Abstract

Objectives: To assess the extent of neointimal proliferation and the safety and efficacy of stent redilatation in patients with stents implanted for aortic coarctation or branch pulmonary artery stenosis.

Design: Retrospective observational study.

Setting: Tertiary referral centre.

Patients and interventions: Of 60 patients with Palmaz stents, 12 with coarctation and 12 with branch pulmonary artery stenosis (with 21 stented sites) underwent recatheterisation and stent redilatation.

Results: Neointimal thickening > 1 mm was detected in six of the 12 coarctation stents and at nine of the 21 stented sites in branch pulmonary arteries (five of which had been overdilated at implantation). Eight of the coarctation stents were electively underdilated at implantation. Coarctation stent redilatation increased median (range) lumen diameter from 9.2 (6.3–11.1) mm to 11.7 (9.8–14.1) mm (p = 0.002), decreased gradient from 10.5 (0–20) mm Hg to 0.5 (0–15) mm Hg (p = 0.008), and increased the ratio of stent diameter to descending aorta diameter from 0.66 (0.38–1.02) to 0.85 (0.52–1.2) (p = 0.008). Pulmonary artery stent redilatation increased lumen diameter from 6.9 (3.8–13.5) mm to 8.8 (4.8–14.1) mm (p < 0.001), decreased gradient from 24 (2–62) mm Hg to 12 (0–29) mm Hg (p < 0.001), and increased the ratio of stent diameter to diameter of distal pulmonary artery from 0.66 (0.44–1.5) to 0.86 (0.48–1.88) (p = 0.001). Dilatation of one peripheral pulmonary artery stent resulted in rupture of the vessel distal to the stent.

Conclusions: Neointimal proliferation is precipitated by overdilating stents at implantation. Redilatation using balloons matched to distal vessel diameter increases stent lumen size, but may not optimise vessel diameter. Redilatation is effective whether the indication for redilatation is a resistant stenosis at implantation, underexpansion at implantation, neointimal proliferation, or relative stenosis caused by growth.