[Children with cardiovascular disorders].
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Biomedical subjects
Publications and source records attributed to C Bruins.
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The family of juxtaductal coarctation includes pseudocoarctation, local stenosis and hypoplasia, atresia or interruption of aortic arch or isthmus. The cause is usually VSD with LV outflow obstruction. Abnormal length of the preductal aorta is characteristic. VSD closure makes infantile hypoplasia evolve into adult stenosis, sometimes before birth. Normal subclavian 'migration' is interrupted in 2 out of 3 cases. So-called typical coarctation is either stenosis of the isthmic orifice or the isthmus in toto. Ductus wall tissue radiates too far into the descending aortic wall. Juxtaductal coarctation is displaced from a pre- into a postductal position by flow and secondary tissue formation. A straddling ductus does not straddle the stenosis but a circular fold in the descending aortic wall, caused by ductus tissue. Patent ductus arteriosus is too frequent a complication, prolonged as well as persistent. Ductus closure causes loss of femoral pulse pressure in different ways. Infantile hypoplasia is treated by promoting its development into adult stenosis, then resection.
A case of tricuspid atresia by sealing of the valves, associated with an intact ventricular septum, a hypoplastic right ventricle and the absence of the pulmonary valve, is described. The foramen ovale and the ductus arteriosus were widely patent but there was no interventricular communication. The pulmonary flow was assured by the ductus which had a saccular continuation in the pulmonary trunk. It is postulated that the lesions probably occurred during the period between the XIX and XXII horizons and that the malformed right coronary artery may have played an important role in producing the lesions of the right ventricle.
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