--- title: Left ventricular noncompaction description: What left ventricular noncompaction is, why experts disagree on whether it is a disease or a feature of heart structure, what complications it can cause, how it is detected and which treatment approaches guidelines and reference texts describe. type: disease aliases: - LV noncompaction - LVNC - noncompaction cardiomyopathy - non-compaction cardiomyopathy - spongy myocardium - left ventricular hypertrabeculation sources: - tier: guideline org: minzdrav-rf title: Желудочковые нарушения ритма сердца. Внезапная сердечная смерть year: 2025 doi: 10.15829/1560-4071-2025-6670 url: https://cr.minzdrav.gov.ru/view-cr/569_2 - tier: guideline org: minzdrav-rf title: Дилатационная кардиомиопатия year: 2025 url: https://cr.minzdrav.gov.ru/view-cr/1008_1 - tier: guideline org: esc title: 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death year: 2022 doi: 10.1093/eurheartj/ehac262 url: https://doi.org/10.1093/eurheartj/ehac262 - tier: guideline org: esc title: 2023 ESC Guidelines for the management of cardiomyopathies year: 2023 doi: 10.1093/eurheartj/ehad194 url: https://doi.org/10.1093/eurheartj/ehad194 - tier: guideline org: aha-acc title: 'Clinical Considerations for Competitive Sports Participation for Athletes With Cardiovascular Abnormalities: A Scientific Statement From the American Heart Association and American College of Cardiology' year: 2025 doi: 10.1161/CIR.0000000000001297 url: https://doi.org/10.1161/CIR.0000000000001297 - tier: reference org: msd-manuals title: Non-Compaction Cardiomyopathy year: 2026 url: https://www.msdmanuals.com/professional/cardiovascular-disorders/arrhythmogenic-cardiac-disorders/non-compaction-cardiomyopathy - tier: reference org: statpearls title: Left Ventricular Noncompaction Cardiomyopathy year: 2024 url: https://www.ncbi.nlm.nih.gov/books/NBK537025/ sources_checked: 2026-10-13 review: null --- Noncompaction is a feature of the structure of the ventricular wall: its inner layer is made of many prominent muscle strands (trabeculae) with deep recesses between them, and the outer dense (compact) layer is often thin. The changes are usually found in the left ventricle and less often in the right. Many people with noncompaction have no symptoms at all. Experts still disagree on what to call this finding. The 2025 Russian Ministry of Health guideline calls noncompaction a distinct type of cardiomyopathy, and the 2022 European Society of Cardiology (ESC) guideline on ventricular arrhythmias speaks of a left ventricular noncompaction (LVNC) cardiomyopathy phenotype. The 2025 scientific statement of the American Heart Association and American College of Cardiology (AHA/ACC), by contrast, prefers the term "left ventricular hypertrabeculation" and no longer considers it a distinct cardiomyopathy. The question remains open, and this article uses both names.

The diagram shows a long-axis section of the left ventricle, base at the top and apex at the bottom. Normally most of the wall's thickness is dense (compact) myocardium, and the spongy layer is not thickened. A normal ventricle also has fine muscle strands; the diagram simplifies its inner surface as smooth.

In noncompaction the outer compact layer is thin, and inside it lies a thick spongy layer of prominent trabeculae; the deep recesses between them open into the ventricular cavity. The changes are usually most marked at the apex, then elsewhere in the left ventricle. Blood can pool in the deep recesses. The ventricle in the diagram is the same size as the normal one: the diagram shows only the structure of the wall.

## Why it happens The traditional explanation is that the ventricular wall fails to "compact" in the embryo, so its inner layer keeps a spongy structure. This explanation is now disputed: newer studies suggest that the spongy and compact layers develop independently of each other, so the word "noncompaction" itself may be a misnomer. According to the MSD Manual, the cause is most often inherited: changes in genes that shape the heart muscle cells; there are probably also acquired cases. Noncompaction can occur together with neuromuscular disorders, chromosomal defects and congenital heart defects. Increased trabeculation also occurs in healthy people: in athletes and during pregnancy it is found by chance, it is often reversible and usually does not mean disease. The Russian Ministry of Health guideline defines noncompaction as a distinct type of cardiomyopathy with prominent trabeculation and deep intertrabecular recesses of the left and/or right ventricle, often combined with a thin compact epicardial layer. StatPearls calls the classification of noncompaction as a primary genetic cardiomyopathy somewhat controversial: the same ratio of trabecular to compact tissue is found in some people without cardiomyopathy, and increased trabeculation is seen in pregnancy and in athletes, likely due to increased preload. The mechanism of complications, according to MSD: the disordered myocardial architecture and associated microvascular abnormalities lead to fibrosis, which predisposes to systolic and diastolic heart failure and to ventricular tachyarrhythmias, while the deep intertrabecular recesses produce areas of blood flow stasis that predispose to thromboembolic events, including stroke. ## Symptoms In many people noncompaction causes no symptoms at all. According to the MSD Manual, when there are symptoms they are most often signs of [heart failure](../heart-failure/): breathlessness on exertion, tiredness and swelling. Some people have rhythm and conduction problems: episodes of palpitations, fainting and sometimes cardiac arrest; dangerous ventricular arrhythmias can be triggered by physical exertion. Blood can pool in the deep recesses of the wall, which raises the risk of thromboembolism, including stroke. The Russian Ministry of Health guideline notes that many patients with left ventricular noncompaction are completely asymptomatic, but it can occur together with any type of cardiomyopathy and progress to chronic heart failure, thromboembolism, arrhythmias or sudden cardiac death. MSD also describes, in some forms, [atrial fibrillation](../atrial-fibrillation/), [Wolff-Parkinson-White syndrome](../wpw-syndrome/), conduction system [blocks](../av-block/), an early repolarisation pattern or a [long QT interval](../long-qt-syndrome/) on the ECG, and an association with skeletal muscular dystrophies. According to MSD, patients with a reduced left ventricular ejection fraction or significant myocardial fibrosis have a worse prognosis. ## How it is diagnosed Noncompaction is seen on [heart ultrasound (echocardiography)](../../diagnostic/echocardiography/) and cardiac MRI; according to the MSD Manual, MRI with a contrast agent is more sensitive than ultrasound. Telling the disease apart from a normal variant can be difficult, especially when the left ventricular wall is thickened, in other cardiomyopathies and in pregnancy. Doctors also record an [ECG](../../diagnostic/ecg/) and [monitor the heart rhythm over a longer period](../../diagnostic/holter-monitoring/), and offer genetic testing when there are signs of the condition. According to MSD, first-degree relatives should have a clinical check, an ECG and a heart ultrasound; if a disease-causing gene change has been found in the patient, relatives are offered a genetic test, and those who do not carry the change need no further testing. In the wording of the Russian Ministry of Health guideline, the diagnosis is made on echocardiographic and/or MRI criteria, with a ratio of noncompacted to compact layer thickness > 2. MSD adds that several different consensus criteria have been developed for echocardiography and MRI: they typically use the ratio of noncompacted (trabeculated) to compacted myocardium among other factors, and it is frequently difficult to distinguish the findings from normal variants. The general ESC 2023 recommendations for all patients with suspected or established cardiomyopathy (not specific to noncompaction) include systematic evaluation using a multiparametric approach: clinical evaluation, pedigree analysis, ECG, Holter monitoring, laboratory tests and multimodality imaging (I C); contrast-enhanced cardiac MRI is recommended in patients with cardiomyopathy at initial evaluation (I B). When a pathogenic or likely pathogenic variant has been identified, the ESC recommends offering cascade genetic testing, with pre- and post-test counselling, to adult at-risk relatives (I B). ## How it is treated According to the MSD Manual, treatment targets the manifestations and complications: heart failure, rhythm problems and the risk of blood clots. With hypertrabeculation alone and no signs of disease, physical activity usually does not need to be restricted; restrictions may be needed, for example, when the ventricle works poorly, is enlarged, has a thickened or thinned wall, or when there are ventricular arrhythmias or thromboembolism. The AHA/ACC statement says that athletes with hypertrabeculation who have no symptoms and no pathologic features of cardiomyopathy should be considered unaffected and can continue competitive sport. Heart failure is treated by the usual standards, in severe cases up to a heart transplant. Rhythm problems are treated with antiarrhythmic medicines, including beta-blockers, and some people receive an implantable cardioverter-defibrillator (ICD) to protect against sudden death. Atrial fibrillation, a previous stroke, clots in the wall or reduced ventricular function may call for medicines that lower the risk of blood clots. The doctor decides together with the patient which treatment is needed. ESC 2022 suggests that in patients with an LVNC cardiomyopathy phenotype based on cardiac MRI or echocardiography, implantation of an ICD for primary prevention of sudden cardiac death should be considered following the recommendations for DCM and hypokinetic non-dilated cardiomyopathy (IIa C). In patients with DCM associated with left ventricular noncompaction, the Russian Ministry of Health guideline allows radiofrequency ablation of the arrhythmogenic substrate of ventricular tachycardia to prevent recurrences (no ESC class; Russian grade of recommendation C, level of evidence 4). ## When to call an ambulance Complications of noncompaction can be life-threatening: fainting, ventricular arrhythmias, cardiac arrest and thromboembolism, including stroke. The Russian Ministry of Health guideline advises calling an ambulance if an episode of arrhythmia comes with dizziness, weakness, loss of consciousness or a racing heartbeat. Call your local emergency number (112 in the EU, 911 in the US and Canada, 999 in the UK) for fainting, especially during exertion, and for signs of a stroke. Dangerous ventricular arrhythmias are covered in the article on [ventricular tachycardia](../ventricular-tachycardia/), and cardiac arrest in the article on [ventricular fibrillation](../ventricular-fibrillation/). As with any heart condition, call an ambulance for fainting, chest pain or severe breathlessness: this is the site's general safety rule, repeated at the bottom of every page.