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Steve Cheung's avatar

But wait. We are ALWAYS referring to absence of evidence. That should go without saying.

To require evidence of absence would be to require proof of a negative. That’s a logical impossibility. That’s not how trials work…ever.

So a trial starts with a hypothesis, and pre-specified statistical parameters upon which one can reject the null and accept the hypothesis. In this case, the statistical analysis showed we could not reject the null and accept the hypothesis; so instead, we must reject the hypothesis and accept the null: ie. accept that “X” does NOT work (in this case; in how the trial was done in this instance). That is of course different from stating one has PROOF that X doesn’t work. This is how it is, and how it has always been.

Hence, there is always the possibility that a larger trial with more endpoints MIGHT show that X in fact does work (and we can reject the null, that it doesn’t). Or that an identical study using different power assumptions may have yielded different statistical results. The onus is on the proponents, of whatever, to do that work, and show that proof.

You can always say…under different trial and statistical circumstances….”X might have worked”….but that still absolves precisely nobody from having to go out and proving it.

That said, the interesting thing with this trial to me is still the metrics for determining atrial cardiopathy as a predictor of future overt AF. We already know DOAC is better than ASA in clinical AF. That’s news to nobody. What I take from this is that the way this study tried to determine atrial cardiopathy has not been shown to be effective (ie absence of evidence). I would not, on the basis of this study, yet conclude that the entire concept of atrial cardiopathy is without merit (ie. evidence of absence).

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Carlos Valladares's avatar

Very educative and kudos to dr Mandrola for his lack of prestige! This just cements my confidence in his assessments. Not everyone is so wise to be humble.

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