Sincerely appreciate your detailed thoughts. I believe we are arguing different points (more below).
1. I am absolutely not ignoring the previous studies and I explicitly stated the preponderance of evidence supports concerns of myocarditis after vaccination being a serious issue. The preponderance of evidence is quite damning for VAM. However this study, while well intentioned, has strong flaws.
2. False positive: The issue is not if these elevated controls are 'real' or false. I agree with you statement that the children serve as their own controls. However, does that elevation correlate with a diagnosis of 'subliminal myocarditis'? Even patients presenting for ACS serve as their own controls if the first 2 troponin are negative. The third one can be positive and subsequent stress test or Cath still be normal (i.e., no ACS). The false positive is not to state the elevated values are 'normal' but rather if the elevated values alone are suffieicnt for diagnosis of sublinical myocarditis independent of a CMR. Without CMR, elevated troponin is abnormal but diagnostic of subliminal myocarditis.
Also, the 4 with 'positive' troponin (but lower than threshold for sublcinial myocarditis specificity had normal CRP and normal CK-MB. That should definitely raise doubt about the clinical relevance of these elevated troponin levels? In adults have you ever diagnosed 'myocarditis' in an asymptomatic patient with normal ESR, CRP, CK-MB, and Echo? Not sure any colleague would accept that as a diagnosis in actual clinical practice.
Agreed that elevated troponin in 4 children after Vx without symptoms is 'concerning'. The issue is: is it diagnostic of 'subclinical myocarditis'. NO (not without CMR) And at those levels found in the trial he specificity is low. I have seen elevated troponin from fall and rhabdo in adults and from excessive endurance training. None of that yields a diagnosis of myocarditis. As you know, one can have elevated troponin without 'inflammayong' of cadriomyocytes.
Yes, Vx was the preceding event. This study just doesn't prove causation. All they had to do was perform CMR in those 4 and the study would have been much stronger.
3 Sample size:1 clinical myocarditis in 301 (1:301) is absolutely an outlier compared to the 1:3000 that most large scale studies suggest. Outliers of this extreme in statistics are almost always contextuliazed as not indicative of the overall pattern (until larger scale studies corroborate).
Ask yourself this: if the study revealed 0 in 301 clinical myocarditis would you accept zero percent as the rate? No. Same size is too small. That is precisely the critique we have all had with the small sample size used to justify EUA in children and adolescents (sample size was too small to assess safety and clinical efficacy)
Overall, we are staying two different things (IMHO). Your point that the elevated troponin is a safety signal is important and no disagreement there. My point is one of diagnostic definitions. Research has already been doing demonstrating elevated troponin can have negative CMR and thus diagnosis of myocarditis (subliminal or clinical) is not appropriate. What the alternate explanation is: we don't know. More research is needed.
As you know in adults with suspected ACS, a Cath with no CAD could mean troponin was from microvascular disease or other causes that we may never know. .
Anyway, thank you very much for your thoughtful analysis and feedback. Appreciate your time.
