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Background: Previous studies have demonstrated structural changes in the heart and cardiac dysfunction in foetuses with intrauterine growth restriction. There are no available data that evaluated left ventricular dimensions and mass in neonates with symmetric and asymmetric intrauterine growth restriction. Therefore, we aimed to evaluate left ventricular dimensions, systolic functions, and mass in neonates with symmetric and asymmetric intrauterine growth restriction. We also assessed associated maternal risk factors, and compared results with healthy appropriate for gestational age neonates., Methods: In all, 62 asymmetric intrauterine growth restriction neonates, 39 symmetric intrauterine growth restriction neonates, and 50 healthy appropriate for gestational age neonates were evaluated by transthoracic echocardiography., Results: The asymmetric intrauterine growth restriction group had significantly lower left ventricular end-systolic and end-diastolic diameters and posterior wall diameter in systole and diastole than the control group. The symmetric intrauterine growth restriction group had significantly lower left ventricular end-diastolic diameter than the control group. All left ventricular dimensions were lower in the asymmetric intrauterine growth restriction neonates compared with symmetric intrauterine growth restriction neonates (p>0.05), but not statistically significant except left ventricular posterior wall diameter in diastole (3.08±0.83 mm versus 3.54 ±0.72 mm) (p<0.05). Both symmetric and asymmetric intrauterine growth restriction groups had significantly lower relative posterior wall thickness (0.54±0.19 versus 0.48±0.13 versus 0.8±0.12), left ventricular mass (9.8±4.3 g versus 8.9±3.4 g versus 22.2±5.7 g), and left ventricular mass index (63.6±29.1 g/m2 versus 54.5±24.4 g/m2 versus 109±28.8 g/m2) when compared with the control group., Conclusions: Our study has demonstrated that although neonates with both symmetric and asymmetric intrauterine growth restriction had lower left ventricular dimensions, relative posterior wall thickness, left ventricular mass, and mass index when compared with appropriate for gestational age neonates, left ventricular systolic functions were found to be preserved. In our study, low socio-economic level, short maternal stature, and low maternal weight were found to be risk factors to develop intrauterine growth restriction. To our knowledge, our study is the first to evaluate left ventricular dimensions, wall thicknesses, mass, and systolic functions in neonates with intrauterine growth restriction and compare results with respect to asymmetric or symmetric subgroups.

Chiari's network (CN) is an embryologic remnant of eustachian valve located in the right atrium (RA). Incomplete involution of the fetal sinus venosus valves results in ''redundant'' CN. CN has been found in 1.3-4 % of autopsy studies and is believed to be of little clinical consequence. However, a redundant CN may favor persistence of a patent foramen ovale, formation of an atrial septal aneurysm, atrial thrombus, or paradoxic embolism, or cause intense right-to-left shunting. It may also cause arrythmias or compromise cardiovascular functions. We report an asymptomatic newborn with a prominent CN prolapsing into the right ventricle and discuss the clinical consequences of a CN. Although the patient herein presented is asymptomatic, CN may cause persistent cyanosis in the newborns mimicking congenital heart disease. It can also be confused with other curvilinear, highly mobile pathologic structures in the RA, such as vegetation, flail tricuspid leaflet, ruptured chordae tendinae, thrombus, or tumor. CN is not always a benign structure; therefore, identification and accurate diagnosis by echocardiography is important.

Pierre-Robin sequence or syndrome (PRS) (OMIM #261800) is characterized by a small mandible (micrognathia), posterior displacement/retraction of the tongue (glossoptosis), and upper airway obstruction. It has an incidence varying from 1 in 8,500 to 1 in 30,000 births. Congenital heart defects (CHDs) occur in 20 % of the patients with PRS. Ventricular septal defect, patent ductus arteriosus, and atrial septal defects are the most common lesions. Noncompaction of the ventricular myocardium is a rare cardiomyopathy characterized by a pattern of prominent trabecular meshwork and deep intertrabecular recesses. It is thought to be caused by arrest of the normal endomyocardial morphogenesis. Isolated left ventricular noncompaction (LVNC) in patients with PRS has not been reported previously. This report describes a newborn with PRS and isolated LVNC. Previously, LVNC has been reported in association with mitochondrial disorders, Barth syndrome hypertrophic cardiomyopathy, zaspopathy, muscular dystrophy type 1, 1p36 deletion, Turner syndrome, Ohtahara syndrome, distal 5q deletion, mosaic trisomy 22, trisomy 13, DiGeorge syndrome, and 1q43 deletion with decreasing frequency. Karyotype analysis of the reported patient showed normal chromosomes (46, XX), and a fluorescent in situ hybridization study did not show chromosome 22q11.2 deletion. This is the first clinical report of a patient with isolated LVNC and PRS. Noncompaction of the ventricular myocardium is a rare and unique disorder with characteristic morphologic features that can be identified by echocardiography. Long-term follow-up evaluation for development of progressive LV dysfunction and cardiac arrhythmias is indicated for these patients.

Noncompaction of the ventricular myocardium is a rare cardiomyopathy characterized by a pattern of prominent trabecular meshwork and deep intertrabecular recesses. The prevalence of left ventricular noncompaction is 0.01% in adults and 0.14% in pediatric patients. Although the usual site of involvement is the left ventricle, the right ventricle and septum can be affected as well. Previously, right ventricular noncompaction has been described only in a few cases of newborns with congenital heart defects and in adult patients. This report presents a newborn with isolated right ventricular noncompaction. To the authors' knowledge, this is the first newborn patient with isolated right ventricular noncompaction but no congenital heart defect involving only the right ventricle.

Background/aims: No data are available examining the relationship between carotid intima media thickness (IMT) and left ventricular mass (LVM) in obese adolescents with non-alcoholic fatty liver disease (NAFLD). Therefore, we investigated LVM and carotid IMT in obese adolescents with NAFLD., Methods: Eighty obese adolescents and 37 lean subjects were enrolled in the study. The obese subjects were divided into two subgroups based on the presence or absence of fatty liver with high transaminases (NAFLD group and non-NAFLD group). Fasting blood samples were assayed for serum transaminases, glucose and insulin levels. Insulin resistance was calculated by the homeostasis model assessment (HOMA-IR)., Results: LVM measurements were higher in both NAFLD and non-NAFLD obese patients in comparison with the lean children. The NAFLD group had significantly higher LVM measurements than the non-NAFLD and lean groups. Carotid IMT was higher in both the NAFLD and non-NAFLD obese patients in comparison with the lean group. The NAFLD group had significantly higher carotid IMT measurements than the non-NAFLD and lean groups. LVM was positively correlated with HOMA-IR and serum alanine aminotransferase levels in the NAFLD obese group. Carotid IMT was positively correlated with HOMA-IR, serum alanine aminotransferase levels and LVM in the NAFLD obese group., Conclusions: We demonstrated that obese adolescents with NAFLD have increased LVM and carotid IMT and low insulin sensitivity. Obese adolescents with NAFLD and increased carotid IMT may demonstrate a more adverse cardiovascular risk profile and higher LVM. Therefore, assessment of carotid IMT, in addition to echocardiography, may assist in risk stratification in obese adolescents with NAFLD with elevated cardiovascular risk factor levels.