Abstract
A wide spectrum of cardiac arrhythmias has been observed in patients with isolated ventricular non-compaction, which is defined by hypertrabeculated ventricular myocardium with deep intertrabecular recesses, in the absence of concomitant congenital heart disease. In this genetically diverse phenotype, the development of fibrosis contributes to an arrhythmogenic substrate underlying atrioventricular conduction diseases, supraventricular tachycardias and ventricular tachycardias. Within this spectrum, monomorphic ventricular tachycardia is the most frequently observed arrhythmia, and this prevalence has important implications for sudden cardiac death risk.
Highlights
Isolated left ventricular non-compaction (LVNC) is a cardiomyopathy defined by hypertrabeculation of the ventricular myocardium, and was first described in 1990.1 The clinical course of this cardiomyopathy often includes the development of systolic dysfunction with heart failure symptoms, mural thrombosis and systemic embolism, and cardiac arrhythmias
Cardiac arrhythmias most likely result from the development of fibrosis in non-compacted myocardium, with the occurrence of the development of conduction delays and reentrant circuits at the border zones of fibrosis and normal myocardium
Arrhythmic manifestations can range from conduction disease to supraventricular tachycardia (SVT) and ventricular arrhythmias
Summary
Isolated left ventricular non-compaction (LVNC) is a cardiomyopathy defined by hypertrabeculation of the ventricular myocardium, and was first described in 1990.1 The clinical course of this cardiomyopathy often includes the development of systolic dysfunction with heart failure symptoms, mural thrombosis and systemic embolism, and cardiac arrhythmias. A wide spectrum of cardiac arrhythmias has been described in case reports and series, which are discussed in this article
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