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Radiology · Chest Radiology

Diagnostic imaging of cardiomyopathies

Cardiomyopathia

Modern diagnostic imaging plays a crucial role in verifying cardiomyopathies and differentiating them from other cardiac disorders. Computed tomography and magnetic resonance imaging tools not only allow for the assessment of anatomy and contractile function, but also enable the determination of myocardial tissue characteristics.

Advantages of CTAbility to reliably rule out coronary artery disease
Tissue assessmentMRI allows differentiation between amyloidosis, sarcoidosis, and Fabry disease
Pericardial thicknessA value ≥ 4 mm is a predictor of pericardial constriction
T2* mappingCritically important for assessing myocardial iron overload in thalassemia
5 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Capabilities of CT and MRI

Computed tomography (CT) is widely used for the precise assessment of cardiac chamber volumes and ejection fraction (ejection fraction). A major advantage of this method is its ability to non-invasively rule out atherosclerotic lesions of the coronary bed, which is critically important for distinguishing between ischemic and non-ischemic myocardial pathologies. Furthermore, CT demonstrates high accuracy in detecting left ventricular intracavitary thrombi. The main disadvantage of the method compared to MRI is its lower contrast resolution, making the late gadolinium enhancement (late enhancement) technique less informative.

Magnetic resonance imaging (MRI) readily detects morphological and functional anomalies. T1- and T2-weighted images provide reliable tissue characterization, while non-contrast techniques and late gadolinium enhancement assist in the differential diagnosis of amyloidosis, sarcoidosis, and Anderson-Fabry disease. Parametric mapping methods hold great promise in this field.

Restrictive phenotype: etiology and diagnostics

The restrictive phenotype is based on increased wall stiffness (wall stiffness). Consequently, chamber pressures rise rapidly even with a minimal increase in blood volume. Diastolic and systolic volumes, as well as ventricular wall thickness, generally remain within normal limits.

The disease is very rarely familial (with autosomal dominant inheritance). More frequently, the cause is systemic processes: amyloidosis, sarcoidosis, hemochromatosis, carcinoid heart disease, anthracycline toxicity, as well as endomyocardial fibrosis (including Loeffler syndrome with hypereosinophilia) and endocardial fibroelastosis.

Instrumental findings:

  • Radiography: unremarkable for a long time. In late stages, the left atrium enlarges and signs of pulmonary venous hypertension appear (presenting a picture resembling mitral stenosis).
  • Echocardiography: normally sized ventricles combined with dilated atria. In Loeffler syndrome or carcinoid syndrome, marked endocardial thickening, a thrombotic layer, calcification, and thickening of the mitral valve leaflets are visible. Mitral inflow dopplerography plays a key role (increased early diastolic velocity, short deceleration time).
  • Cine MRI: visualizes the characteristic "tubular" shape of the ventricles against the background of a marked enlargement of the atria.
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Specific MRI patterns

The MRI picture directly depends on the stage of the pathological process:

  1. Acute phase: T2-weighted images reveal focal signal hyperintensity reflecting inflammatory edema. With gadolinium enhancement (LGE), intramyocardial, subepicardial, or epicardial foci of enhancement are identified.
  2. Chronic stage: characterized by the presence of nodular LGE regions without signs of edema on T2, indicating the formation of fibrosis and scar tissue.

In sarcoidosis, the presence of LGE is an excellent predictor of risk, but it may "miss" early stages of the disease. This is where T2 mapping comes to the aid, revealing active granulomatous inflammation prior to scar formation. Such a condition is potentially reversible with appropriate treatment.

Particular attention should be paid to the assessment of iron overload (e.g., in major thalassemia). For this purpose, the T2* parameter is used — the transverse relaxation time in a gradient echo sequence. The myocardial signal intensity fades rapidly as the echo time increases. Quantitative T2* assessment allows for the modulation of chelation therapy, which reliably reduces mortality from heart failure.

Restrictive cardiomyopathy or constrictive pericarditis?

A clinical and dopplerographic picture similar to restriction can be produced by constrictive pericarditis, in which a rigid pericardium impedes chamber filling. Ultrasound performs poorly in visualizing the pericardium, thus CT or MRI is required for differentiation.

The key criterion is pericardial thickness. A value of 4 mm or more has high prognostic value for constriction, although the process can occur without marked leaflet thickening. The kinetics of the interventricular septum and inferior vena cava blood flow during inspiration and expiration are also evaluated. MRI may show incomplete blood signal suppression in the right atrium due to slowed flow (slow flow). However, CT has a major advantage over MRI in this situation — it allows reliable visualization of pericardial calcification.

Briefly: answers to topical questions

What late gadolinium enhancement (LGE) pattern is characteristic of cardiac amyloidosis?

Cardiac amyloidosis is characterized by a specific pattern of late gadolinium enhancement. In AL amyloidosis, a global subendocardial distribution is more commonly observed. In ATTR amyloidosis, failure to null the myocardial signal at any given inversion time is frequently noted. Additionally, late enhancement images reveal diffuse subendocardial late enhancement visualized in both the left and right ventricles, as well as a lack of myocardial signal suppression due to interstitial amyloid deposition.

Which dopplerographic parameters indicate a restrictive type of mitral inflow?

Mitral inflow dopplerography in the restrictive phenotype is a key diagnostic method. It shows an increased early diastolic velocity, a short deceleration time, and a low or shortened atrial velocity. An early-to-late filling peak velocity ratio greater than 1.5 is also indicative of restrictive filling.

What are the main types of cardiomyopathies identified in current classification?

In the current classification of non-familial cardiomyopathies, the following main types are distinguished:

  • Hypertrophic cardiomyopathy (HCM) — includes conditions such as obesity, fatty acid metabolism disorders, and amyloidosis.
  • Dilated cardiomyopathy (DCM) — includes myocarditis, toxic damage, pregnancy, and alcoholic damage.
  • Arrhythmogenic right ventricular cardiomyopathy (ARVC) — includes putative inflammatory factors.
  • Restrictive cardiomyopathy (RCM) — includes amyloidosis, scleroderma, and endomyocardial fibrosis.
  • Unclassified (Unclassified) — includes Takotsubo cardiomyopathy.

Class and exam questions

What is the main limitation of CT compared to MRI in cardiomyopathies?

The late enhancement technique in CT is significantly less informative due to lower tissue contrast resolution.

What changes in mitral inflow are characteristic of the restrictive phenotype?

Increased early diastolic velocity, short deceleration time, and low atrial velocity on dopplerography.

Why is T2 mapping performed in cardiac sarcoidosis?

T2 mapping allows the detection of active granulomatous inflammation at an early stage, even before the formation of an irreversible myocardial scar.

What is the advantage of CT over MRI when constrictive pericarditis is suspected?

Unlike MRI, computed tomography allows clear visualization of pericardial calcification.

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What else to study on this topic

  • Parametric mapping (T1, T2, T2*)
  • Dopplerographic parameters of mitral inflow
  • Systemic diseases leading to restriction (amyloidosis, Fabry disease)
  • MRI semiotics of myocardial iron overload and assessment of chelation therapy

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