Must-watch lecture on cardiomyopathy and CMR by @cshenoy.bsky.social „more often than what is the EF we should ask the why?“ youtube.com/live/9or85hk...

“CMR phenotyping can be used immediately in clinical practice to identify patients with suspected cardiac sarcoidosis who would benefit from a primary prevention ICD," said Chetan Shenoy, MD. Read more about how this can prevent life-threatening ventricular arrhythmias: www.tctmd.com/news/cmr-may...

Thank you, @toddneale.bsky.social, for your excellent reporting on our EHJ paper! @tctmd.bsky.social @escardio.bsky.social @paragbawaskar.bsky.social

#EHJCVI 🫀 What's the value of ventricular strain in systemic sclerosis? 📉 Both LVGLS and RVGLS are linked to death or MACE, unlike LVEF and RVEF 🧠 How does strain compare to traditional prognostic markers? 🔍 Read more 👉 doi.org/10.1093/ehjc... #CardioSky @jgrapsa.bsky.social @escardio.bsky.social

Prediction of ventricular arrhythmic outcomes in suspected cardiac sarcoidosis: a comparison of cardiovascular magnetic resonance phenotyping vs. societal recommendations for implantable cardioverter-defibrillator placement academic.oup.com/eurheartj/ad... #Cardiosky #WhyCMR #Epeeps #Medsky

Cardiac sarcoidosis is a undervalued disease and difficult to diagnose and treat, considering potential life-threatening arrhythmias. Nice to have some more guidance. #cardiosky.

academic.oup.com/eurheartj/ad... @escardio.bsky.social #Cardiosky #WhyCMR #Epeeps #Medsky Please DM me if you would like a full-text PDF of the paper!

pmc.ncbi.nlm.nih.gov/articles/PMC... #HCM #CardioSky #Cardiomyopathy

In patients with suspected cardiac sarcoidosis, cardiac FDG-PET is recommended after a normal CMR if there is a high clinical suspicion. What are the data supporting this recommendation? #CardioSky #MedSky #Sarcoidosis

Query sarcoid, normal #WhyCMR, so then should we do FDG-PET? Not much benefit.

In patients with suspected cardiac sarcoidosis, cardiac FDG-PET is recommended after a normal CMR if there is a high clinical suspicion. What are the data supporting this recommendation? #CardioSky #MedSky #Sarcoidosis

This paper reports the coexistence of cardiac sarcoidosis and arrhythmogenic cardiomyopathy in 5 patients. heart.bmj.com/content/earl... #CardioSky #MedSky

Great thread on LV thrombus and embolism risk - especially if RWMA I discuss lifelong anti coagulation with my pts even if it looks resolved on echo, good to have some data to help back this up 👇

Amazing achievement by rising star and post-doc in my lab @paragbawaskar.bsky.social, winner of the prestigious 2024 Melvin Judkins Early Career Investigator Award at #AHA24!! Congratulations!!! @ahascience.bsky.social

It’s great that journals are coming over here, but what I have really missed after my departure from Twitter 2 years ago is this, the authors themselves presenting their works and discussing it with peers. #cardiosky #medsky #emimcc

With the big caveat that obvious alternative causes are not present such as AF.

All patients with stroke is unrealistic in terms of cost, access and resourcing. However in patients with ischaemic stroke, LV dysfunction and/or recent MI I agree (if #echofirst + contrast is negative for thrombus).

Thanks for your insights. Fascinating area.

Thanks. So for example - post anterior infarct, persisting WMA on CMR at 6 months despite OMT (but improvement in overall LVEF). Lifelong anticoagulation or would you reimage at a further interval (I.e. 12 months) to look for improvement in wall motion abnormality?

Great work Chetan. An important area where as a community we need to get better at managing - particularly in the post (anterior) STEMI space. What are your thoughts on stopping anticoagulation at 3 or 6 months post MI with persisting wall motion defects but resolved thrombus?

Congratulations for this work! Do you have data for patients with CMR and echo to evaluate the discrepancy? We need a well designed RCT to answer this important although infrequent question. And to assess the effectiveness of DOAC in these cases

In 2019, we wrote a paper showing that patients with left ventricular thrombus have a long-term risk of embolism, extending to at least 8 years. We were puzzled by the finding… #CardioSky www.ahajournals.org/doi/10.1161/...

It depends!

Read our editorial on avoiding errors when diagnosing myocarditis using CMR: www.sciencedirect.com/science/arti... @paragbawaskar.bsky.social #CardioSky

Finally, many thanks to @cshenoy.bsky.social for his mentorship, our outstanding team for their contributions, and the editors and reviewers at Circulation for all their efforts to make our paper better!

Read our paper here –https://www.ahajournals.org/doi/abs/10.1161/CIRCULATIONAHA.123.067032 And if you will be at #AHA23, come visit the poster session on Monday, Nov 13, 10:00-11.30 am, Zone 2. eppro01.ativ.me/src/EventPil...

An important trial related to this topic was just funded in the UK – Peter Swoboda at the University of Leeds is the PI of an RCT to identify the best initial test for newly diagnosed HF… we look forward to the results of CROSS-HF in a few years.

And if NICM and dualCM do influence outcomes, the next trial should investigate whether the routine use of CMR to identify the cause of cardiomyopathy improves the selection of patients for coronary revascularization, and overall long-term outcomes.

We need to investigate whether NICM or dualCM in patients with CAD influences outcomes after coronary revascularization. An ancillary study of the STICH3C trial by Mario Gaudino and Jonathan Weinsaft at Cornell will give us some answers in about 5 years.

So what? Patients with CAD+NICM or dualCM should be treated with a statin, aspirin, and guideline-directed HF therapy the same as those with CAD+ICM. But do patients with CAD+ NICM or dualCM benefit from coronary revascularization in the same manner as those with CAD+ICM?

Prior studies have found better outcomes for NICM vs. ICM. What explains worse outcomes for NICM in our study? We can only speculate, but it may be because patients in our study had 2-3 diseases – CAD+NICM… or CAD+ICM+NICM. Prior studies compared NICM without CAD to ICM+CAD.

And we looked at their long-term outcomes. Patients with CAD+NICM or dualCM had a greater risk of all-cause death or heart failure hospitalization, all-cause death, and heart failure hospitalization compared with CAD+ICM. The risk of CV death was not different.

We found NICM or dualCM in 1 of every 6 patients with CAD. CAD+NoCM - 18.2% CAD+ICM - 64.8% CAD+NICM - 9.3% CAD+dualCM - 7.7% The prevalence of CAD+NICM or dualCM was 16.9% or 1 in 6 patients with CAD.

We looked at their CMRs and coronary angiography data and classified them into one of: 1. No cardiomyopathy (CAD+NoCM) – normal LVEF and no LGE 2. Ischemic cardiomyopathy (CAD+ICM) 3. Non-ischemic cardiomyopathy (CAD+NICM) 4. Dual cardiomyopathy (CAD+dualCM) – both ICM and NICM

We did a large retrospective observational study of 3,023 patients with obstructive CAD who had CMR for any clinical indication at our health system.

So how often do patients with CAD have NICM or dual (both ICM and NICM) cardiomyopathy? How do these patients do compared to patients with ICM? We tried to answer these questions.

There has been interest in this topic of late because trials of coronary revascularization other than STICHES have not shown revascularization to be beneficial.

Currently, we determine the cause of cardiomyopathy based on coronary angiography findings… CAD=ICM; No CAD=NICM However, pathology and small CMR studies have shown that NICM can occur with “bystander” CAD ICM can occur without CAD Both ICM and NICM can occur together

A thread about our latest paper from star post-doc @paragbawaskar.bsky.social 👇