Aneurysm of the pulmonary trunk with patent arterial duct.

We present a 14-year-old female with a massive aneurysm of the pulmonary trunk occurring secondary to bacterial endocarditis of the patent arterial duct. Echo Doppler imaging, magnetic resonance and angiography confirmed the diagnosis. On intermediate follow-up after surgical correction, the echo studies and cardiac catheterization disclosed no residual lesions. The patient is now asymptomatic.     

Stenting of the arterial duct: a new approach to palliation for pulmonary atresia.

OBJECTIVE--To assess the possibility of maintaining ductal patency in neonates with complex pulmonary atresia by percutaneous implantation of balloon expandable stents. PATIENTS--Two duct-dependent neonates with long segment pulmonary atresia, right sided aortic arch, and left sided arterial duct. RESULTS--Stents with final diameter of 3.5 or 4 mm and initial length of 7 or 15 mm were successfully positioned in the arterial duct. Two stents were required in one child and four in the other in order to stent the entire length of the duct. After the procedures the ducts remained widely patent and arterial oxygen saturations remained above 80%. Complications of the procedures included perforation of a peripheral pulmonary artery and cardiac perforation, both caused by guide wire manipulation. Both babies died suddenly, one at five weeks, and the other at nine days after successful stenting of the duct. Both ducts were patent at necropsy; the exact cause of one death was not clearly defined, but the second seemed to be caused by pneumococcal septicaemia. CONCLUSIONS--Stenting of the arterial duct is technically feasible. It provides adequate palliation for neonates with pulmonary atresia at least in the short term and it seems to result in balanced, central perfusion of both pulmonary arteries. This preliminary report suggests that this previously untried technique may prove to be a promising and attractive alternative to neonatal aortopulmonary shunt operation.     

Stenting of the arterial duct: a new approach to palliation for pulmonary atresia.

OBJECTIVE--To assess the possibility of maintaining ductal patency in neonates with complex pulmonary atresia by percutaneous implantation of balloon expandable stents. PATIENTS--Two duct-dependent neonates with long segment pulmonary atresia, right sided aortic arch, and left sided arterial duct. RESULTS--Stents with final diameter of 3.5 or 4 mm and initial length of 7 or 15 mm were successfully positioned in the arterial duct. Two stents were required in one child and four in the other in order to stent the entire length of the duct. After the procedures the ducts remained widely patent and arterial oxygen saturations remained above 80%. Complications of the procedures included perforation of a peripheral pulmonary artery and cardiac perforation, both caused by guide wire manipulation. Both babies died suddenly, one at five weeks, and the other at nine days after successful stenting of the duct. Both ducts were patent at necropsy; the exact cause of one death was not clearly defined, but the second seemed to be caused by pneumococcal septicaemia. CONCLUSIONS--Stenting of the arterial duct is technically feasible. It provides adequate palliation for neonates with pulmonary atresia at least in the short term and it seems to result in balanced, central perfusion of both pulmonary arteries. This preliminary report suggests that this previously untried technique may prove to be a promising and attractive alternative to neonatal aortopulmonary shunt operation.     

Ectopic right coronary artery to pulmonary artery fistula masquerading as patent arterial duct

A patient is described in whom communication between an ectopic right coronary artery and the main pulmonary artery presented with clinical features of a patent arterial duct. Full clinical data documented by Doppler echocardiography, cardiac catheterisation and intra-operative findings are described.     

Thoracoscopic closure of the patent arterial duct

Video assisted thoracoscopic surgery for closure of the persistently patent arterial duct is an effective answer to the modern effort of seeking repair of congenital cardiac malformations with minimally invasive techniques. Between June, 1994, and December, 2002, 150 consecutive patients with an echocardiographic diagnosis of isolated patency of the arterial duct were referred to our Institution for video assisted thoracoscopic closure. The median age at the time of operation was 45 months, with a range from 3 to 161 months, and mean weight was 18 kg, with a range from 4.2 to 73 kg. Video assisted closure was possible in 139 patients (93%). The mean operative time was 37 min, with a range from 14 to 89 min. In the remaining 11 patients (7%), seen early in our experience, we converted to a mini-thoracotomy to achieve closure. In no instance did we encounter major haemorrhage requiring blood transfusion, and there were no hospital deaths. The mean period of stay in hospital was less than 24 h in 61 patients, less than 48 h in 88 patients seen earlier in our experience, and 21 days in 1 patient because of a persistent chylothorax. Other complications included palsy of the left recurrent laryngeal nerve in 1 patient, with partial regression at 6 months follow-up. We conclude that closure of the arterial duct by video-assisted thoroscopy combines the advantages of safe and complete extraluminal occlusion with an excellent clinical and aesthetic result, minimal postoperative pain, and short stay in hospital at low cost.     

Stenting the neonatal arterial duct in duct-dependent pulmonary circulation: new techniques, better results

OBJECTIVES: The goal of this study was to assess a new approach to stent the arterial duct in neonates with a duct-dependent pulmonary circulation. BACKGROUND: Previous attempts to stent the neonatal arterial duct were unsatisfactory. Learning from these failures, we speculated that covering the complete length of the duct with current low-profile stents might avoid previous problems. METHODS: Ten neonates with duct-dependent pulmonary circulations through a short straight duct were treated with stent implantation. The duct was crossed with an atraumatic 0.014-inch wire. A low-profile premounted coronary stent (outer diameter <4F, length 13 to 24 mm, diameter 3.0 to 4.0 mm) was positioned within the duct, not protected by a sheath; care was taken to cover the complete length of the duct from the aortaductal junction until well within the pulmonary trunk. RESULTS: All stents could safely be deployed with adequate pulmonary flow at early- and medium-term follow-up. There were no procedure-related complications; one patient died early from sepsis. All patients had adequate relief of cyanosis for at least three to four months. During follow-up, the pulmonary vasculature bed had grown without distortion. Acute occlusion of a stented duct was not observed. Ductal flow progressively decreased slowly over several months by luminal narrowing, until the stented duct had either become redundant or was dilated/restented or until elective staged surgery was performed. CONCLUSIONS: With current technology, complete stenting of a short straight duct is a safe and effective palliation, allowing adequate growth of the pulmonary arteries.     

Coil occlusion of the small patent arterial duct without arterial access

BACKGROUND: Arterial access is traditionally considered mandatory during coil occlusion of the patent arterial duct. Arterial access necessitates heparinization and carries the risk of femoral artery occlusion in small children. METHODS AND RESULTS: Between July 1999 and May 2001, we attempted coil occlusion of patent arterial ducts in 104 patients without arterial access. The patients were aged from 3 months to 14 years. The median age was 2 years. They weighed 3-35 kg. The median weight was 9.8 kg. The duct diameter at pulmonary artery insertion was 1.8-3.5 mm. The patients were selected on basis of echocardiographic evaluation of duct diameter at pulmonary artery insertion and morphology of the ampulla. Doppler color flow imaging was used in the catheterization laboratory to confirm duct closure. Arterial access was required in 21 patients. The reasons included accidental puncture in 5 patients, failure to obtain venous access in 1 patient, aortic embolization in 3 patients, poor echo images in 2 patients, requirement for additional coils in 8 patients and, failure to cross the duct from pulmonary artery in 2 patients. The fluoroscopic time ranged from 2.2 to 20 min with a mean of 5.3+/-3.8 min. Immediate closure was achieved in 98 patients and this included 79 of the 83 patients in whom arterial access was avoided. Color Doppler 3-24 h later showed residual flow in 2 patients. Four patients had new-onset left pulmonary artery turbulence with peak gradients below 5 mm of mercury. Coil embolization occurred in 6 patients and all coils were retrieved. Three-month follow up information was available for 78 patients. Small residual ductal leaks were seen in 4 patients, 2 of whom had leaks at 24 h. Two patients had recanalized their ducts. CONCLUSION: It is feasible to occlude small patent arterial ducts with coils using venous access alone in carefully selected patients with excellent immediate and short-term results.     

Cannulation of patent arterial duct in patients with pulmonary atresia and ventricular septal defect.

During cardiac catheterization in patients with pulmonary atresia and ventricular septal defect, cannulation of the arterial duct was attempted in 23 children via antegrade approach. It was successful in all but two children. Injection of contrast through antegradely placed catheter resulted in improved opacification of pulmonary arteries. This technique facilitated transcatheter dilation of spontaneously closed arterial duct in two children.     

Evolution of strategies for management of the patent arterial duct

Persistent patency of the arterial duct represents one of the most common lesions in the field of congenital cardiac disease. The strategies for management continue to evolve. In this review, we focus on management beyond the neonatal period. We review the temporal evolution of strategies for management, illustrate the currently available the techniques for permanent closure of the patent arterial duct, review the expected outcomes after closure, discuss the current controversy over the appropriate treatment of the so-called "silent" duct, and provide recommendations for the current state of management of patients with persistent patency of the arterial duct outside of the neonatal period.At the Congenital Heart Institute of Florida, we now recommend closure of all patent arterial ducts, regardless of their size. Before selecting and performing the type of procedure, we explain the natural history of the persistently patent arterial duct to the parents or legal guardian of the child. Particular emphasis is placed on the risks of endocarditis, including the recognition that many cases of endocarditis may not be preventable. The devastating effects of endocarditis, coupled with the perception of more anecdotal reports of endocarditis with the silent duct, as well as the low risk of interventions, has led us to recommend closure of the patent arterial duct in these situations. We now recommend intervention, after informed consent, for all patients with a patent arterial duct regardless of size, including those in which the patent duct is "silent". We recognize, however, that this remains a controversial topic, especially given the new recommendations for endocarditis prophylaxis from American Heart Association. Since 2003, our strategy for closure of the patent arterial duct has changed subsequent to the availability of the Amplatzer occluder. This new device has allowed significantly larger patent arterial ducts to be closed with interventional catheterization procedures that in the past would have been closed at surgery. During the interval between 2002 and 2006 inclusive, the overall surgical volume at our Institute has been stable. Over this period, the number of patients undergoing surgical ligation of the patent arterial duct has decreased, with this decline in volume most notable for the subgroup of patients weighing more than five kilograms. This decrease has been especially notable in thoracoscopic procedures and is attributable to the increased ability to close larger ducts using the Amplatzer occluder. For infants with symptomatic pulmonary overcirculation weighing less than 5 kilograms, our preference is for the surgical approach. For patients who have ductal calcification, significant pleural scarring, or "window-like" arterial ducts, video-assisted ligation is not an option and open surgical techniques are used. When video-assisted ligation is possible, the approach is based on family and surgeon preference. When open thoracotomy is selected, we usually use a muscle-sparing left posterolateral thoracotomy. For patients weighing more than 5 kilograms, we currently recommend percutaneous closure for all patent arterial ducts as the first intervention, reserving surgical treatment for those cases that are not amenable to the percutaneous approach. For symptomatic infants weighing greater than 5 kilogram with large ducts, we prefer to use the Amplatzer occluder. In rare instances, the size of the required ductal occluder is so large that either encroachment into the aorta or pulmonary arteries is noted, and the device is removed. The child is then referred for surgical closure. We can now often predict via echocardiography that a duct is too large for transcatheter closure, even with the Amplatzer occluder, and refer these patients directly to surgery. For patients with an asymptomatic patent arterial duct, we prefer to wait until the weight is from 10 to 12 kilograms, or they are closer to 2 years of age. If the patent arterial duct is greater than 2.0 to 2.5 millimetres in diameter, our preference is to use the Amplatzer occluder. For smaller ducts, we typically use stainless steel coils. Using this strategy, we close all patent arterial ducts, regardless of their size.     

Impaired increase of retinal capillary blood flow to flicker light exposure in arterial hypertension

We hypothesized that the increase of retinal capillary blood flow (RCF) to flicker light exposure is impaired in subjects with arterial hypertension. In 146 nondiabetic untreated male subjects with (n=50) or without (n=96) arterial hypertension, RCF was measured before and after flicker light exposure noninvasively and in vivo using scanning laser Doppler flowmetry. In addition, in a subgroup of 28 subjects, the change of RCF to flicker light exposure was again assessed during parallel infusion of nitric oxide synthase inhibitor N-monomethyl-l-arginine (L-NMMA). The increase of RCF to flicker light exposure was lower in patients with untreated hypertension compared with normotensive subjects when expressed in absolute terms (7.69±54 versus 27.2±44 AU; P adjusted=0.013) or percent changes (2.95±14 versus 8.33±12%; P adjusted=0.023). Systolic (β=-0.216; P=0.023) but not diastolic blood pressure (β=-0.117; P=0.243) or mean arterial pressure (β=-0.178; P=0.073) was negatively related to the percent change of RCF to flicker light exposure, independently of other cardiovascular risk factors. In the subgroup of 28 subjects, the increase of RCF to flicker light exposure was similar at baseline and during parallel infusion of L-NMMA when expressed in absolute terms (20.0±51 versus 22.6±56 AU; P=0.731) or percent changes (7.12±16 versus 8.29±18%; P=0.607). The increase of RCF to flicker light exposure is impaired in arterial hypertension. In the subgroup of the total study cohort, nitric oxide was not a major determinant of the increase of RCF to flicker light exposure.