We are and already do. This trial created a permission structure to do the easiest thing for patients in complex situations. Not saying it’s always wrong, but binary decision making in shock leads to many unintended consequences. This is why we use shock teams to think of all possible futures.

Ask me about the time we found a part of one sticking through the right ventricle 🏹

😂

Would definitely be helpful!

Totally agree. The obsession over EF has hamstrung research efforts and clinical progress.

Amen

Otherwise other afterload reducers would be just as effective in HFrEF and that is just not the case (prazosin, amlodipine, metoprolol tartrate)

Agree, but more than that, EF is an artifact of LV dilatation; a function of a specific type of cardiomyopathy. GDMT works independently of afterload reduction by reducing beta receptor downregulation and preventing neurohormonal pathways to fibrosis.

HFpEF pathology is completely different

So you’re selecting a treatment group that can tolerate SGLT2i that had a high rate of discontinuation for hypotension in the trials.

Skeptical of these results for a few reasons. The HFpEF trials of late benefit from enrollment of EF down to 40% which we know includes a HFrEF phenotype that responds to GDMT.

Propensity matching in this group is frought. Sick amyloids can barely tolerate any meds due to dysautonomia.

Quick comment on my end. The app is great, but reporting the % size is problematic.

We insist that the PHM RATIO is reported to avoid communication errors between team members with a misplaced or missing minus sign.

I don’t yet have an avenue to help but I’ll be happy to speak with them if they need advice

Not the best level of evidence but this is consistent with my clinic experience using Entresto in ESRD patients. Have managed to get some recovered EFs to kidney transplant alone!

www.ahajournals.org/doi/10.1161/...