Myocardial Infarction & Viability (CMR)
- Late gadolinium enhancement (LGE) is the star of the show: scarred myocardium holds onto contrast and lights up bright white, while healthy muscle goes dark.
- For ischemic scar, the brightness starts at the subendocardium (the inner layer) and works outward — because that inner layer starves first.
- The transmural extent of that bright scar predicts viability: thin scar = muscle that can wake up after revascularization; full-thickness scar = muscle that's gone for good.
- CMR also catches the complications of infarction — thrombus, microvascular obstruction, aneurysm — in one sitting.
When a coronary artery clogs and stays clogged, the heart muscle downstream doesn't die all at once or all at the same depth. It dies from the inside out. Cardiac MRI (CMR) is the one test that can show you, layer by layer, exactly how much muscle was lost and — the genuinely useful part — how much is still alive and worth saving. That's the whole game here: telling dead muscle from sleeping muscle.
Why the inside dies first
Think of the heart wall as a steak cooking on a grill where the heat source is inside the meat. The coronary arteries run along the outside (the epicardial surface) and dive inward, so the deepest layer — the subendocardium, the lining right next to the blood pool — is the farthest from supply and the first to starve. Squeeze the artery a little and only that inner rim suffers. Squeeze it hard and long enough and the damage marches outward toward the epicardium, like a scorch creeping up through the steak.
This "wavefront of death" is why ischemic scar always touches the subendocardium. Hold that thought — it's the single most useful pattern in all of CMR.
Late gadolinium enhancement: where scar glows
Here's the trick. We give a gadolinium contrast agent, then wait about ten minutes before imaging — hence late gadolinium enhancement. Gadolinium can't get inside living cells; it loafs around in the space between them. In healthy muscle that extracellular space is tight and the contrast washes out fast. In scar — where dead cells have been replaced by loose, spread-out collagen — there's far more room for contrast to pool, and it lingers.
So on the delayed images we set the scanner to make normal muscle null out to black, and the scar pops bright white against it. Dead tissue, caught glowing red-handed.
The pattern of LGE tells you the cause. Subendocardial or transmural enhancement that follows a coronary territory says "this is ischemic — a heart attack." Enhancement that spares the subendocardium (mid-wall or epicardial) points away from infarction toward things like myocarditis.
From "how much scar" to "will it come back"
This is where CMR earns its keep. Some hibernating muscle is alive but stunned — chronically underfed, barely contracting, playing dead. Revascularize it and it can recover. The question for the surgeon is: is it worth re-plumbing this artery, or is the muscle behind it already a lost cause?
LGE answers it by measuring transmural extent — how deep the bright scar goes through the wall thickness:
| Transmural extent of scar | What it usually means |
|---|---|
| No LGE (0%) | Muscle is viable — strong recovery expected. |
| Less than ~50% of wall thickness | Likely viable — good chance of improving after revascularization. |
| More than ~50% of wall thickness | Less likely to recover — mostly scar. |
| Full thickness (near 100%) | Not viable — re-opening the artery won't bring it back. |
The intuition is just plain carpentry: a board with a shallow scratch is still a board, but one that's rotted nearly all the way through isn't holding up the porch no matter what you do.
CMR isn't the only viability test — nuclear imaging (PET and SPECT) and stress echo also assess it. CMR's advantage is resolution: it resolves that thin subendocardial rim of scar that lower-resolution methods can blur right past.
The complications CMR catches in the same visit
A heart attack doesn't stop at scar. Because you're already in the magnet, CMR mops up the dangerous sequelae:
- Microvascular obstruction (MVO): a dark core inside the bright acute scar. The infarct was so severe the tiny vessels clogged too, so contrast can't even reach the center. It's a marker of a nastier infarct and worse outcomes.
- Left ventricular thrombus: a clot clinging to akinetic wall, usually at the apex. On LGE it stays black (no blood supply, no contrast) against the bright ventricular blood pool — CMR is more sensitive for this than echo.
- Aneurysm and wall thinning: a stretched, thinned, bulging scar that can host that thrombus.
Don't mistake acute infarct edema for chronic scar. In an acute MI the muscle is also bright and swollen on T2-weighted images because of edema; chronic scar is not edematous. Pairing T2 (edema) with LGE (necrosis/scar) lets you date the injury — fresh versus old.
The one thing to remember
When you see bright LGE that starts at the subendocardium and respects a coronary territory, you're looking at an old heart attack — and the depth of that brightness is your crystal ball for whether the muscle behind it is salvageable. For the bigger picture of how the artery got blocked in the first place, see coronary artery disease; for how each CMR sequence contributes, see cardiac MRI technique.