Left Ventricular Non-Compaction (LVNC)
This condition is characterized by the formation of prominent trabeculations in the left ventricle and deep intertrabecular recesses (recesses). As a result, the wall segment consists of a thin compacted epicardium and an abnormally thickened endocardial layer. The question of whether LVNC is an independent cardiomyopathy or a common phenotype for other diseases remains open.
Developmental features and genetics:
- Can occur in an isolated form.
- Often associated with muscular dystrophies or congenital heart defects (Ebstein's anomaly, complex cyanotic defects).
- Shows a strong familial pattern: approximately 25% of asymptomatic relatives of the patient exhibit myocardial ultrasound abnormalities.
Imaging diagnostics of LVNC:
- Echocardiography: The primary and often only method in pediatrics. Typical localization of increased trabeculation is the mid-apical (midapical) segments of the lateral wall and interventricular septum (which normally lacks trabeculations).
- Cardiac MRI: Used in complex cases. Cine-MRI (horizontal long axis) is convenient for measuring the layer ratio: the criterion is a non-compacted to compacted myocardium ratio of > 2.3. T1-weighted images (dark-blood technique) clearly demonstrate trabecular thickening.
- Late Gadolinium Enhancement (LGE): Contrast accumulates in the compacted layer at the septal level due to fibrotic changes. Subendocardial sparing (subendocardial sparing) is characteristic.
- T1 mapping: Native T1 values are significantly higher than normal, allowing the detection of fibrosis earlier than on standard LGE. Multiple thrombi are frequently found in the intertrabecular spaces.
Takotsubo Cardiomyopathy
The disease is also known as transient left ventricular apical ballooning syndrome. It is characterized by reversible regional myocardial systolic dysfunction. Functional recovery usually occurs within a few days or weeks.
The typical patient profile is a postmenopausal woman. The onset of the syndrome is usually triggered by severe emotional or physical stress, resulting in a massive release of norepinephrine (norepinephrine).
Clinically, Takotsubo flawlessly mimics acute coronary syndrome (chest pain, ECG changes), yet invasive coronary angiography reveals no hemodynamically significant stenoses. Performing CAG is mandatory according to clinical guidelines to rule out obstructive coronary artery disease.
Differential Diagnosis on MRI
Magnetic resonance imaging is indicated for acute symptoms with clean coronary arteries. Its main goal is to differentiate Takotsubo from acute myocarditis and myocardial infarction with non-obstructive coronary arteries (MINCA).
MRI signs of Takotsubo:
- Functional apical ballooning.
- Diffuse myocardial edema (hyperintensity on T2-weighted scans).
- Absence of late gadolinium enhancement (delayed enhancement), which proves the lack of macroscopic necrosis and the complete reversibility of the process.
To confirm edema in hypokinetic zones, T1 and T2 mapping are used, which offer greater diagnostic accuracy compared to routine T2 STIR sequences.
Differences from other pathologies:
- Acute myocarditis: Characterized by the localization of edema and late gadolinium enhancement in the subepicardial layer (more frequently lateral and inferior walls). If necrosis is absent, early gadolinium enhancement helps detect inflammatory hyperemia.
- Acute myocardial infarction: The area of late gadolinium enhancement always involves the subendocardial layer or is transmural.
For Takotsubo: "Stress — adrenaline — balloon without necrosis" (ACS-like clinical presentation, but CAG is clean, and MRI shows no late enhancement).
Class and exam questions
On angiography in Takotsubo, there is no coronary artery obstruction, and MRI lacks the late gadolinium enhancement pattern characteristic of myocardial necrosis.
On angiography in Takotsubo, there is no coronary artery obstruction, and MRI lacks the late gadolinium enhancement pattern characteristic of myocardial necrosis.
How is the MRI criterion for left ventricular non-compaction (LVNC) calculated?
The ratio of the thickness of the non-compacted layer to the compacted layer is determined in the diastolic phase on cine-MRI. The diagnosis is confirmed if this ratio exceeds 2.3.
Where does the contrast agent accumulate on MRI (LGE) in LVNC?
In the presence of fibrosis, contrast accumulates in the compacted myocardial layer, predominantly in the interventricular septum, while the subendocardium remains spared.
What else to study on this topic
- Pathogenesis and morphological stages of acute myocarditis
- Dallas criteria for endomyocardial biopsy
- The role of T1 and T2 mapping in detecting occult edema and fibrosis
- MRI semiotics of arrhythmogenic right ventricular cardiomyopathy (ARVC)
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