The incidence of myocarditis and pericarditis in unvaccinated Covid patients
pubmed.ncbi.nlm.nih.gov
pubmed.ncbi.nlm.nih.gov
> 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-...)
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.
From my limited understanding, 2.56x next to none is still pretty close to next to none.
> 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.
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.
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?
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.
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.
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.
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.
> 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"?
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. Like living in a very polluted city, exposure to lots of dust or chemicals, or living in a building with black mold for extended periods. The minor feeling or easy to ignore/temporary damage done by those experiences creating cellular damage that makes cells in CV systems pop like popcorn when COVID does its very unique number on vascular structures. The word Blood Foam was used once in a very early study on people who died from COVID. The images I remember from that study demonstrated that it is a pretty accurate term for what happens in the worst cases. I'm sure there are people with genetic properties that could just make them more susceptible as well.
I would also not be surprised if it ended up being correlated to heavy metals, dust/fiber, or fungal exposure specifically one or a pair of those things, even staggered exposure, being the biggest contributor. I expect that once its mechanisms are understood, the condition will not share a designation with other known pathologies. An interaction to an exposure and the damage certain coronaviruses do when given the right scaffold.
[0] https://www.frontiersin.org/articles/10.3389/fmed.2020.60682...
[1]https://www.heart.org/en/news/2022/03/31/after-covid-19-expe...
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
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...
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.)
https://www.nationalgeographic.com/science/article/persistin...
Thinking about this now though gives me some ideas that could even be testable that could help. Thank you for sharing this.
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...
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.
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!
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!
> 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?
What does censored mean in this context?
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.