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Transcatheter recanalisation and stenting of a closed ductus arteriosus in duct dependent lung perfusion
  1. C Kampmanna,
  2. C-F Wippermanna,
  3. F-X Schmidb
  1. aDepartment of Pediatric Cardiology, Johannes Gutenberg University, Mainz, Germany, bDepartment of Heart and Cardiovascular Surgery, Johannes Gutenberg University
  1. Dr med C Kampmann, Johannes Gutenberg Universität zu Mainz, Pädiatrische Kardiologie, Langenbeckstrasse 1, D-55101 Mainz, Germany. email: kampmann{at}

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In patients with the congenital cardiac malformation of tetralogy of Fallot, occasionally one pulmonary artery, usually the left, seems angiographically to be absent.1 This pulmonary artery is usually present, but discontinuous with the pulmonary trunk, having originally been supplied by a patent arterial duct. With closure of the duct, the receiving flow to that pulmonary artery is by small collateral vessels, which leads to reduced growth of the involved pulmonary vessels and impedes definite surgical repair.

We report a case of a 2 day old, 1890 g, premature, cyanotic boy (oxygen saturation 82%) with tetralogy of Fallot, right sided aortic arch, and discontinuity between the pulmonary trunk and the left pulmonary artery with a distance of 6 mm, and a complete left sided pulmonary perfusion deficiency. Six hours after starting prostaglandin E1 (PGE1) infusion (100 ng/kg/min) there was still no flow to the left pulmonary artery or any increase in saturation.

Antegrade angiography from the right femoral vein confirmed the diagnosis. A closed patent arterial duct, originating from the left subclavian artery, could be seen selectively after passing the right ventricle into the overriding aorta (fig 1). To recanalise the closed patent arterial duct, an additional 50 ng/kg/min PGE1 was given over 10 minutes into the origin of the patent arterial duct, while it was attempted to pass a 0.014 inch floppy guidewire through the patent arterial duct. After successfully passing the wire, PGE1 infusion was stopped and dilatation was performed up to 3 mm. The length of ductal obliteration was 11 mm. To maintain ductal patency, a 9 mm long coronary NIR stent was mounted on a 3.5 mm balloon catheter and implanted at the pulmonary end of the duct (fig 2). Postinterventional angiography showed a well developed left sided pulmonary arterial system, but without a main left pulmonary artery (fig3).

Figure 1

Selective posterior-anterior angiogram of the origin of the closed arterial duct from the left subclavian artery.

Figure 2

Angiogram of the arterial duct during stent implantation at the pulmonary end of the patent arterial duct.

Figure 3

Selective angiogram of the left pulmonary artery after ductal stenting.

Immediately after stenting, the child developed left sided lung oedema with pleural effusion that necessitated drainage. After stenting, dilatation of the right ventricular outflow tract was performed up to 7 mm. All interventions were without complication. Total fluoroscopy time was 18.6 minutes. Before stenting, antithrombin III was substituted to a blood level of 100% and a bolus of 100 U/kg heparin was given intravenously followed by continuous infusion of 400 U/kg/day for the next three days. The child was extubated on the next day and discharged 14 days later in very good condition (oxygen saturation 91%); he was treated with 2 mg/kg/day propranolol and dipyridamole.

Redilatation of the stent up to 4.2 mm was necessary after 235 days. Selective angiograms of the right and left pulmonary arteries showed adequate development with diameters of 8 and 7.6 mm, respectively, and mean right and left pressures of 10 and 13 mm Hg. At the age of 1 year the child had successful transatrial–transpulmonary repair of the tetralogy of Fallot with connection of the left pulmonary artery to the pulmonary trunk.


In symptomatic newborns with tetralogy of Fallot, percutaneous balloon dilatation of the right ventricular outflow tract and the application of propranolol is used palliatively to provide ideal conditions for repair,2 although the dysplastic pulmonary valve may be damaged.3 Stenting of the patent arterial duct to maintain patency was first reported by Gibbset al in patients with pulmonary atresia4 but required redilatation.5 In our case with duct dependent lung perfusion, adequate left pulmonary artery growth could be established by stenting the patent arterial duct. Interventional recanalisation combined with stenting of a closed patent arterial duct in man has not been reported previously. Early interventional recanalisation of closed patent arterial ducts is feasible even in premature neonates, and the procedure supports age appropriate development of pulmonary arteries. This should contribute to a reduction in perioperative mortality.