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[Total correction of pseudotruncus arteriosus in infancy (author's transl)].
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[Surgical repair of truncus arteriosus (author's transl)].
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[NO inhalation therapy for post-operative pulmonary hypertensive crisis of the case of truncus arteriosus].
Two-months-old baby underwent complete correction by Barbero-Marcial's procedure for type I truncus arteriosus. Postoperative hemo-dynamics was fairly stable immediately after the operation. However, the acute rise in pulmonary pressure occurred on the 2nd postoperative day. The pulmonary vasodilation therapy with prostaglandin E1 and amrinone had failed. Thirty ppm of inhaled nitric oxide (NO) was started and it resulted in an immediate decrease in pulmonary arterial pressure. Complete weaning from NO was achieved 9 days after surgery by simultaneous administration of PGE1 and amrinone. Although inhalation of NO reduced pulmonary arterial pressure, combination of PGE1 and amrinone with NO inhalation exerted a pulmonary vasodilation and brought the patient to full recovery in this case with pulmonary hypertensive crisis.
[Rastelli's procedure].
In 1969, Rastelli conceived a new technique to repair of transposition of the great arteries in the presence of ventricular septal defect and severe pulmonary stenosis (TGA III), based on the redirection of ventricular outflows. An intracardiac tunnel connected the left ventricle to the aorta and an external valved conduit established continuity between the right ventricle and the pulmonary artery. TGA III and truncus arteriosus are underwent a Rastelli operation. The present report is an analysis of indication, operative technique, early and late results with this procedure. Early deaths were related to unfavourable anatomy, conduit compression and sepsis. Residual VSD and postoperative infection were the main factors contributing to the late deaths. A current Re-Rastelli operation for the problems of extracardiac valved conduit is a good result.
Biventricular repair of conotruncal anomalies associated with aortic arch obstruction: 103 patients.
BACKGROUND: Biventricular repair of conotruncal anomalies associated with aortic arch obstruction is a complex surgical procedure that combines a cardiac repair and a aortic arch reconstruction. METHODS AND RESULTS: From January 1984 to April 1996, such a repair was performed in 103 patients. The conotruncal anomalies included: 15 transpositions of the great arteries (TGAs) with intact ventricular septum, 44 TGAs with ventricular septal defect, 32 double outlet right ventricle with subpulmonary ventricular septal defect, 10 truncus arteriosus, one double outlet left ventricle, and one tetralogy of Fallot. The arch obstruction included 88 coarctation and 15 interrupted aortic arch. One-stage repair has been the favored technique since 1990 and was performed in 58 neonates, including 38 TGAs or double outlet right ventricle and ventricular septal defect, 10 TGAs with intact ventricular septum, and all of the 10 truncus arteriosus. The cardiac repair included 89 arterial switch operations, 2 Kawashima rerouting, 10 truncus arteriosus repairs, and one double-outlet left ventricle repair and one tetralogy of Fallot repair. The aortic arch was reconstructed by direct anastomosis in 85 patients, with a Gore-Tex conduit in three patients and more recently by an ascending aortic patch augmentation in 15 patients. The hospital mortality was 12% (7 of 58) for the one-stage repair and 20% (9 of 45) for the two-stage repair. There were six late deaths. Reoperations or angioplasties were mandatory for 12 right ventricle outflow tract obstructions after arterial switch, involving 10 patients with double outlet right ventricle (P=.02), 10 recurrent arch obstruction, and six miscellaneous lesions. CONCLUSIONS: One-stage biventricular repair of conotruncal anomalies associated with aortic arch obstruction can be achieved in selected patients with an 83% survival rate at 7 years.
Polyhydramnios as a prenatal symptom of the digeorge/velo-cardio-facial syndrome.
Prenatal diagnosis of the DiGeorge/velo-cardio-facial syndrome has become possible since it was recognized that this syndrome is caused by a submicroscopic deletion in chromosome 22q11. In a sporadic patient presenting a conotruncal heart defect and polyhydramnios, the del 22q11 was made prenatally by fluorescence in situ hybridization (FISH) after amniocentesis. Seven additional patients with a del 22q11 were identified, who presented during pregnancy with polyhydramnios. In one of them, unilateral hydronephrosis was present. These findings further add to a growing list of clinical presentations of a del 22q11 and suggest that in patients with polyhydramnios and a conotruncal heart defect or uropathy, fetal karyotyping should be complemented by FISH for a del 22q11.
Early root resorption of maxillary primary first molars in a child with severe congenital heart disease.
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[Pathoanatomical criteria of the common arterial trunk].
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[Congenital isolated unilateral absence of the left pulmonary artery with dextrorotation of the aorta (2 cases)].
In connection with two cases of congenital absence of the left pulmonary artery with dextro-rotation of the aorta, the authors recall the clinical and radiological signs of this rare abnormality, explaining it by the theory of failure in partitioning of the troncus arteriosus. They particularly insist on the normal pulmonary venous return.
Cyanotic heart lesions with increased pulmonary blood flow.
This article examines common cyanotic congenital heart lesions that result in an increase in pulmonary blood flow. These lesions include transposition of the great arteries, truncus arteriosus, total anomalous pulmonary venous connection, tricuspid atresia, and single ventricle. The complications caused by increased pulmonary blood flow are examined. The hemodynamics, presentation, diagnosis, medical management, and surgical treatment of each lesion are discussed. Support and teaching needs of the parents are also addressed.
Pulmonary artery banding for truncus arteriosus in the first year of life.
Results of pulmonary artery banding (PAB) for truncus arteriosus (TA) in infancy are reviewed in 15 children between 1957 and 1974. There were ten hospital and one late deaths (73%). A policy of early correction of severely symptomatic infants with TA was adopted in 1974. Since October, 1974, four infants with TA and one with hemitruncus had a complete correction. Three of these are surviving 22, 17, and 9 months after the operation. Their weight at operation was 4.7, 6.0, and 3.5 kg.
Repair of truncus arteriosus.
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Prenatal detection of truncus arteriosus by ultrasound.
This report describes the echocardiographic findings of truncus arteriosus, right aortic arch, and persistent left superior vena cava draining into the coronary sinus in a 32-week-old fetus, in whom the diagnosis was confirmed by autopsy.
First case of human infection caused by Pasteurella gallinarum causing infective endocarditis in an adolescent 10 years after surgical correction for truncus arteriosus.
OBJECTIVE: To report the first case of human infection (infective endocarditis [IE]) caused by Pasteurella gallinarum and to review the literature regarding IE caused by the genus Pasteurella. SETTING: University hospital based. PATIENT: An adolescent boy who underwent successful correction for truncus arteriosus 10 years before the present illness. RESULTS: Persistent fever, pallor, and a palpable spleen suggested IE clinically. Echocardiography documented vegetation in the conduit that was used for surgical correction. Blood cultures grew P. gallinarum and confirmed its role as the causative organism for IE in the patient. CONCLUSION: This case illustrates that IE may develop in a child with congenital heart disease several years after surgical intervention using material that is foreign to the body (conduit), and that such a complication may involve unusual pathogens. These observations emphasize the need for careful long-term follow-up of children with congenital heart disease even after successful surgical correction.
Aspergillus ball thrombus occluding a homograft conduit.
Almost total occlusion of an aortic homograft conduit by a ball of Aspergillus terreus was found postmortem in a 6-month-old infant following repair of a type I truncus arteriosus. Signs of pulmonary hypertensive crisis, fever, anaemia, and thrombocytopenia were present. However, blood cultures were persistently negative. A 2-D echocardiogram failed to demonstrate any vegetation. The clinical, pathological, and postmortem findings are described and difficulties in the diagnosis of Aspergillus infection are discussed.
Abnormal systemic venous connection possibly associated with a persistent right umbilical vein; a case report.
BACKGROUND: Abnormal venous connections involving a persistent right umbilical vein are rare. In a minority of cases the liver is entirely bypassed and the condition is associated with multiple congenital malformations. CASE PRESENTATION: The described case illustrates a systemic venous drainage that was severely abnormal in a newborn girl with a truncus arteriosus type II congenital heart defect. Injection of contrast medium through the umbilical vein catheter revealed a very peculiar venous connection that passed anterio-laterally through the right hemithorax before crossing in an oblique fashion towards the superior vena cava. CONCLUSIONS: This venous drainage may be the result of a persistent right umbilical vein connecting with the superior vena cava.
Di George anomaly and velocardiofacial syndrome.
The velocardiofacial syndrome is an autosomal dominant disorder characterized by cleft palate, cardiac anomalies, characteristic facies, and learning disabilities. The Di George anomaly involves developmental defects of the third and fourth pharyngeal pouches, resulting in thymic and parathyroid hypoplasia and cardiac defects. The cases of individuals in two families help substantiate the notion that the Di George anomaly occurs as a feature of the velocardiofacial syndrome. The proband in family 1 was a male infant with persistent hypocalcemia and cardiac defects consisting of truncus arteriosus, atrial septal defect, ventricular septal defect, and abnormal aortic arch vessels. Autopsy revealed absence of thymic and parathyroid tissue, and the Di George anomaly was diagnosed. His father had a submucous cleft palate, T cell dysfunction, and facial features consistent with the velocardiofacial syndrome. This is the third case of male-to-male transmission of velocardiofacial syndrome. The proband of family 2 was a 4-year-old girl with developmental delay, persistent neonatal hypocalcemia, ventricular septal defect, T cell dysfunction, and facial features of the velocardiofacial syndrome. The Di George anomaly has been reported to occur in at least 18 different disorders. The observation that the Di George anomaly is a component manifestation of the velocardiofacial syndrome in these two families provides further evidence that the Di George anomaly is not a distinct syndrome of a single origin but rather a heterogeneous developmental field defect. It is proposed that all previously reported cases of autosomal dominant Di George anomaly are examples of the velocardiofacial syndrome.