For reference, here's our work on CMR phenotyping:
pubmed.ncbi.nlm.nih.gov/40400457/
pubmed.ncbi.nlm.nih.gov/36103165/
pubmed.ncbi.nlm.nih.gov/31954639/
pubmed.ncbi.nlm.nih.gov/31070111/
#WhyCMR #sarcoidosis #cardiacsarcoidosis #CardioSky
Posts by Chetan Shenoy
They even extended our findings.
CMR phenotyping had much greater interobserver reproducibility than LGE quantification.
CMR phenotyping was 5-fold faster than LGE quantification.
FDG-PET added no incremental predictive value beyond CMR phenotyping.
In a prospective cohort of 206 patients (CHASM-CS), they found that ALL ventricular arrhythmia events occurred exclusively in patients with the high-risk (pathology-frequent) LGE phenotype.
There were NO events in the low-risk patients.
This study confirms, for the first time in a fully prospective cohort, the prognostic importance of CMR phenotyping in cardiac sarcoidosis. The high-risk CMR phenotype had 100% NPV, indicating the absence of VA events among patients without the high-risk phenotype. LGE phenotyping showed much higher interobserver reproducibility than LGE quantification and was five-fold faster.
In science, successful replication is the ultimate quality check!
This is a highlight for our research group—David Birnie's group (one of the biggest names in cardiac sarcoidosis) just independently replicated our CMR phenotyping work!
doi.org/10.1093/ehji...
#EHJIMP #CardioSky #sarcoidosis
Related: you’ve definitely made me more conscious about not calling something «ischemic cardiomyopathy» just because there is coronary disease as it might just be a bistander.
Sensitivity and localization accuracy of CMR for acute and chronic MI.
The sensitivity of CMR for acute non-Q-wave MIs was 91% in this multicenter study:
www.ahajournals.org/doi/10.1161/...
So yes, that's one part of it, but only a small part.
🧵 Are OCT and CMR really "complementary" in MINOCA? Or are they telling us conflicting stories?
Reynolds et al (Circulation 2026) combined both modalities in 284 MINOCA patients. The results raise more questions than answers.
📄 www.ahajournals.org/doi/abs/10.1...
1/7
Have you ever wondered whether your patient with CAD and cardiomyopathy truly has ischemic cardiomyopathy, or whether the CAD is a “bystander”?
You might be interested in our paper now out in Circulation
#simultaneouspublication
#AHA23
#cardiosky
#Medsky
#WhyCMR
academic.oup.com/eurheartj/ad...
#CardioSky #WhyCMR #Medsky
Thanks for the shoutout! A minor clarification - the high risk phenotype does not even incorporate an abnormal LVEF!!!!
Important multicenter study in #EHJ
#CMR outperforms societal recs for ICD placement in cardiac sarcoidosis
📈AUC=0.86 for 5-yr risk of fatal/life-threatening arrhythmias
⚡Highest risk = abnl LVEF + LGE that is multifocal, septal, subepicardial, or involves RV freewall
buff.ly/Nc2upbU
#cardiotwitter
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...
Here's our paper in Circulation on the topic - bsky.app/profile/para...
Here's my talk on how to identify the etiology of cardiomyopathy using CMR - www.youtube.com/watch?v=9or8...
In my opinion, both trials are fundamentally useless.
What is ischemic cardiomyopathy?
Both trials defined ischemic cardiomyopathy as LV dysfunction + obstructive CAD.
This does not identify the etiology of cardiomyopathy as ischemic, but identifies the presence of CAD. Two different things!!!
I don't exactly know. But...
1 - There was no real change in ECV in Explorer HCM (PMID 33190524).
2 - An increase in ECV is not necessarily bad. It increases after AVR (PMID 29471937).
3 - The amount of dead myocardium will never decrease. So, a "decrease in LGE" does not mean less badness.
Interesting. The ECV increased 1.1% (25 min) to 2.2% (5 min), which is difficult to explain. But it explains why LGE was less; it was quantified as the amount of myocardium 6SD brighter than "remote". LGE amount will be less if the remote myocardium is brighter after mavacamten than at baseline.
“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
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#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.
VT and VF/cardiac arrest - correct. That would be secondary prevention.
AV block is a Class IIa indication for an ICD in the guidelines for cardiac sarcoidosis. But who has cardiac sarcoidosis is not always clear.
What if patient has extracardiac sarcoidosis and complete AV block but no LGE? 🤔
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@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.
We discuss this in our editorial:
academic.oup.com/ehjcimaging/...