Premium
Pulmonary artery and lung parenchymal growth following early versus delayed stent interventions in a swine pulmonary artery stenosis model
Author(s) -
Pewowaruk Ryan,
Hermsen Joshua,
Johnson Cody,
Erdmann Alexandra,
Pettit Kevin,
Aesif Scott,
Ralphe J. Carter,
Francois Christopher J.,
RoldánAlzate Alejandro,
Lamers Luke
Publication year - 2020
Publication title -
catheterization and cardiovascular interventions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.988
H-Index - 116
eISSN - 1522-726X
pISSN - 1522-1946
DOI - 10.1002/ccd.29326
Subject(s) - medicine , pulmonary artery , left pulmonary artery , lung , stenosis , right pulmonary artery , cardiology , stent , hemodynamics , perfusion
Objectives Compare lung parenchymal and pulmonary artery (PA) growth and hemodynamics following early and delayed PA stent interventions for treatment of unilateral branch PA stenosis (PAS) in swine. Background How the pulmonary circulation remodels in response to different durations of hypoperfusion and how much growth and function can be recovered with catheter directed interventions at differing time periods of lung development is not understood. Methods A total of 18 swine were assigned to four groups: Sham ( n = 4), untreated left PAS (LPAS) ( n = 4), early intervention (EI) ( n = 5), and delayed intervention (DI) ( n = 5). EI had left pulmonary artery (LPA) stenting at 5 weeks (6 kg) with redilation at 10 weeks. DI had stenting at 10 weeks. All underwent right heart catheterization, computed tomography, magnetic resonance imaging, and histology at 20 weeks (55 kg). Results EI decreased the extent of histologic changes in the left lung as DI had marked alveolar septal and bronchovascular abnormalities ( p = .05 and p < .05 vs. sham) that were less prevalent in EI. EI also increased left lung volumes and alveolar counts compared to DI. EI and DI equally restored LPA pulsatility, R heart pressures, and distal LPA growth. EI and DI improved, but did not normalize LPA stenosis diameter (LPA/DAo ratio: Sham 1.27 ± 0.11 mm/mm, DI 0.88 ± 0.10 mm/mm, EI 1.01 ± 0.09 mm/mm) and pulmonary blood flow distributions (LPA‐flow%: Sham 52 ± 5%, LPAS 7 ± 2%, DI 44 ± 3%, EI 40 ± 2%). Conclusion In this surgically created PAS model, EI was associated with improved lung parenchymal development compared to DI. Longer durations of L lung hypoperfusion did not detrimentally affect PA growth and R heart hemodynamics. Functional and anatomical discrepancies persist despite successful stent interventions that warrant additional investigation.