Cardiac magnetic resonance (CMR) is the non-invasive reference method for characterising myocardial tissue in cardiomyopathies. The 2023 ESC cardiomyopathies guideline gives it a Class I recommendation with Level of Evidence B when cardiomyopathy is first suspected, so that unexplained ventricular dysfunction meets tissue imaging early rather than after everything else is exhausted. Alongside tissue detail, CMR supplies the standardised reference for biventricular size, function, and mass — more reproducible than echocardiography.
Why tissue detail changes the workup
Echocardiography shows wall thickness, systolic function, and filling pressures, but it cannot say what the wall is made of. Before tissue imaging became routine, around 2006, dysfunction with normal coronaries often stopped at a dead-end label. CMR looks into the microstructure instead: fibrosis, infiltration, storage, and oedema each leave a different combined signature, so the scan narrows the differential rather than merely confirming that dysfunction exists.
The core sequences
Five measurements build the tissue picture: cine imaging gives the shape and function of the ventricle, and the remaining four probe what the wall is made of — native T1, T2, late gadolinium enhancement, and extracellular volume.
Cine imaging
Steady-state free precession cine loops show the cardiac cycle in any plane and measure volumes, ejection fraction, wall thickness, and mass. In cardiomyopathy work, cine establishes the morphological phenotype: dilated, hypertrophic, or restricted.
T1 mapping
T1 mapping measures the longitudinal relaxation time of the tissue — how long magnetised tissue takes to return to its resting state — without contrast, assigning every pixel a value in milliseconds on a colour-coded map; a typical range is roughly 400–1200 ms.
- Raised native T1 is sensitive but not specific. It says something is wrong with the tissue without naming the cause — fibrosis, oedema, and amyloid infiltration all raise it.
- Lowered native T1 is more specific and narrows the differential considerably. In practice the main cause is intracellular storage, such as the glycosphingolipid accumulation of Fabry disease.
T2 mapping
T2 mapping measures the transversal relaxation time and is specific for myocardial oedema — free water or water bound to large molecules such as collagen. Oedema signals an active process. Extensive oedema across segments argues for active inflammation, while severe dysfunction with almost no oedema argues for chronic, already-established damage.
Late gadolinium enhancement
After gadolinium contrast and a wait of about 10 minutes, damaged myocardium retains contrast and appears grey or white while normal myocardium appears black.
- Ischaemic pattern follows a coronary territory, typically subendocardial or transmural, reflecting the wavefront of necrosis spreading outward from the endocardium after occlusion.
- Non-ischaemic pattern ignores coronary territories: midmyocardial bands, subepicardial patches, circumferential subendocardial involvement, or focal scar at the right ventricular insertion points.
Extracellular volume
Extracellular volume (ECV) quantifies the fraction of myocardium that is extracellular space — matrix, collagen, vessels — calculated from native T1, post-contrast T1, and the haematocrit. A normal ECV sits below 30%, meaning cells compose roughly 70% of the tissue. Raised ECV marks extracellular expansion from fibrosis, amyloid deposition, or inflammation. The distribution matters as much as the number: diffuse elevation in every segment means something different from elevation confined to scarred segments.
Reading the pattern together
No single sequence diagnoses; the combination does. Three patterns recur, each pointing toward a different disease.
| Pattern | Native T1 | Oedema (T2) | ECV | Enhancement | Points toward |
|---|---|---|---|---|---|
| Diffuse high | Raised everywhere | Variable | Raised diffusely | Circumferential subendocardial, transmural when advanced | Cardiac amyloidosis |
| Diffuse low | Lowered everywhere | Minimal | Raised only where scar sits | Midmyocardial band, segmental | Fabry disease |
| Focal high | Raised in patches | Usually quiet | Raised focally | Insertion points and patchy scar in thickened segments | Fibrosis of hypertrophic cardiomyopathy |
One test, repeated over time
CMR also follows disease along its continuum. In storage disease the sequence runs from intracellular storage to cellular oedema to cell death with fibrosis to progressive systolic decline, with early oedema spatially matching where scar later appears. Because mapping quantifies tissue rather than merely picturing it, serial T1 and ECV track response to therapy: improvement on treatment predicts a better course than worsening, a relationship reported from the National Amyloidosis Centre in London in JAMA Cardiology.
The focal pattern in the table raises the next question: what disease thickens the wall and scars it in patches. In hypertrophic cardiomyopathy the answer lies in the sarcomere, the contractile unit of the muscle cell.