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Udgivet

Effects of Interatrial Shunt on Pulmonary Vascular Function in Heart Failure With Preserved Ejection Fraction

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DOI

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  • Masaru Obokata
  • Yogesh N V Reddy
  • Sanjiv J Shah
  • David M Kaye
  • Finn Gustafsson
  • Gerd Hasenfuβ
  • Elke Hoendermis
  • Sheldon E Litwin
  • Jan Komtebedde
  • Carolyn Lam
  • Daniel Burkhoff
  • Barry A Borlaug
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BACKGROUND: Implantation of an interatrial shunt device (IASD) in patients with heart failure (HF) reduces left atrial hypertension by shunting oxygenated blood to the right heart and lungs. The attendant increases in pulmonary blood flow (Qp) and oxygen content may alter pulmonary vascular function, while left-to-right shunting might compromise systemic perfusion.

OBJECTIVES: The authors hypothesized that IASD would improve indexes of pulmonary artery (PA) function at rest and during exercise in HF patients without reducing systemic blood flow (Qs).

METHODS: This is a pooled analysis from 2 trials assessing the effects of the IASD on resting and exercise hemodynamics in HF patients (n = 79) with EF ≥40% with baseline and repeated hemodynamic evaluation between 1 and 6 months. Patients with pulmonary vascular resistance (PVR) >4 WU or right ventricular dysfunction were excluded.

RESULTS: Qp and PA oxygen content increased by 27% and 7% following IASD. These changes were associated with salutary effects on pulmonary vascular function (17% reduction in PVR, 12% reduction in PA elastance [pulmonary Ea], and 24% increase in PA compliance). Qp increased during exercise to a greater extent following IASD compared with baseline, which was associated with reductions in exercise PVR and pulmonary Ea. Patients with increases in PA compliance following IASD experienced greater improvements in supine exercise duration. There was no reduction in Qs following IASD at rest or during exercise.

CONCLUSIONS: Implantation of an IASD improves pulmonary vascular function at rest and during exercise in selected patients with HF and EF ≥40%, without compromising systemic perfusion. Further study is warranted to identify underlying mechanisms and long-term pulmonary hemodynamic effects of IASD. (REDUCE LAP-HF Trial [REDUCE LAP-HF]; NCT01913613; and REDUCE LAP-HF Randomized Trial I [REDUCE LAP-HF I]; NCT02600234).

OriginalsprogEngelsk
TidsskriftJournal of the American College of Cardiology
Vol/bind74
Udgave nummer21
Sider (fra-til)2539-2550
Antal sider12
ISSN0735-1097
DOI
StatusUdgivet - 26 nov. 2019

Bibliografisk note

Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

ID: 59169624