Educational scope notice: This is a study note for medical students, not medical advice, diagnosis, or treatment guidance. Clinical management should follow local protocols and current guidelines.
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 — the teaching material dates that change to roughly the pre-2006 era — 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
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 without contrast, assigning every pixel a value in milliseconds on a colour-coded map; the teaching material describes a typical range of 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.
| 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 |
Exact thresholds and segment-by-segment values belong to the disease notes; this note teaches the logic that connects them.
When echocardiography understates disease
A recurring lesson is the disproportion between a reassuring echocardiogram and severe tissue disease. Mild hypertrophy with preserved ejection fraction on echo can coexist with pancardiac infiltration on mapping. The echocardiogram remains the frontline tool — available, inexpensive, real-time, with Doppler filling pressures and strain — but a mild echo never excludes diffuse tissue disease.
One test, repeated over time
CMR also follows disease along its continuum. In storage disease the teaching 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.
Evidence anchors
- Arbelo E, et al. 2023 ESC Guidelines for the management of cardiomyopathies: https://doi.org/10.1093/eurheartj/ehad194
- Society for Cardiovascular Magnetic Resonance: https://scmr.org/
- Kittleson MM, et al. Cardiac amyloidosis: evolving diagnosis and management (AHA scientific statement): https://www.ahajournals.org/doi/10.1161/CIR.0000000000000792