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Cardiac MRI report: LGE, scar burden and viability

Also called: cardiac MRI · CMR · CMRI · cardiovascular magnetic resonance · MRI heart · contrast MRI of the heart

Medically reviewed by Dr Kunal Patankar, MBBS, MD (Medicine), DrNB (Cardiology) Last reviewed 4 August 2026 ~17 min read

A cardiac MRI is a scan of your heart that uses a strong magnet rather than X-rays or sound waves. If you have read how your heart works, an echo inspects the shape of the rooms and how the walls move. A cardiac MRI goes one step further and looks at what the wall is actually made of.

That is the whole reason it gets ordered. By the time someone asks for a cardiac MRI, the question has usually stopped being how well is the heart pumping — an echo answered that — and become why.

This page explains the report. The scan itself is done in the radiology department and reported by a radiologist; your cardiologist ordered it with a particular question in mind and reads it alongside everything else they know about you.

Two practical things, because people arrive expecting an echo. This takes considerably longer — allow a good part of a morning rather than the fifteen minutes an echo takes — and you lie inside a tube, in a machine that is loud, holding your breath when you are asked to. If enclosed spaces frighten you, say so when the appointment is made, not on the day. That is a solvable problem if anyone knows about it in advance, and a wasted scan if nobody does.

The questions a cardiac MRI is asked

When the pumping is down, or a wall is thicker than it should be, there are only a handful of explanations, and they need completely different treatment. A cardiac MRI is how they are told apart:

  • Was the blood supply cut off? An old heart attack, sometimes one nobody knew about.
  • Was there inflammation? An insult to the muscle that has since settled, or is still active.
  • Is something being deposited in the muscle? An infiltrative disease such as amyloidosis or sarcoidosis, where an abnormal substance builds up inside the wall.
  • Is the muscle itself abnormally thickened? Hypertrophic cardiomyopathy, and if so, where — and is the thickened part still made of good muscle?

Those four are all versions of what is it. There is a fifth question of a different kind, and it is often the one that sent you for the scan:

  • Is the muscle behind a blocked pipe still alive? Not what happened to it, but what can still be done about it — whether reopening that artery would give anything back. This is called viability, and it has its own section below.

Almost every line in the report exists to answer one of those five.

LGE — the line that matters most

LGE stands for late gadolinium enhancement, and it is the centrepiece of the scan. Your report may call it delayed enhancement, or simply describe an area as enhancing.

Gadolinium is the contrast dye given through a drip during the scan. Here is what it does.

The dye cannot get inside a living heart cell. It is too large to cross an intact cell membrane, so wherever it goes, it is travelling in the spaces between cells. That single fact is the whole basis of the scan.

Healthy heart muscle is packed tight — the cells sit shoulder to shoulder, and the space between them is small. The dye has little room to occupy there, and what does get in drains away quickly.

Scar is not muscle. Where heart tissue is lost, it is not replaced by more heart tissue — it is replaced by something else: putty, cardboard, bhoosa. It fills the space and holds the shape, but it is not the working material and it never becomes the working material again. And unlike muscle, it is loose-packed: the dye spreads into all that extra space between its fibres, and it is slow to drain back out.

So the pictures are taken late — about ten minutes after the injection, once the healthy muscle has washed clean. Anything still holding the dye and glowing bright is no longer working muscle. That is why late is in the name: looking early would show dye everywhere and tell you nothing.

It also explains something that puzzles people about a fresh heart attack, where the damage lights up very brightly indeed. When muscle cells die, their membranes break down — and the space that was closed to the dye a moment ago is suddenly open to it.

What does a bright patch mean for you? Nothing you can feel directly — scar has no sensation and causes no symptom of its own, which is exactly why a scan is needed to find it. It matters in two other ways. Putty does not squeeze, so a large enough patch means less of the wall is doing the work, and that is one reason the pumping number falls. And putty does not carry electricity the way muscle does, which is the subject of the next section.

Where the enhancement sits tells you the cause

This is the part that turns a bright patch into a diagnosis, and it is why the report describes the pattern, not just the presence:

Where the LGE is What it usually points to
Inner layer of the wall, or the full thickness, following one artery’s territory An old heart attack — the inner layer dies first when supply is cut off
The middle of the wall, not matching any artery A non-ischaemic cause — an old inflammation, or a genetic muscle disease
Patchy and multifocal, often at the base of the septum Suggestive of sarcoidosis
Widespread across the inner layer of both ventricles, with the muscle hard to darken normally Suggestive of amyloidosis
At the points where the right ventricle joins the septum, or within thickened segments Common in hypertrophic cardiomyopathy

So “LGE present” on its own answers nothing. “LGE present, mid-wall, not in a coronary territory” answers a great deal — it says this was not a heart attack, and redirects the whole search.

How much of it — scar burden

The report may also quantify it: scar burden, given as a percentage of the left ventricular muscle.

This matters because of what scar cannot do. Working heart muscle carries the electrical signal smoothly and in step, the whole sheet moving together. Putty does not carry it at all.

So where a patch of scar sits in the middle of working muscle, the electrical wave arriving at it cannot pass through — it has to travel around the edges. And a current forced around an obstacle can catch itself: instead of passing on and dying away, it starts going round and round that patch, like water caught in a whirlpool. A heart driven by that loop beats far too fast to fill or to pump properly, and that is the rhythm the scan is quietly asking about.

That is why a number is put on it — more scar means more edges for a current to catch on. Broadly:

Scar burden How it is generally read
Under 5% The most favourable group
5–15% Risk begins to rise measurably above the lowest group
Over 15% What guidelines describe as extensive LGE, and treat as a risk marker

What LGE can miss — and the numbers that cover for it

There is one blind spot worth knowing about, because it explains extra numbers on some reports.

LGE works by contrast — bright abnormal muscle against normal muscle deliberately darkened to black. That works beautifully for a patch of scar sitting among healthy tissue. But when the scarring is spread evenly through the whole muscle rather than concentrated in patches, there is no normal muscle left to compare it against, and the images can look deceptively uniform.

This is why your report may carry T1 mapping or ECV — extracellular volume — given as a percentage. Rather than relying on a bright-versus-dark comparison, these measure the space between the cells directly, across the whole muscle. A raised ECV says the spaces have expanded everywhere, which is exactly the pattern of diffuse fibrosis and of infiltration.

Viability — whether opening the artery would give anything back

Everything so far has been about what the muscle is. This section is about a different kind of question, and it is often the reason the scan was ordered at all: if a pipe has been blocked for a long time, is the muscle behind it still worth reopening it for?

Your report may put this as viable or non-viable, as hibernating myocardium, or simply by giving the transmural extent of the enhancement — how much of the wall’s thickness is scar.

Here is how I explain it in clinic. Think of a tree.

A tree that has shed all its leaves and dried up completely is dead. However much water you give it, however much fertiliser, it will not come back, because there is nothing alive left inside to respond. That is non-viable muscle — scar. Restoring the blood supply to it gives nothing back, because there is nothing there to recover.

But there is a second kind of tree. It has no leaves either. It looks just as bare — only dry branches and a stem. Yet inside, it is still alive. Water that tree and it will come back. That is hibernating myocardium: muscle that has been so short of supply for so long that it has stopped contracting to survive, but has not died. Reopen its pipe and it can begin working again.

This is the one thing an echo cannot tell you. An echo sees a wall that is not moving. It cannot tell you whether that wall is a dead tree or a sleeping one — and the treatment is completely different.

How the scan answers it

By the thickness of the scar through the wall. The heart wall dies from the inside out, so a short interruption of supply scars only the inner layer, while a long one goes all the way through.

The original work behind this scanned people before their arteries were reopened and then measured whether each piece of wall started moving again afterwards. The result was a clean gradient with no cut-off in it: the more of the wall’s thickness was scar beforehand, the less likely it was to recover. Wall with no scar at all mostly came back. Wall that was scar nearly all the way through almost never did.

So a wall with a thin rim of inner-layer scar and good muscle above it is a tree with sap in it. A wall enhancing through its full thickness is firewood.

What the trials actually showed — and it is not what you would expect

The idea was reasonable: scan first, find the sleeping trees, and reopen only those pipes. It was tested properly, and it did not hold up.

In the STICH trial, people with a weak heart were assigned at random to bypass surgery plus medicines, or medicines alone, and in a large group of them viability was measured beforehand. People with viable muscle did live longer — but that difference faded once other differences between them were taken into account, and, critically, viability did not identify who gained more from the surgery. Bypass helped about equally whichever answer the viability test had given. Following the same patients for ten years found exactly the same thing.

REVIVED-BCIS2 then asked the question of stents rather than surgery, and enrolled only people who already had demonstrable viability. Over about three and a half years, stenting made no difference to death or admission with heart failure compared with medicines alone. Most of those viability assessments were done by cardiac MRI, so this is not a case of the wrong test being blamed.

And yet bypass surgery itself does help this group. Ten years on, fewer of the operated patients had died than of those treated with medicines alone. The honest summary is that bypass helps people with a weak heart and extensive disease, but a viability scan is not what tells you which of them it will help.

One thing worth knowing about that survival benefit: it was not there at five years. It appeared only with longer follow-up — which is its own lesson about how long a decision of this kind takes to show its worth, and why a five-year result is not the last word.

Guidelines have followed the evidence rather than the idea: bypass carries a strong recommendation in this group on the strength of that ten-year result, while viability imaging sits at the level of may be considered — a piece of information, not a gatekeeper.

One finding from REVIVED-BCIS2 does survive, and it is the one this whole page has been building towards: the amount of scar predicted how people did regardless of which treatment they had. Scar burden is a measure of how much heart has already been lost. That is worth knowing whatever is decided next.

Oedema — is it still active

Oedema means swelling in the muscle, and it is reported from a different set of images (you may see T2 on the report).

The distinction it draws is between now and then. Scar without swelling is an old, settled injury. Scar with swelling around it suggests the process is still active — a myocarditis that has not finished, or sarcoidosis still inflaming the muscle.

That distinction decides the treatment, which is why it earns its own images. An old scar is managed; an active inflammation may be treatable. Putty that has already set cannot be undone, but muscle that is still being damaged can sometimes be protected from further damage — and that is a different conversation with a different urgency. If the swelling is what brought you here, your cardiologist may also ask again about the weeks before your symptoms began, because a viral illness some time earlier is a common opening to this story.

Thickened muscle — and whether it is still muscle

Where the walls are thick, a cardiac MRI answers two questions an echo struggles with.

First, where exactly. Hypertrophic cardiomyopathy is not one shape. It may involve the base of the septum, or it may be apical — confined to the tip of the left ventricle, which is the area an echo most often misses or underestimates. Naming the pattern changes what your cardiologist watches for and what they plan — and it explains a frustrating experience some people have had, of symptoms that were real and echoes that kept coming back normal.

Second, and more important: is the thickened part still good muscle? This is the distinction that runs through the whole scan.

Infiltration — when something is being deposited

Some conditions do not damage the muscle so much as fill it with something that does not belong. The two looked for most often are:

  • Amyloidosis — an abnormal protein deposited throughout the muscle. It produces a characteristic look on the scan: widespread enhancement across the inner layer of both ventricles, and muscle that behaves abnormally when the radiologist tries to darken it in the usual way.
  • Sarcoidosis — patches of inflammatory tissue scattered through the wall, classically including the base of the septum, often with a patchy distribution that follows no artery’s territory.

Both are worth naming precisely because they are treated quite differently from a heart weakened by blocked arteries, and neither can be identified from an echo alone.

Would you have known? Almost certainly not, and that is the honest answer rather than an evasion. These conditions produce breathlessness, tiredness and swollen ankles — the same things a heart weakened by any other cause produces. Nothing about the way they feel tells them apart from anything else, which is precisely why the question gets settled by a scan of what the wall is made of rather than by asking you more questions.

Clot at the apex

A cardiac MRI is also very good at answering a specific question: is there a clot sitting in the tip of the left ventricle?

When a heart pumps weakly, blood at the apex moves sluggishly, and slow-moving blood can clot. The concern is that a piece breaks off and travels — most seriously to the brain. A clot can be hard to see on an echo, especially at the apex, and the contrast images on an MRI show it clearly because a clot takes up no dye at all: it appears as a dark mass against a bright cavity.

The report may be answering one of two questions: is a clot there, or — after months on blood-thinning medicine — has it gone? A repeat scan to confirm the clot has dissolved is a normal, planned part of treatment, not a sign that anything is wrong.

Volumes and ejection fraction

You will also find the familiar numbers: end-diastolic and end-systolic volumes, ejection fraction, and muscle mass — for both the left and the right ventricle.

Cardiac MRI is regarded as the reference standard for these, because it measures the chambers directly rather than estimating them from a handful of views. So do not be alarmed if the MRI’s ejection fraction differs by a few points from your echo’s. It is not that one machine was wrong; they are different methods, and the MRI is generally the more precise of the two. What your doctor follows is the trend measured the same way.

The impression

The last lines are the conclusion — the radiologist’s summary of what mattered. Read it first, then use the detail above it as the evidence behind it.

Two honest cautions, the same as for any report. It is written for the doctor who requested the scan, in their shorthand. And it describes this scan alone — not your symptoms, your history, your other tests or your treatment, all of which change what it means.

What happens next

A cardiac MRI is usually a scan that settles a question rather than opening one. Once your cardiologist knows whether the muscle is scarred, inflamed, infiltrated or simply thickened, the plan generally follows from that answer.

Depending on what was found, that might mean starting or changing heart-protective medicines, treating an active inflammation, investigating an infiltrative disease properly, starting blood thinners for a clot with a repeat scan planned, discussing rhythm risk and whether anything should be done to protect against it, or — where a pipe is blocked and the muscle behind it is still alive — a conversation about whether reopening it is worth doing.

Common questions

My report says late gadolinium enhancement is present. Does that mean I had a heart attack?

Not necessarily. Late gadolinium enhancement means part of the muscle is no longer normal working muscle, but where it sits tells you what caused it. Enhancement in the inner layer of the wall, following the territory of one artery, points to an old heart attack. Enhancement in the middle of the wall, or patchy and not following any artery, points to something else entirely — an old inflammation, a genetic muscle disease, or an infiltrative condition. The pattern is the diagnosis, not the presence.

What does scar burden or percentage mean on a cardiac MRI report?

It is how much of the heart muscle is scar rather than working muscle, given as a percentage of the left ventricle. It matters because scar does not conduct electricity the way muscle does, so a larger burden carries a higher risk of dangerous rhythms. It is one input into a risk assessment, not a verdict on its own, and your cardiologist reads it alongside your symptoms, your family history and everything else on the scan.

Why was a cardiac MRI ordered when I already had an echo?

An echo shows the shape of the rooms and how the walls move. A cardiac MRI shows what the wall is actually made of — working muscle, scar, swelling, or an abnormal substance deposited in it. When the question has moved from how well is it pumping to why is it not pumping, only the MRI answers it.

My report says the muscle is viable. Does that mean I need a stent or bypass?

Not on its own. Viable means the muscle is still alive and could work again if its blood supply were restored — it does not by itself mean that reopening the artery will make you live longer or feel better. That surprised everybody: large trials that scanned for viability first found it did not identify who benefits from having the artery opened. Bypass surgery does help people with a weak heart and extensive disease, but the decision rests on the whole picture — your symptoms, which arteries are involved, your heart function and your own preferences — not on the viability line alone.

What does non-viable mean on a cardiac MRI report?

It means that part of the muscle is scar rather than living muscle, so restoring blood flow to it would not bring movement back. Think of a tree that has dried out completely: no amount of water will revive it, because nothing living is left inside. A wall that enhances through its full thickness is in that state. A wall with only a thin rim of inner-layer scar still has living muscle above it, and that muscle can recover.

What is hibernating myocardium?

It is heart muscle that has been short of blood for so long that it has shut down to survive, but has not died — like a tree that has lost every leaf and looks dead, yet is still alive inside and comes back when it is watered. On an echo it looks the same as scar, because neither is moving. Telling the two apart is one of the things a cardiac MRI is for.

Does scar on the MRI mean I definitely need a defibrillator?

No. Scar burden is one factor among several in a risk assessment, and the decision is made for you as an individual — weighing the amount and location of scar, your rhythm, your symptoms, your family history and your own preferences. It is a conversation to have with your cardiologist and your family, not something a percentage decides by itself.

Can the clot in my heart go away?

Often, yes. A clot at the apex of the left ventricle is usually treated with blood-thinning medicines, and a repeat scan some months later is done specifically to see whether it has dissolved. That follow-up scan is a common and expected part of the plan, not a sign that something has gone wrong.

Is the gadolinium dye safe?

For most people it is well tolerated, and your kidney function is generally checked before it is given because the dye is cleared by the kidneys. Tell the radiology team about any kidney problems, allergies, previous reaction to contrast, or the possibility of pregnancy, and tell them about any pacemaker, defibrillator or other implant well before the appointment — those need checking for MRI compatibility.

Who actually does the scan, and who explains the result?

The scan is done in the radiology department, and a radiologist reports the images. Your cardiologist ordered it with a specific question in mind and reads the report in the context of everything else they know about you — which is why the person who explains what it means for you is your cardiologist, not the report itself.

References

  1. Arbelo E et al. 2023 ESC Guidelines for the management of cardiomyopathies, Eur Heart J 2023 — when cardiac MRI is indicated, and what LGE contributes
  2. Ommen SR et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR Guideline for the Management of Hypertrophic Cardiomyopathy, Circulation 2024 — extensive LGE as a risk marker
  3. Quantitative Late Gadolinium Enhancement Cardiac Magnetic Resonance and Sudden Death in Hypertrophic Cardiomyopathy: A Meta-Analysis, JACC Cardiovasc Imaging 2024 — risk rises continuously with scar burden
  4. Assessment of late gadolinium enhancement in hypertrophic cardiomyopathy improves risk stratification based on current guidelines, Eur Heart J 2023 — outcomes across the under-5%, 5–15% and over-15% bands
  5. 2019 HRS expert consensus statement on evaluation, risk stratification, and management of arrhythmias associated with cardiac sarcoidosis, Heart Rhythm 2019
  6. Kim RJ et al. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction, N Engl J Med 2000 — transmural extent predicts recovery: segments with no enhancement improved in 78% of cases, those with more than three-quarters wall-thickness scar in 1 of 58
  7. Bonow RO et al. Myocardial viability and survival in ischemic left ventricular dysfunction, N Engl J Med 2011 — the STICH viability substudy, 601 patients: viability did not identify who gained more from surgery
  8. Panza JA et al. Myocardial viability and long-term outcomes in ischemic cardiomyopathy, N Engl J Med 2019 — the same question at ten years, with the same answer
  9. Velazquez EJ et al. Coronary-artery bypass surgery in patients with ischemic cardiomyopathy, N Engl J Med 2016 — STICH at ten years: 58.9% of surgical patients had died against 66.1% on medicines alone, about one death prevented per fourteen operated; the difference was not statistically significant at five years
  10. Perera D et al. Percutaneous revascularization for ischemic left ventricular dysfunction, N Engl J Med 2022 — REVIVED-BCIS2, 700 patients with demonstrable viability: death or heart-failure admission in 37.2% after stenting against 38.0% on medicines alone; about 70% of viability assessments were by cardiac MRI
  11. Viability and outcomes with revascularization or medical therapy in ischemic ventricular dysfunction, JAMA Cardiol 2023 — the prespecified viability analysis of REVIVED-BCIS2: scar burden predicted outcome regardless of which treatment was given
  12. ASNC/AHA/ASE/EANM/HFSA/ISA/SCMR/SNMMI expert consensus recommendations for multimodality imaging in cardiac amyloidosis, J Nucl Cardiol 2021

Written and medically reviewed by Dr Kunal Ajay Patankar, MBBS, MD (Medicine), DrNB (Cardiology) — interventional cardiologist, Mumbai, India.

First published
4 August 2026
Last medical review
4 August 2026

Reviewed against the guidelines cited below. Found an error?drkunalpatankar@gmail.com— corrections are made promptly. How this site is reviewed.