The three-vessel view is a transverse view of the fetal upper mediastinum is as simple to obtain as the four-chamber view. It demonstrates the main pulmonary artery, ascending aorta and superior vena cava in cross- or oblique sections. The purposes of this study were to describe the normal anatomy of the three-vessel view and to analyze what anatomical changes would occur in this view when there are lesions of the ventricular outflow tracts and/or great arteries. Sonograms of 29 fetuses with lesions involving the ventricular outflow tracts and/or great arteries were reviewed. Three-vessel views were evaluated in terms of vessel size, number, arrangement and alignment. Twenty-eight of 29 fetuses showed an abnormal three-vessel view that included abnormal vessel size (n = 12), abnormal alignment (n = 8), abnormal arrangement (n = 7) and abnormal vessel number (n = 3). The vessel size was abnormal in obstructive lesions of the right (n = 4) or the left (n = 8) side of the heart. An abnormal alignment was seen in tetralogy of Fallot (n = 6) and double-outlet right ventricle (n = 2) that showed anterior displacement of the aorta. An abnormal arrangement was seen in complete (n = 4) and corrected (n = 1) transposition, double-outlet right ventricle (n = 1) and pulmonary atresia with ventricular septal defect (n = 1). Only two vessels were seen in truncus arteriosus (n = 1). Four vessels were seen in persistent left superior vena cava (n = 2). A fetus with pulmonary atresia and intact ventricular septum showed a normal three-vessel view. In conclusion, most of the lesions involving the ventricular outflow tracts and/or great arteries showed an abnormal three-vessel view.

ABSTRACT:Life expectancy and quality of life for those born with congenital heart disease (CHD) have greatly improved over the past 3 decades. While representing a great advance for these patients, who have been able to move from childhood to successful adult lives in increasing numbers, this development has resulted in an epidemiological shift and a generation of patients who are at risk of developing chronic multisystem disease in adulthood. Noncardiac complications significantly contribute to the morbidity and mortality of adults with CHD. Reduced survival has been documented in patients with CHD with renal dysfunction, restrictive lung disease, anemia, and cirrhosis. Furthermore, as this population ages, atherosclerotic cardiovascular disease and its risk factors are becoming increasingly prevalent. Disorders of psychosocial and cognitive development are key factors affecting the quality of life of these individuals. It is incumbent on physicians who care for patients with CHD to be mindful of the effects that disease of organs other than the heart may have on the well-being of adults with CHD. Further research is needed to understand how these noncardiac complications may affect the long-term outcome in these patients and what modifiable factors can be targeted for preventive intervention.

T HE RECENTLY RECOGNIZED MYOCARDIAL malformation known as ventricular noncompaction is a fascinating disorder, characterized by the presence of an extensive trabeculated myocardial layer reinforcing the luminal aspect of the compact portion of the ventricular wall. Usually described thus far in the left ventricle, it is typically associated with abnormal systolic function, albeit also recorded with restrictive physiology and segmental hypokinesis. 1-5 Seen most frequently in the structurally normal heart, increasing recognition shows that the lesion can also accompany diverse forms of congenital cardiac disease (Figs 1 and 2). 1-10 When seen in the left ventricle, it is currently considered an unclassified form of cardiomyopathy, being neither dilated, hypertrophic, nor restrictive. 2,3,11,12 Although once considered rare, 13-15 it is now being seen with increasing frequency, from the fetus to the adult. 16-29 Diagnosis has now moved from the autopsy table to recognition during life, albeit the debate continues with regard to the features displayed by angiography, echocardiography, computed tomography, and magnetic resonance imaging that permit unequivocal recognition. In this review, we will consider myocardial noncompaction from the stance of comparative vertebrate biology, as well as discussing the genetic, developmental, clinical, and imaging characteristics of patients with noncompaction, seen both in isolation and in the setting of congenital cardiac disease. In the latter setting, we must ask whether noncompaction is a homogeneous process that, in its many clinical and pathological expressions, can be explained on the basis of a developmental abnormality. In this respect, it is of interest to note that, in the evolution of the vertebrates, myocardial noncompaction is advantageous, and indeed necessary, for the circulatory function of some