Author + information
- Received June 3, 2019
- Revision received August 22, 2019
- Accepted August 26, 2019
- Published online November 18, 2019.
- Masaru Obokata, MD, PhDa,
- Yogesh N.V. Reddy, MBBS, MSca,
- Sanjiv J. Shah, MDb,
- David M. Kaye, MD, PhDc,
- Finn Gustafsson, MD, PhDd,
- Gerd Hasenfuβ, MDe,
- Elke Hoendermis, MD, PhDf,
- Sheldon E. Litwin, MDg,
- Jan Komtebedde, DVMh,
- Carolyn Lam, MBBS, PhDf,i,j,
- Daniel Burkhoff, MD, PhDk and
- Barry A. Borlaug, MDa,∗ (, )@bborlaugmd@mayoclinicCV
- aDepartment of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota
- bDivision of Cardiology, Northwestern University, Chicago, Illinois
- cBaker IDI Heart and Diabetes Institute and Alfred Hospital, Melbourne, Victoria, Australia
- dDepartment of Cardiology, Rigshospitalet, Copenhagen, Denmark
- eGeorg-August Universität, Heart Centre, Gottingen, Germany
- fUniversity Medical Center Groningen, Groningen, the Netherlands
- gMedical University of South Carolina, Charleston, South Carolina
- hCorvia Medical, Tewksbury, Massachusetts
- iNational Heart Centre Singapore and Duke-National University of Singapore, Singapore
- jThe George Institute for Global Health, Newtown, New South Wales, Australia
- kDivision of Cardiology, Columbia University, New York, New York
- ↵∗Address for correspondence:
Dr. Barry A. Borlaug, Mayo Clinic and Foundation, 200 First Street SW, Rochester, Minnesota 55905.
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)
The Cardiovascular Research Foundation is the recipient of an unrestricted educational grant from Abiomed. Dr. Shah is supported by grants from the National Institutes of Health (R01 HL107577, R01 HL127028, and R01 HL140731) and the American Heart Association (#16SFRN28780016 and #15CVGPSD27260148); has received research grants from Actelion, AstraZeneca, Corvia, and Novartis; and has served as a consultant/Advisory Board/Steering Committee Member for Abbott, Actelion, AstraZeneca, Amgen, Bayer, Boehringer Ingelheim, Cardiora, Coridea, CVRx, Eisai, Ionis, Ironwood, Merck, MyoKardia, Novartis, Pfizer, Sanofi, Tenax, and United Therapeutics. Dr. Kaye has served on the Scientific Advisory Board of Corvia. Dr. Gustafsson has served as an unpaid advisor to Corvia; has served as an advisor to Abbott, Pfizer, and Novartis; and has received speaker honoraria from Abbott, Boehringer Ingelheim, Carmat, and Orion. Dr. Komtebedde is an employee of and has equity in Corvia Medical. Dr. Lam has received research support from Boston Scientific, Bayer, Roche Diagnostics, AstraZeneca, Medtronic, and Vifor Pharma; and has served on the Advisory Board/Steering Committee/Executive Committee for Boston Scientific, Bayer, Roche Diagnostics, AstraZeneca, Medtronic, Vifor Pharma, Novartis, Amgen, Merck, Janssen Research & Development, LLC, Menarini, Boehringer Ingelheim, Novo Nordisk, Abbott Diagnostics, Corvia, Stealth BioTherapeutics, JanaCare, Biofourmis, and Darma. Dr. Burkhoff has served as a consultant to Corvia Medical (Hemodynamic Core Laboratory). Dr. Borlaug is supported by RO1 HL128526 and U10 HL110262. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received June 3, 2019.
- Revision received August 22, 2019.
- Accepted August 26, 2019.
- 2019 American College of Cardiology Foundation
This article requires a subscription or purchase to view the full text. If you are a subscriber or member, click Login or the Subscribe link (top menu above) to access this article.