Cardiac defects were present in three-quarters of our patients. Pulmonary arterial lesions generally improved, while supravalvar aortic stenosis often progressed. Atypical cardiac malformations, particularly ventricular septal defects, occurred frequently. Systemic hypertension was found in one-fifth, even in the absence of structural cardiac defects. The short-term mortality was low.

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Computed tomography (CT) has a well-established diagnostic role in the assessment of coronary arteries in adults. However, its application in a pediatric setting is still limited and often impaired by several technical issues, such as high heart rates, poor patient cooperation, and radiation dose exposure. Nonetheless, CT is becoming crucial in the non-invasive approach of children affected by coronary abnormalities and congenital heart disease. In some circumstances, CT might be preferred to other noninvasive techniques such as echocardiography and magnetic resonance imaging for its lack of acoustic window influence, shorter acquisition time, and high spatial resolution. The introduction of dual source computed tomography (DSCT) has expanded the role of CT in the evaluation of pediatric cardiovascular anatomy and pathology. Furthermore, technical advances in the optimization of low-dose protocols represent an attractive innovation. DSCT can play a key role in several clinical settings in children, namely in the evaluation of patients with suspected congenital coronary artery anomalies, both isolated and in association with congenital heart disease. Moreover, it is able to assess acquired coronary artery abnormalities, as in patients with Kawasaki disease and after surgical manipulation, especially in case of transposition of the great arteries treated with arterial switch operation and in case of coronary reimplantation.

A 64 year old man presented with a traumatic ventricular septal defect following blunt chest trauma 40 years before. Echocardiography and left ventriculography were helpful in locating the unusual septal defect, which was subpulmonary. The shunt was small, but the anomalous chronic overload led to right ventricular failure. The surgical correction was thus too late to improve right ventricular function. (Heart 2001;86:e6)