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.”
In the main text, they elaborate:
“Our data demonstrated that LGE in the acute phase of myocarditis is not necessarily synonymous with irreversible damage, because in 11% of our patients, LGE completely disappeared at follow-up.”
What do I think?
- What does LGE in acute myocarditis mean?
- It certainly does not mean fibrosis… fibrosis is another word for scar, and the human body takes time to heal and form a scar. In the acute setting, it is necrosis. This means dead myocardium with edema.
- Is LGE in the acute myocarditis synonymous with irreversible damage?
- Absolutely. See above. Until we figure out a way to regenerate human myocardium, the death of myocardium is irreversible damage.
- But wait, if LGE represents irreversible injury, then why did it disappear in 11% of the cases in this paper?
- Because LGE detects focally dead myocardium and the technique has a minimum threshold for detection. Generally, it’s around 1 cm3 of myocardium.
In acute myocarditis, the volume of the dead myocardium is larger because of edema (think of a swollen bruise or cut on your knee).
In healed myocarditis, the volume of the same dead myocardium is smaller due to scar formation, shrinkage, and compaction (think of healed scar tissue on your knee).
And in some instances, the volume of the healed dead myocardium may be below the threshold of detection by LGE.
Think of the injury in terms of the fraction of the cardiac cells that are dead. It’s the same in both the acute and healed stages, even if “LGE disappears”.
So LGE in the acute stage indeed represents dead myocardium even if it disappears in some. The "disappearance" is explained by changes in the dead myocardium over time and thresholds of detection of dead myocardium by LGE.
The investigators also write: “For this reason, myocarditis differs from myocardial infarction, where LGE is always associated with irreversible myocardial damage, the extent of which usually decreases at follow-up due to scar shrinkage, although it never disappears completely.”
- So why does LGE disappear in myocarditis but not MI?
- Actually, LGE can "disappear" in MIs as well, and for the same reasons. It happens less often than in myocarditis because the dead myocardium in MIs is often larger in size than in myocarditis and MIs are serially imaged less often than myocarditis (so we don’t see it as much).
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A CMR 4 months later showed a near resolution of the anteroseptal/anterior/anterolateral LGE (red arrows). The inferior LGE (blue arrow) that did not disappear matched the fat seen on cine images.
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).
In the septum, the LGE spares the very RV side of the septum (also a distinguishing feature from cardiac sarcoidosis) and is therefore often midmyocardial… the ring is subepicardial laterally and midmyocardial septally.
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)?
I tried looking at published CMR images and autopsy studies to get some insights into what happens in the hearts of Covid-19 patients. I’ll share my thoughts on 10 papers with CMR images and 2 papers each with autopsy data in >10 patients:
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
Next, I try to identify how many and where the MIs are. For this, I look at the extent and locations of ischemic LGE and decide which of the 17 LV segments are likely to be supplied by each of the coronary arteries. 3/18