studies? What were the impacts on heart conditions, strokes, neurological, SADS and other medical conditions?
The silence is truly deafening.
And to further increase my chances of getting censored - it's those same spheres of influence that likely created COVID in the first place and continue to allow institutions to dabble with genetic modification of these viruses. No one cares about the definition of "gain of function". We (humanity) dabbled with the code of life and messed up; we messed up big. Let's learn from this mistake and move on.
As for censorship, I don't think anyone is censoring truly good studies on this stuff right now. And I don't think there is that much central control of the entire medical and scientific community.
Take ivermectin, for example. Low power, poorly conducted studies trying to point to the benefits of Ivermectin to treat covid are still coming out. Doesn't seem like they are being censored.
If you're only hearing silence in the vaccination debate (which, mind you, has been raging since before the first SARS outbreak, let alone the current SARS 2: CoV Boogaloo), then you might want to get your ears checked ;)
There is no shortage of medical professionals with all sorts of opinions on whether or not to vaccinate for any manner of disease, COVID included. Sure, the overwhelming majority have reached a consensus in favor of vaccination doing more good than harm (for good reason), but the tiny minority with contrary opinions are not at all being censored (if anything, they're being anti-censored, e.g. by social media posts and your usual gaggle of conspiracy-theory-peddling news outlets).
Do you believe they have all the data needed to make that a final conclusion? Or are most of those medical professionals simply following certain leaders and descission makers? Would that even count as (useful) consensus then?
There is no "final conclusion". There will always be more data. So far the data have rather strongly indicated greater benefit than harm, even among the reports asserting correlations between vaccines and adverse reactions, so it doesn't seem very surprising to see consensus on that among medical experts.
The consensus ain't always right, to be clear. Maybe the small minority of experts asserting more harm than good are onto something. The body of data supporting such assertions is far more lacking, so I wouldn't bet on it.
> Or are most of those medical professionals simply following certain leaders and descission makers?
It's usually the other way around: the "certain leaders and decisionmakers" in the pro-vaccination camp largely lead/decide based on how experts are informing them - and there's certainly no shortage of said experts.
It's a fair bit more varied in the anti-vaccination camp; some such leaders/decisionmakers do defer to experts (and it's simply a case of their pool of experts being in the anti-vaccination camp), but it seems like most instead assume they know better than the experts; they tend to be the sorts of folks who already reject scientific methodology for various reasons, and thus are not inclined to defer to experts informed by said methodology.
I still think it's important to point out that in this situation, with a) a lack of primary data and especially b) considering the political and societal implications for publicly disagreeing with the "accepted opinion" consensus might just not be a great measure in this case.
Put simply, not every single patient in the study was appropriately tested for myocarditis and/or pericarditis. The statistics provided by this retrospective cohort study depend on the outcome of patients traversing the healthcare system of the population in question. These statistics are really telling you the outcome of multiple probabilistic events (listed below). Once you think through each of these events, it quickly becomes apparent that all of the biases lead these conditions to be dramatically undercounted.
1. Patient sought healthcare 2. Patient reported symptoms doctor could identify as potential myocarditis and or pericarditis 3. Doctor recognized symptoms 4. Doctor ordered appropriate diagnostic testing 5. Radiologist recognized the condition.
Let's look at each of these.
1. Given this was a retrospective study, we know that (1) happened 100% of the time. No problem here.
2 and 3. A patient with myocarditis may have one or more of the symptoms below. Some of these symptoms, such as swelling in the lower extremities, are likely a dead give away. However, most are extremely common in COVID.
- Signs of a viral infection, such as body aches, joint pain, fever, headaches, vomiting, diarrhea or a sore throat. - Rapid or abnormal heart rhythms (arrhythmias). - Chest pain. - Shortness of breath, both at rest and during physical activity. - Swelling of your lower extremities (legs, ankles and feet). - Fatigue.
I would wager that most patients who demonstrated one or more of these symptoms indicative for potential myocarditis/pericarditis were not actually tested for the disease. To get tested, a patient lacking extreme myocarditis would likely have to push and push hard to get the doctor to test. This *heavily* biases the results toward under counting.
4. Diagnosing COVID-caused myocarditis and pericarditis is hard. The typical standard of care, at least in the US, is an echocardiogram. This diagnostic ultrasound can indeed pick up some forms of the disease but multiple papers have shown that COVID-caused myocarditis and pericarditis can be invisible on an echocardiogram. The definitive scan is a specialized MRI machine capable of a particular scan sequence. This machine is hard to find even in major health centers (there are three of them total in the Washington DC area). The cost of an MRI is at least an order of magnitude more than an echocardiogram. The echo takes about 15 minutes whereas the cardiac MRI is about 90 minutes. Thus, it is highly unlikely that the doctors in question ordered the appropriate test that can actually detect the disease in question. This further biases the findings in the same direction.
Finally, the study looks at patients from March 2020 and January 2021. The fact that COVID myocarditis and pericarditis can typically only be resolved on a specialized cardiac MRI was not common knowledge for most of the study period.
Thus, the conclusions from this study are DRAMATICALLY underestimated.