Alain Batisse

Video-assisted thoracoscopic surgical interruption: the technique of choice for patent ductus arteriosus. Routine experience in 230 pediatric cases.

Video-assisted thoracoscopic surgical interruption for patient ductus arteriosus is a well-standardized procedure already described. We present our entire series of such cases, from the first case (performed on Sept. 5, 1991) to March 1, 1995. Two hundred thirty patients in a variety of age groups underwent video-assisted interruption: younger than 6 months (70 patients, 30%), 6 to 48 months (123 patients, 54%), and older than 48 months (37 patients, 16%). The mean weight was 12.6 kg (range 1.2 to 65 kg). Thirty-nine patients had symptomatic pulmonary hypertension. Associated intracardiac anomalies included atrial septal defect (three), ventricular septal defect (five), and anomalous pulmonary venous return (one). All patients underwent video-assisted interruption of the patient ductus arteriosus with two titanium clips. Closure was evaluated by postoperative echocardiography before extubation. Five patients had a persistent patent ductus after video-assisted interruption, all early in our experience and related to insufficient dissection resulting in inadequate clip placement. Four patients had successful immediate clip repositioning (three by video-assisted interruption and one by thoracotomy). Subsequent echocardiography revealed persistent closure in these patients. A persistent patent ductus arteriosus with minimal flow was discovered in one patient without symptoms after discharge. Recurrent laryngeal nerve dysfunction was noted in six patients (2.6%, five transient and one persistent). There were no deaths, hemorrhages, transfusions required, or chylothoraces in this series. Mean operative time was 20 +/- 15 minutes, and hospital stay averaged 48 hours for patients younger than 6 months and 72 hours for patients older than 6 months. This is a safe, rapid, cost-effective technique that results in excellent results and a shortened hospital stay. Video-assisted interruption represents the technique of choice for closure of a patient ductus arteriosus.

Video-thoracoscopic surgical interruption of patent ductus arteriosus. Routine experience in 332 pediatric cases.

OBJECTIVE Pediatric video-assisted thoracic surgery closure of patent ductus arteriosus can now be performed on a routine basis. We review here our entire experience with this technique. METHODS Three hundred and thirty two consecutive patients underwent video-assisted closure of patent ductus arteriosus from September 1991 to September 1996. Indications were symptomatic ductus or failure of closure in older children. All complications were carefully noted, as well as intensive care unit stay, and operating room time. RESULTS Patients were divided in three age groups: less than 6 months (101 patients, 31%), 6-48 months (179 patients, 54%), greater than 48 months (52 patients, 16%). The mean weight was 12.6 kg (range 1.2-65 kg). Associated cardiac anomalies were atrial septal defect (3), ventricular septal defect (5), anomalous pulmonary venous return (1). Six patients had a residual shunt following video-assisted interruption. Five patients had successful immediate clip repositioning (three via video-assisted interruption, two via thoracotomy). One patient continued to have a small shunt, which is followed medically. Complications included recurrent laryngeal nerve dysfunction in six patients (1.8%) (five transient, one persistent). Mean operating time was 20 +/- 1.5 mn and hospital stay averaged 48 h (> 6 months), 72 h (< 6 months). CONCLUSIONS Interruption of patent ductus can be safely performed by video-assisted technique with minimal morbidity and no mortality. It can be performed in all age group with minimal hospital stay.

Foetal echocardiographic assessment of tetralogy of Fallot and post-natal outcome

AIMS Outcome of foetuses diagnosed with tetralogy of Fallot (TOF) or pulmonary atresia with ventricular septal defect (PA-VSD) and the reliability of foetal echocardiography to predict post-natal surgical outcome. METHODS AND RESULTS Outcome of 218 foetuses having been diagnosed with TOF (n = 153) or PA-VSD (n = 65) was reviewed. Abnormal karyotyping, 22q11 deletion, and extracardiac anomalies were found, respectively, in 11, 18, and 46%. Pregnancy was terminated in 75 cases (34%), and in three cases foetuses died in utero. Presence or absence and confluence of PA branches were confirmed after birth or pregnancy termination in all but five (5%) cases. Main pulmonary trunk (MPA) was incorrectly described in 11 (10%) cases and major aorto-pulmonary collateral arteries in 16 (13%) cases. Among live born infants, 110 (88%) were operated and 92 (74%) underwent complete repair in the first year of life. Size of confluent PAs and presence of MPA were related to the probability of having a complete repair in the first year of life. CONCLUSION Foetal diagnosis of TOF and PA-VSD has a major impact on pregnancy outcome, as associated anomalies are frequently found. Pre-natally determined size of PA branches and presence of MPA are good predictors of complete repair in the first year of life.

Right superior vena cava draining into the left atrium

The right superior vena cava draining into the left atrium is a rare malformation causing cyanosis and clubbing in patients in whom no other signs of congenital heart defect are present. Diagnosis may be difficult as cyanosis may be mild and the anomaly is not always easily detectable by echocardiography. For this reason we report a 13-month-old male in whom we confirmed the clinical and echocardiographic suspicion of anomalous drainage of the right superior vena cava using multidetector CT. This allowed successful surgical reconnection of the right superior vena cava to the right atrium.

Aortic coarctation, multiple ventricular septal defects, and anomalous coronary artery arising from the right pulmonary artery ☆ ☆☆ ★ ★★

The literature reveals no reports of a left coronary artery arising from the right pulmonary artery in association with aortic coarctation and multiple ventricular septal defects. The patient we describe here died of left myocardial infarction after palliative operation because this defect was unanticipated. Case report. The patient was admitted at the age of 12 days with a diagnosis of aortic coarctation and multiple ventricular septal defects. She had classic signs of aortic coarctation and predominantly left-sided heart failure, which responded partially to prostaglandin E1 and diuretics. Chest radiography revealed severe cardiomegaly and symmetrically plethoric lungs. The electrocardiogram showed sinus rhythm at 140 beats/min, right ventricular hypertrophy, and no signs of myocardial ischemia. Echocardiography demonstrated an aortic coarctation with long, severe hypoplasia of the arch, a large ductus arteriosus, and multiple ventricular septal defects. The left ventricle was neither hypokinetic nor hypoplastic. No coexisting mitral regurgitation was documented. There was also a left superior caval vein draining into the coronary sinus and a large ostium secundum–type atrial septal defect. The patient underwent pulmonary artery banding, division of the ductus arteriosus, and aortic coartectomy. Within 2 hours of the patient’s return to the intensive care unit, her condition deteriorated rapidly and dramatically, with a global but predominantly left-sided intractable heart failure, complete atrioventricular block, and cardiogenic shock. The postoperative electrocardiogram revealed signs of severe myocardial anterolateral ischemia and necrosis and a third-degree atrioventricular block (Fig. 1). Creatine kinase had increased to 530 U/L (normal range 15 to 100 U/L) with an MB fraction of 365 U/L (68%), representing a significant acute myocardial necrotic phenomenon. Postoperative cross-sectional echocardiography visualized a mildly dilated and severely hypokinetic left ventricle (less than 10% of shortening fraction) with severe impairment of diastolic function. The pulmonary artery banding was adequate, and there was no residual aortic coarctation. The right coronary artery was predominant, and the left coronary artery’s origin was not seen from the corresponding aortic Valsalva sinus. This raised suspicion of an anomalous left coronary artery arising from the pulmonary artery, which would provide an explanation for the myocardial infarction. Unfortunately, the child’s deteriorating condition did not allow performance of any further investigations. Despite maximum hemodynamic support and intravascular cardiac pacing with a 5F bipolar balloon pacing electrode (USCI International, BARD, C.R. Bard Ireland Ltd., Galway, Ireland), she died on the third postoperative day. Postmortem examination. The heart weighed 30 gm. There was, as expected, an abnormal left superior caval vein draining into the coronary sinus, a large ostium secundum–type atrial septal defect, and one large perimembranous and multiple muscular ventricular septal defects. The right ventricle was predominant, and the left one was small but not hypoplastic. Necrotic patches, confirmed by histologic analysis, were evident in the left anterolateral wall. The endocardium did not exhibit fibroelastosis. The aortic coarctation was well repaired, and the pulmonary banding was found to be in place. A tortuous, dilated right predominant coronary artery originated from the right aortic Valsalva sinus. The left coronary artery arose from the posterior right pulmonary artery wall immediately after the pulmonary bifurcation and followed a tortuous course over the anterior interventricular groove (Fig. 2). Discussion. Within the wide variety of left coronary anomalous origin, left coronary artery arising from the right pulmonary artery is extremely uncommon. The chief reason for this report, however, is the association of this origin with lesions producing high pulmonary flow, with consequent lack of clinical data suggesting such a diagnosis. Many factors led to misdiagnosis. First, this finding is not classically anticipated in cases of ventricular septal defects and aortic coarctation. Second, the left-to-right shunt provided normal perfusion to the aberrant coronary artery before the operation. Until palliation, this child’s left coronary blood flow was normal, and so were the left ventricular myocardial perfusion and oxygenation, because the pulmonary and aortic pressures and saturations were similar. The fall in pulmonary pressure to a low level after the pulmonary artery banding was therefore accompanied by a decline in the left coronary flow, with drops in coronary perfusion pressure and oxygen saturation leading to left ventricular ischemia and myocardial infarction. A similar physiopathologic condition related to closure of From the Department of Pediatric Cardiac Surgery, Centre Medico-Chirurgical de la Porte de Choisy, and the Department of Pediatric Cardiology, Institut de Puericulture de Paris, Paris, France.