Objective To examine our experience of the detection of a right aortic arch in the fetus over an 8-year period.Methods Between February 1998 and December 2005, all

Assessment of the four chambers of fetal heart early in pregnancy was feasible and allowed the detection of 45% of CHD. Additional parameters of fetal cardiac anatomy during the NT scan may further improve the detection rate providing pregnancy management information early in the first trimester.

Isolated left ventricular non-compaction (LVNC) is a rare disorder, classified as a primary genetic cardiomyopathy by the American Heart Association or as an unclassified cardiomyopathy by the European Society of Cardiology CASE REPORTA 28-year-old primigravida with spontaneous singleton pregnancy was referred at 25 + 4 weeks of gestation because of extreme dilatation of the left ventricle (LV) diagnosed during the anomaly scan. First-trimester nuchal translucency measurement was normal. Detailed cardiac examination performed by a fetal cardiologist revealed biventricular hypokinesia with depressed systolic and diastolic function as a result of the highly dilated LV and flat motion of the intraventricular septum. Heart failure was attributed to the presence of non-compacted LV apical myocardium. An extensive trabeculated layer with multiple deep intratrabecular recesses filled with blood directly from the LV cavity was visualized (Figures 1 and 2).The trabeculae were protruding into the cavity whereas the recesses were extending towards the compacted layer of the ventricular wall. The ratio of non-compacted to compacted myocardium was about 2 (Figure 3).Depressed LV global systolic function with an ejection fraction of 19-20% was present, and a coexisting finding was a single muscular ventricular septal defect extending from the inlet portion to the outlet portion of the septum at the subaortic area. The rest of the cardiac anatomy was normal. After detailed counseling, the couple declined to have an amniocentesis and decided to continue with the pregnancy. The fetus was further assessed at 31 + 3 weeks and at 38 + 4 weeks by echocardiography, showing stable cardiac findings.Because of the fetal cardiac manifestations, both parents were screened by echocardiography and were found to be negative for non-compaction as well as for any other cardiac defects. Furthermore, their siblings were negative for cardiac defects and related metabolic, neuromuscular or chromosomal diseases.A male infant weighing 3640 g was born by uncomplicated vaginal delivery at 39 + 5 weeks, with Apgar scores of 9 and 10 at 1 and 5 min, respectively. No resuscitation was needed, oxygen saturation was 99-100% and the neonate reached 3700 g on the 15 th postnatal day. The neonate received digoxin, furosemide and spironolactone for 5 days postnatally because of an LV ejection fraction of 26%. Response to medication was excellent and the baby remained asymptomatic. The prenatal diagnosis of left ventricular non-compaction (LVNC) was confirmed postnatally and the single muscular ventricular septal defect measured 3 mm. DISCUSSIONLVNC is a congenital defect affecting the structure of the ventricular myocardium and is caused by arrest of the compaction process between the 5 th and 8 th weeks of embryonic life 1 . It involves failure of the gradual compaction of the myocardium fibers, leading to

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