Pulmonary Artery Banding in Post-tricuspid Congenital Cardiac Shunting Defects with High Pulmonary Vascular

Thomas J Kulik1,2, Julia E McSweeney3, Joseph Tella4

  • 1Division of Cardiac Critical Care, and the Pulmonary Hypertension Program, Department of Cardiology, Boston Children's Hospital, 300 Longwood Ave, Boston, MA, 02115, USA. thomas.kulik@cardio.chboston.org.

Pediatric Cardiology
|January 24, 2019
PubMed

Insights

Treating post-tricuspid cardiac shunts with high pulmonary vascular resistance (PVR) using pulmonary artery banding is challenging. Many patients do not achieve sufficient PVR reduction, and PVR can increase long-term after repair.

Area of Science:

  • Cardiology
  • Pediatric Cardiology
  • Pulmonary Hypertension

Background:

  • "Treat and repair" strategies for cardiac shunts with inoperably high pulmonary vascular resistance (PVR) are complex, especially for post-tricuspid defects.
  • Pulmonary artery (PA) banding is a palliative approach, but its efficacy in significantly reducing PVR in these cases is debated.

Purpose of the Study:

  • To evaluate the effectiveness of PA banding and targeted pulmonary hypertension medications in patients with large ventricular septal defects (VSDs) and inoperably high PVR.
  • To review previous reports on PA banding for post-tricuspid defects to assess long-term outcomes.

Main Methods:

  • Retrospective analysis of 5 patients with large VSDs and high PVR treated with PA banding and medications.
  • Review of existing literature on PA banding for post-tricuspid defects.

Main Results:

  • Three patients had persistent high mean pulmonary artery pressure (>50 mmHg) post-banding with minimal PVR reduction.
  • Two patients achieved lower PVR post-banding and underwent VSD closure, but experienced progressive PVR increase over 3.5 and 7.7 years.
  • Previous reports indicate difficulty in achieving adequate band gradients and limited success in surgical repair post-banding.

Conclusions:

  • PA banding for post-tricuspid defects with high PVR is technically challenging, often failing to achieve sufficient PVR reduction.
  • Long-term PVR monitoring is crucial as it can increase significantly even after successful defect closure.
  • Further research is needed, emphasizing accurate pre-treatment characterization of pulmonary circulation and long-term follow-up.

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