Chetan Shenoy Profile picture
Cardiologist and researcher, in cardiovascular magnetic resonance imaging, at the University of Minnesota
Dec 12, 2021 12 tweets 5 min read
This is an interesting study by @amritlota et al.

“LGE has no prognostic value if LV volumes and EF are normal” is the wrong interpretation, @MAecocardio.

These are my thoughts…
#WhyCMR First, was the LGE in this study an artifact ("overcalling")?

No, because:

- This paper comes from pioneers and some of the biggest names in CMR
- Our anecdotal experience matches these findings
- The images in the paper very clearly demonstrate LGE.

Apr 29, 2021 11 tweets 4 min read
I previously did a thread on what the disappearance of LGE means. I’ll share two cases to illustrate some of my thoughts…

The first is a case of Desmoplakin cardiomyopathy that we published a few years ago:
ahajournals.org/doi/10.1161/CI…
Apr 28, 2021 9 tweets 4 min read
I think it’s genetic ACM because of the pattern of LGE involvement. There is circumferential LGE (the "ring sign") with lateral wall predominance vs. septal (unlike in cardiac sarcoidosis). The lateral wall involvement spares the most subendocardial portion and/or the papillary muscles and trabeculations, indicating it is subepicardial (unlike a transmural MI that started subendocardially and involves the papillary muscles/trabeculations).
May 19, 2020 28 tweets 7 min read
It’s been over 2 months since the first descriptions of cardiac manifestations of Covid-19. There have been many papers and reviews on this topic. What have we learned about how SARS-CoV-2 can affect the heart? #whyCMR #cardiotwitter Troponin elevations and low EFs are frequently described. Why do they happen? Most papers use the term Covid-19 myocarditis. But can SARS-CoV-2 cause fulminant myocarditis (= extensive focal myocardial necrosis, as seen with viral lymphocytic or giant cell myocarditis)?
Nov 12, 2019 13 tweets 3 min read
Here’s an interesting paper published in JACC yesterday. The investigators studied 187 acute myocarditis patients with CMR (within a week) and repeated the CMR at 6 months.
onlinejacc.org/content/74/20/… They found that LGE was present in 96% at the initial presentation and 86% at 6 months. They conclude:

“In the acute setting, LGE does not mean definite fibrosis, and it may disappear at 6 months.”
Aug 24, 2019 18 tweets 4 min read
With all the discussion about viability in the past few days, I would like to share how I interpret and report viability on CMR. I first look for LGE. Rarely, there’s no LGE and it’s all viable or more likely, a non-ischemic cardiomyopathy. #WhyCMR 1/18 When I see LGE, I confirm it’s in an ischemic pattern – subendocardial or transmural, and limited to a coronary territory, i.e., an MI. If not, it's again a non-ischemic cardiomyopathy and not a viability issue anymore. 2/18
Jul 15, 2018 11 tweets 33 min read
@jameschilee @purviparwani @krychtiukmd @DrRyanPDaly @venkmurthy @journalofCMR @MarcDweck @AmitRPatelMD @onco_cardiology @ash71us @SHummelMD @SCMRorg 1/11 Why CMR for newly diagnosed HF? First, CMR is the gold standard for LVEF assessment and LVEF is used to diagnose cardiomyopathy, to decide medications and other treatments such as ICD and CRT. Sometimes, we don’t find a cardiomyopathy on CMR that was diagnosed on echo. @jameschilee @purviparwani @krychtiukmd @DrRyanPDaly @venkmurthy @journalofCMR @MarcDweck @AmitRPatelMD @onco_cardiology @ash71us @SHummelMD @SCMRorg 2/11 Second, CMR tells us about the etiology of the cardiomyopathy. This is critical because the etiology is closely linked to prognosis and management. The prognostic relevance was nicely shown by @dukehfdoc in a landmark NEJM paper 18 years ago - goo.gl/xQP6JT