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
This paper has data that I find useful to know which coronary artery is responsible for an MI involving a particular segment or a combination of segments: imaging.onlinejacc.org/content/1/3/282
For instance, LGE involving the basal anterolateral and inferolateral segments cannot be anything but an LCx MI but LGE involving the basal inferolateral and inferior segments can also be an RCA MI. 5/18
I also look at the coronary angiogram to know how large the coronaries are, which coronaries supply which LV segments, whether the LAD wraps around the apical LV, etc. 6/18
Angiograms are always available because the two pre-requisites for requesting a viability study are: severe CAD in 1 or more coronary arteries and LV dysfunction. 7/18
Integrating all this information, I know how many MIs there are, which coronary territories they belong to, and I allocate the 17 LV segments between the main coronary arteries. 8/18
Next, I score the LGE in a semiquantitative way on a 17-segment basis based on the area of LGE, using a 5-point scale: 0 = no LGE; 1 = 1% to 25%; 2 = 26% to 50%; 3 = 51% to 75%; 4 = 76% to 100%.
One key point is NOT to look at transmurality at any single location (transmural thickness of LGE) but to consider each segment as a volume and visually estimate the amount of LGE within the volume of the segment (each segment = 1/17 of the LV mass). 10/18
I then estimate the extent of LGE within each territory by adding the segmental scores weighted by the mid-point of the range of LGE = 12.5% for 1 (midpoint of 1-25%), 37.5% for 2 (midpoint of 26-50%), etc. and dividing by the total number of segments in the territory. 11/18
Thus, I get an LGE extent in % for each of the coronary territories. 100 minus LGE extent in % gives me the viability in each territory, which I report in multiples of 5%. So, a patient may have 65% viability in the LAD, 30% in the RCA, and 100% in the LCx territories. 12/18
Viability is not a dichotomous entity. The extent of viability and locations of viability should be integrated with other factors such as quality of target vessels, surgical risk, presence of hibernating myocardium, etc. to decide whether to revascularize and how. 13/18
I assess the presence of hibernating myocardium by comparing LGE extent in a coronary territory to the wall motion and looking for discordance. The coronary supplying this territory should also have severe disease. 14/18
For instance, if there is 0-30% LGE with severe hypokinesis or akinesis (= dysfunction beyond what you would expect from the LGE), there is hibernating myocardium. If there is no or mild hypokinesis, there is no hibernating myocardium. 15/18
Hibernating myocardium = viable myocardium that’s hypocontractile due to severe ischemia. It has the potential for improvement in contractility, and some data suggest that hibernating myocardium is prognostically worse than ischemic-but-not-hibernating myocardium. 16/18
The summary of my typical viability CMR report looks something like this:
Ischemic cardiomyopathy, LVEF 28%, MIs in the LAD and RCA territories, 65% viability with hibernating myocardium in the LAD territory, 100% viability without hibernating myocardium in the LCx territory, and 30% viability without hibernating myocardium in the RCA territory. 18/18
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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.
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:
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.”