ArticlePediatric cardiology2019
Pulmonary Artery Banding in Post-tricuspid Congenital Cardiac Shunting Defects with High Pulmonary Vascular Resistance.
Article in Pediatric cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Common shunt lesions with pulmonary hypertension-who will benefit from surgery?Indian journal of thoracic and cardiovascular surgery · 2025Review
- Article
- A case of a middle-aged patient with a ventricular septal defect complicated by severe pulmonary hypertension-stepwise surgical repair with pulmonary vasodilators.Journal of cardiology cases · 2021Article
- Pulmonary Hypoplasia Resulting from Pulmonary Artery Banding in Infancy: A Neonatal Rat Model Study.Pediatric cardiology · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reports of "treat and repair" of cardiac shunting lesions with inoperably high pulmonary vascular resistance (PVR) mostly concern pre-tricuspid defects; post-tricuspid lesions are different. We report our experience with pulmonary artery (PA) banding ± targeted pulmonary hypertension medications in five patients with a large VSD and inoperably high PVR, and review previous reports of PA banding with post-tricuspid defects. Three of our 5 patients had mean PAP > 50 mmHg after banding and no or only a transient fall in PVR. Two patients had mean PAP < 50 mmHg and lower PVR after banding; they had closure of their VSDs but have since had a progressive increase in PVR (follow-up after closure, 3.5 and 7.7 years). Previous reports have also documented difficulty in achieving sufficient band gradient. Of previously reported patients, only one became operable only after banding and targeted therapy, and was repaired; follow-up after repair was short-term (16 months). Our and previous experience demonstrate the difficulty in placing a PA band sufficiently tight to substantially reduce PA pressure. Reported attempts to "treat and repair" post-tricuspid defects are few and have met with limited success, and we found that PVR may increase significantly over time after repair. But more information is needed. Accurate interpretation of experience with "treat and repair" requires: careful characterization of the pulmonary circulation prior to "treating"; considering spontaneously reversible factors at pre-treatment catheterization before ascribing reduction in PVR to medical therapy; and long-term observation of PVR in patients who have had defect closure.
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