A striking pattern seen on cardiac scans has become one of the most debated findings in pediatric cardiology: a left ventricle with unusually prominent muscular ridges and deep recesses, known as trabeculation. For years, the appearance has often been linked to left ventricular noncompaction, or LVNC, a condition associated with impaired heart contraction, rhythm disturbances, blood clots and, in severe cases, heart failure. Yet a review by C.J. McMahon, published in Pediatric Research, argues that the central clinical challenge is no longer simply identifying trabeculation. The more urgent question is determining which children face genuine cardiac risk and which have a harmless anatomical variation.
The left ventricle is the heart’s main pumping chamber. During fetal development, its inner muscle initially forms a loose, sponge-like network. As the heart matures, this tissue generally becomes more compact, creating a dense muscular wall capable of generating pressure and efficiently ejecting blood into the circulation. In some individuals, prominent trabeculation persists. When imaging shows a relatively thin compacted outer layer and a thicker, heavily trabeculated inner layer, clinicians may consider LVNC. The visual impression can be dramatic, especially on echocardiography or cardiac magnetic resonance imaging. But the appearance alone does not necessarily reveal how the heart will function over time.
That distinction is crucial because trabeculation is not exclusive to children with cardiomyopathy. It can appear in healthy hearts, particularly during periods of rapid growth or increased physiological demand. Athletes may develop more prominent ventricular trabeculae, while pregnancy, altered loading conditions and certain congenital heart abnormalities can also influence cardiac structure. In children, the changing dimensions of the heart make fixed imaging thresholds especially difficult to interpret. A ratio between noncompacted and compacted muscle that appears abnormal in one age group may be less meaningful in another. The same scan can therefore generate very different clinical implications depending on symptoms, family history, ventricular performance and the method used to obtain the images.
McMahon’s “beyond trabeculation” perspective reflects a broader shift in medicine from describing a phenotype to estimating prognosis. A phenotype is a visible or measurable trait—in this case, the architecture of the ventricular wall. Prognosis, by contrast, concerns the likelihood of future outcomes, such as declining systolic function, ventricular arrhythmias, thromboembolism or hospitalization for heart failure. The review emphasizes that these are not interchangeable concepts. A child may have marked trabeculation but preserved ejection fraction, normal chamber dimensions and no symptoms. Another child may show less striking trabeculation but have progressive muscle weakness, electrical instability or a genetic form of cardiomyopathy. The image is a starting point, not a complete diagnosis.
Echocardiography remains a central tool because it is widely available, does not use ionizing radiation and can measure cardiac motion in real time. Clinicians assess ventricular size, wall movement, blood flow and ejection fraction, while also looking for the characteristic recesses associated with noncompaction. Cardiac magnetic resonance imaging can provide higher-resolution anatomical information and more reproducible measurements of muscle mass. It can also detect late gadolinium enhancement, a marker that may indicate myocardial fibrosis or scarring. Fibrosis is clinically important because disrupted cardiac tissue can interfere with electrical conduction and may be associated with a higher risk of arrhythmia. However, even advanced imaging must be interpreted in the context of the child’s age, body size, loading conditions and overall clinical picture.
The review’s clinical message is especially relevant because diagnostic labels can have consequences long after the scan is performed. A diagnosis of LVNC may lead to repeated imaging, restrictions on physical activity, genetic testing, medication or concern about sudden cardiac events. In some families, it may trigger screening of relatives and raise difficult questions about inherited disease. Those steps can be appropriate when there is evidence of cardiomyopathy, but an imaging label based only on trabecular appearance may create unnecessary anxiety. Conversely, dismissing the finding as an incidental variant could delay recognition of a progressive disorder. The challenge is to avoid both overdiagnosis and underdiagnosis by combining structural findings with objective evidence of cardiac health.
Genetics provides one part of that broader assessment. Variants in genes involved in sarcomere structure, cytoskeletal organization, mitochondrial energy production and electrical signaling have been associated with cardiomyopathies that may include a noncompacted appearance. Yet genetic results are not always straightforward. Some variants are clearly pathogenic, while others have uncertain significance and cannot reliably predict an individual child’s future. A negative genetic test also does not eliminate the possibility of inherited disease, since current testing cannot identify every relevant biological mechanism. For this reason, genetic counseling and careful interpretation are essential, particularly when several relatives have unexplained heart failure, arrhythmias, fainting or sudden death.
Prognostic evaluation must therefore be multidimensional. Symptoms such as exercise intolerance, breathlessness, chest discomfort, palpitations or fainting deserve attention, but children may not always recognize or report reduced exercise capacity. Clinicians may track ejection fraction, ventricular volumes, diastolic function, electrocardiographic changes and ambulatory rhythm monitoring. Biomarkers can sometimes provide additional information about myocardial stress, while exercise testing may reveal limitations not obvious at rest. The presence of ventricular dysfunction, myocardial fibrosis, sustained arrhythmias or a strong family history may carry greater prognostic weight than the degree of trabeculation itself. Longitudinal follow-up is also important because the pediatric heart changes continuously with growth.
This approach reflects a larger lesson in modern cardiovascular imaging: anatomy is most powerful when integrated with biology and time. A single scan captures the heart at one moment, but pediatric cardiology is often concerned with trajectories. Does ventricular function remain stable? Are chamber dimensions changing appropriately? Is an arrhythmia emerging? Does a child’s clinical status diverge from what the imaging initially suggested? These questions require surveillance strategies tailored to risk rather than identical protocols for every patient with prominent trabeculae. They also highlight the need for standardized imaging criteria, age-aware reference ranges and research that follows children over many years.
The significance of McMahon’s review lies in its attempt to move the conversation away from a visually compelling but incomplete definition of disease. Left ventricular noncompaction should not be treated as a diagnosis determined by texture alone. Instead, it is better understood as a phenotype that may occur in different biological settings, ranging from normal variation to a manifestation of inherited or acquired myocardial disease. For families and clinicians, the most important outcome is not naming an unusual pattern on an image, but identifying whether the heart is functioning normally, whether risk is evolving and what follow-up is justified. In pediatric cardiology, looking beyond trabeculation may ultimately mean replacing a binary label with a more precise, individualized picture of prognosis.
Subject of Research: Pediatric left ventricular noncompaction, trabeculation, cardiac imaging, and prognosis
Article Title: Beyond trabeculation: from phenotype to prognosis in pediatric left ventricular noncompaction
Article References: McMahon, C.J. Beyond trabeculation: from phenotype to prognosis in pediatric left ventricular noncompaction. Pediatr Res (2026). https://doi.org/10.1038/s41390-026-05392-8
Image Credits: AI Generated
