IJCS | Volume 32, Nº2, May/June 2019

294 Figure 1 - 12-lead electrocardiogram showing ventricular extrasystoles. Nascimento et al. Extrasystoles in non-compacted myocardium Int J Cardiovasc Sci. 2019;32(3)293-296 Case Report of 46%. The 24-hour Holter showed the patient had 33,258 ventricular extrasystoles and one episode of non- sustained ventricular tachycardia. The exercise test results showed sinus rhythm and presence of ventricular bigeminy in the pre-exertion phase, frequent ventricular extrasystoles, with a reduction of arrhythmias with isolated extrasystoles during the exertion. She was submitted to a coronary angiography, which did not show obstructive lesions. The patient started treatment for HF with optimized doses of carvedilol, enalapril and spironolactone. In 2014, she was submitted to an echocardiogram, which showed inferomedial akinesia and mild LV systolic dysfunction. The 24-hour Holter showed a reduction in ventricular ectopies when compared to the initial exam, but still at high incidence (10,583 ectopies). In 2015, the patient’s systolic function normalized, but she still maintained the segmental alteration at the echocardiogram and the high incidence of ventricular ectopies. At that moment, she was submitted to a magnetic resonance imaging (MRI) assessment, which showed an increase in trabeculations in the LV mid- apical portion and a ratio between the non-compacted/ compacted layers of 2.8 (1.4/0, 5 = 2.8) at the end of the diastole (Figures 2). These findings were compatible with the diagnosis of left ventricular non-compaction cardiomyopathy. The last evaluation occurred in 2017, and the patient was in New York Heart Association (NYHA) functional class I, with low-incidence ventricular ectopies and receiving warfarin anticoagulation. Discussion During the embryonic development, the heart consists of a spongy network of muscle fibers and trabeculae, which are separated by recesses that connect the myocardium to the LV cavity. Blood is supplied to the myocardium through the intertrabecular spaces. Between the fifth and eighth weeks of fetal development, the ventricular myocardium undergoes compaction, with the transformation of the intertrabecular spaces into capillaries, and the residual spaces within the trabecular meshwork disappear. The process begins from the epicardium to the endocardium and from the base to the apex of the heart. 2 This trabeculation process is of utmost importance, since it allows a greater surface-to-volume ratio and an increase in muscle mass before coronary arteries are established. 5,6 In the LV non-compacted myocardium, there is a persistence of the trabeculation and deep recesses,