During the research phase it would be easy, just time based for pts committed to a consistent sleep schedule. Once commercialized we’d work with the device manufacturer to develop an app for pts to turn on sleep mode themselves once they’re in bed, or even some sort of NFC with a bed sensor

For those curious, the PAd dropped by 8-9mmHg at zero G. Conclusion: we should send all HFpEF patients to live on in a space colony.

Would this pass IRB and what’s the highest impact factor journal I could publish this in? (For reference, a few weeks ago JAMA Cardiology published a study of 2 HFpEF pts w/ CardioMEMS getting strapped to a zero G simulator to see how PAd would change)

Take a few of these patients to sleep lab for a couple nights and measure sleep latency, REM time, and use surveys for daytime wakefulness. Compare nights w/ and w/o this sleep algorithm.

6/ Sac-Val may have value in this space, but from a cost effectiveness standpoint, we need to demonstrate it has incremental value over RAASi alone for clinically meaningful endpoints before we consider using it outside of a randomized setting.

5/ Lastly, I heard one of the panel discussants for SARAH say at a different conference recently they’ve lost faith in the value of strain (the PEP here) for prognostication.

4/ And the reduction in LVEF in the control arm of this trial didn’t come anywhere near meeting criteria for CTRCD. How clinically meaningful is preventing a 3% decrease in LVEF?

3/ And if I’m wrong about the equipoise/ethics, wouldn’t a more valuable trial have had three arms: placebo, valsartan alone, and sacubitril-valsartan?

2/ Acknowledging that RAASi is not considered standard of care for preventing CTRCD, I’m not sure it was entirely ethical to give the control arm placebo when PRADA and several meta-analyses have shown benefit with ACEi/ARB in regards to the surrogate primary outcome in SARAH.

I want flying cats. X is trying hard to win me back and it might be working.

The other studies you’re referring to (COLCOT and LoDoCo2 for colchicine, CANTOS for canakinumab, in-process ZEUS for ziltevekimab, etc) look at reducing residual inflammatory risk for secondary MACE prevention after AMI or in chronic CAD rather than treating an AMI itself

That’s really interesting. I can’t access the paper right now, but what timeframe was that ACM over? My kneejerk is that there’s probably not too much to study with the totally null signal from RCTs. I did a quick search on clinicaltrials.gov and couldn’t find anything contemporary

I think the answer is A & B. Consider the octopus: two branchial hearts and one systemic heart. I see no reason a centaur wouldn’t have a dual circulation with both a human and an equine heart. Two defibrillators, two sets of pads, push the shock button on whichever monitor shows VT/VF.

This was a pointless first Bluesky post I don’t know why I felt compelled to write that