Abstract
Left ventricular noncompaction (LVNC) is a distinct type of non-classified cardiomyopathy1-3 that features a number of specific echocardiographic features, such as thickening of both myocardial layers with prominent trabeculations4. It may occur in isolation or associated with several heart defects or neuromuscular diseases5. Normal myocardial compaction usually starts in the embryonic period (between six and eight weeks), continuing during the fetal period, between 12 and 18 weeks of gestation, developing from the epicardium to the endocardium and from the base to the apex of the heart2. Chin et al.6 postulated that the interruption of the normal process of myocardial compaction during endomyocardial morphogenesis would be the pathophysiological basis of LVNC6. However, the possibility of the existence of acquired forms of LVNC1 has been recently proposed.
Highlights
Left ventricular noncompaction (LVNC) is a distinct type of non-classified cardiomyopathy[1,2,3] that features a number of specific echocardiographic features, such as thickening of both myocardial layers with prominent trabeculations[4]
The prevalence of isolated LVNC was 3.0% in a clinical study conducted in a heart failure healthcare service[8]
Retrospective study included adult patients diagnosed with LVNC admitted for heart failure (HF) consultation from January 2006 to February 2014 in Hospital Central, a reference for the northern region of Portugal
Summary
Left ventricular noncompaction (LVNC) is a distinct type of non-classified cardiomyopathy[1,2,3] that features a number of specific echocardiographic features, such as thickening of both myocardial layers with prominent trabeculations[4]. It may occur in isolation or associated with several heart defects or neuromuscular diseases[5]. Objectives: To define the clinical characteristics, complications and survival of patients with LVNC assisted in heart failure (HF) healthcare service. It is a small group of patients with short follow-up time
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