Left ventricular non-compaction associated with hypertrophic cardiomyopathy in the same patient

Abstract

A 19-year-old man was referred for lipothymia, episodes of palpitations, and dyspnoea New York Heart Association class II. He had no previous personal medical history; however, his brother experienced sudden cardiac death at the age of 16 years. The physical examination showed a heart rate of 65 bpm and a blood pressure of 130/70 mm Hg; no signs of heart failure were found. Electrocardiogram (ECG) revealed sinus rhythm, incomplete left bundle branch block, and no ST-T segment abnormalities. Two-dimensional echocardiogram showed a dilated left ventricle (LV) with mild systolic dysfunction (ejection fraction [EF] 42%) and hypertrabeculated LV apex, dilated left atrium (area 27 cm 2

Noncompaction may not only be non-isolated but also myopathic. Commentary to the article: “Left ventricular non-compaction associated with hypertrophic cardiomyopathy in the same patient”

“…We do not agree that LVHT is a genetic disease [1]. Although LVHT is frequently associated with mutations in various genes or chromosomal defects, a causal relation has never been proven.…”

“…With interest we read the article by Laaroussi et al [1] about a 19-year-old male with left ventricular hypertrabeculation/noncompaction (LVHT). We have the following comments and concerns.…”

Left ventricular noncompaction associated with genetic disturbance of folic acid metabolism

“…1 Left ventricular noncompaction can present as isolated abnormality or in combination with other hereditary structural defects such as Ebstein's anomaly, bicuspid aortic valve, coronary arteries abnormalities, and septal defects. 2 MTHFR gene codes MTHFR protein that is responsible for intracellular homocysteine transformation to methionine. This enzyme requires pyridoxine, cyanocobalamin, and folic acid to perform its biological role.…”