Prognosis in left ventricular non-compaction is determined primarily by ventricular function, myocardial substrate, and arrhythmic burden rather than by the extent of trabeculation itself.
Prognosis in left ventricular non-compaction is primarily determined by ventricular function and arrhythmic burden rather than the extent of trabeculation.
Left ventricular non-compaction (LVNC) remains one of the most debated phenotypes within the spectrum of cardiomyopathy. Increasing recognition of left ventricular hypertrabeculation (LVHT) in healthy individuals and in physiological adaptive states challenges the concept of LVNC as a distinct morphological entity. In patients with heart failure (HF), distinguishing adaptive trabeculation from true cardiomyopathic LVNC is clinically critical, as misclassification may lead to unnecessary interventions or failure to identify high-risk patients. This review summarizes current evidence on the pathophysiology, imaging features, genetic background, and clinical implications of LVHT and LVNC from an HF-centred perspective. We propose a pragmatic diagnostic approach integrating echocardiography, cardiac magnetic resonance, and selective genetic testing to improve clinical interpretation, risk stratification and management. Importantly, prognosis appears to be determined primarily by ventricular function, myocardial substrate, and arrhythmic burden rather than by the extent of trabeculation itself.
Geavlete et al. (Fri,) conducted a review in Left ventricular non-compaction in heart failure. Left ventricular non-compaction (LVNC) was evaluated. Prognosis in left ventricular non-compaction is determined primarily by ventricular function, myocardial substrate, and arrhythmic burden rather than by the extent of trabeculation itself.
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