In 2023, two large randomized trials addressed the use of oral anticoagulation in short duration atrial fibrillation. This was a really big story. We learned a lot.
1. I would not lump the ESUS population with that of the Noah/Artesia cohort. These 2 studies are of primary stroke prevention. If someone already has had a stroke that a neurologist deems most likely of cardioembolic origin (ie. secondary prevention), and then device detected subclinical AF is found, I would consider that more causally significant and worthy of treatment (as the presumption will be that the event rate will be higher). Of course, I look forward to the trial results.
2. Great point that Noah and Artesia studied somewhat older people who already had a device (as well as their inherent indications) and decently-high chads scores. These are not the same people as the Apple Watch brigade of “worried well”.
3. I am somewhat thrilled that these 2 studies produced nuanced results that will resist “1 size fits all” decrees from guideline writers. This will remain for now in the realm of clinical judgment and patient values and preferences. In addition, the Circulation-published “meta-analysis” (which wasn’t really a meta analysis) was of limited usefulness, but the patient-level combined data of the 2 studies that you mentioned will hopefully provide more context as to the duration of SCAF btw 6 mins and 24 hours after which stroke risk increases more acutely. This would be very useful information for clinical decision-making.
4. I do not fault device and medicine-makers for funding research. Without them, very little research in the cardiology space would occur. In general, their incentives align with patient desires - finding drugs that work. As alluded to yesterday, I fault regulators for not raising the bar for approval. The only way to disincentivize research trainwrecks like Protect/Prevail, Guide HF, or Symplicity et al, is for regulators to say “that is not good enough”….which is the only way to spur companies to fund better studies.
Wonderful summary, as usual.
A few thoughts:
1. I would not lump the ESUS population with that of the Noah/Artesia cohort. These 2 studies are of primary stroke prevention. If someone already has had a stroke that a neurologist deems most likely of cardioembolic origin (ie. secondary prevention), and then device detected subclinical AF is found, I would consider that more causally significant and worthy of treatment (as the presumption will be that the event rate will be higher). Of course, I look forward to the trial results.
2. Great point that Noah and Artesia studied somewhat older people who already had a device (as well as their inherent indications) and decently-high chads scores. These are not the same people as the Apple Watch brigade of “worried well”.
3. I am somewhat thrilled that these 2 studies produced nuanced results that will resist “1 size fits all” decrees from guideline writers. This will remain for now in the realm of clinical judgment and patient values and preferences. In addition, the Circulation-published “meta-analysis” (which wasn’t really a meta analysis) was of limited usefulness, but the patient-level combined data of the 2 studies that you mentioned will hopefully provide more context as to the duration of SCAF btw 6 mins and 24 hours after which stroke risk increases more acutely. This would be very useful information for clinical decision-making.
4. I do not fault device and medicine-makers for funding research. Without them, very little research in the cardiology space would occur. In general, their incentives align with patient desires - finding drugs that work. As alluded to yesterday, I fault regulators for not raising the bar for approval. The only way to disincentivize research trainwrecks like Protect/Prevail, Guide HF, or Symplicity et al, is for regulators to say “that is not good enough”….which is the only way to spur companies to fund better studies.