A surrogate outcome does not mean a new age. This type of study leads to over prescribing based on a soft endpoint with financial detriment to the patient with no proven benefit in hard outcomes. Does the next drug that reduces BNP create a new age for heart failure?.

So that statistically significant ~1.5% reduction of a composite endpoint driven by the weakest of the endpoints in COLCOT was actually just noise? Who would have thought? #colchicine .

If you think finerenone is good, just wait until you hear about this drug called spironolactone.

RT @J_Rosales_MD: 🚨When it is a YES ✅ and not 🚫in DOACS 💊. 👉🏻 J Am Coll Cardiol 2024;83:444-465.

RT @AnnalsofIM: New: Either ACEi or ARB therapy protect against kidney failure in those with advanced CKD. Neither therapy provided a death….

RT @BradSpellberg: Hence my Antibiotic Stewardship for the 21st Century Lecture: slides

Analogous to LVAD ramp studies, a trial assessing RHC to guide optimal pacing rates for HFpEF may allow for further individualization of pacer settings beyond the algorithm used in MyPace .

If there was half as much enthusiasm about initiating spironolactone as there is about sacubitril/valsartan, the world would be a better place 😌.

RT @DanielJDrucker: Clinical strategies for mitigating adverse events with GLP-1 medicines @BevTchangMD #ADA2024 ht….

Patient with ACS found to have new AF. Something commonly overlooked is in Pioneer AF-PCI, rivaroxaban was reduced to 15 mg daily in pts otherwise indicated for 20 mg daily. Make things simple and use apixaban which was studied at the same dose as used in its landmark AF trial.

RT @CardiacTrials: When to suspect cardiac amyloidosis?. Echo features: .🔹Nondilated LV with thickened walls.🔹E/A > 2 and E/e’ > 14.🔹Biatri….

In the end, genomics are one piece of the complex puzzle of antiplatelet response. But - RCT data has failed to show meaningful benefit and scientific statements that call for routine testing and blanket treatment strategies undermine the complexity of medicine & clinical context.

6) Stent technology has vastly improved each decade and uptake of intravascular imaging has reduced procedural factors that contribute to stent thrombosis. As PCI continues to advance, the benefits of more potent antiplatelet therapy has and will continue to diminish IMHO.

5) This scientific statement does not address when the clinical scenario calls for clopidogrel but the genomic data calls for alternatives. Ex: pt with 2C19 LOF with hx of ICH. Or with AF on DOAC (essentially no safety data for DOAC+ticagrelor/prasugel).

4) The COGENT trial randomized CAD pts on DAPT with clopidogrel to omeprazole (a 2C19 inhibitor) or placebo. MACE occurred in 4.9% vs 5.7% in favor of the omeprazole arm (p=ns). Bottom line, 2C19 inhibition (i.e., LOF) had no effect on outcomes.

3) Many studies showing worse outcomes compared LOF clopidogrel vs LOF ticagrelor/prasugel. But, ticagrelor and prasugrel are not neutral comparators. You cant conclude the outcomes are due to genetic mutations when the comparator group gets 💊shown to be superior to clopidogrel.

2) TAILOR-PCI is the best designed RCT and most contemporary trial to test a genotype guided strategy. Yet it was negative and failed to show carriers of LOF 2C19 on clopidogrel had worse MACE outcomes than patients on ticagrelor/prasugrel.

1) yes, numerous OBSERVATIONAL and POST HOC analyses have shown worse outcomes with clopidogrel in pts with 2C19 LOF. But we have been fooled many times by low quality data that was later refuted by RCTs (e.g., HRT for CV risk reduction overturned by WHI).

A scientific statement on CYP2C19 testing to guide anti platelet therapy that I have to respectfully disagree with. A 🧵 on why genomic testing a misguided solution to a complicated problem.

It never made sense that HM3 patients who almost certainly develop acquired von Willebrand syndrome would need an antiplatelet agent and we finally have the data proving it!.