Author + information
- Received February 8, 2018
- Revision received May 17, 2018
- Accepted May 18, 2018
- Published online September 3, 2018.
- Rebecca T. Hahn, MDa,∗ (, )
- Philippe Pibarot, DVM, PhDb,
- Jonathon Leipsic, MDc,
- Philipp Blanke, MDc,
- Pamela S. Douglas, MDd,
- Neil J. Weissman, MDe,
- Samir Kapadia, MDf,
- Vinod H. Thourani, MDe,
- Howard C. Herrmann, MDg,
- Tamim Nazif, MDa,
- Thomas McAndrew, PhDh,
- John G. Webb, MDc,
- Martin B. Leon, MDa and
- Susheel Kodali, MDa
- aColumbia University Medical Center/NY Presbyterian Hospital, New York, New York
- bDepartment of Medicine, Laval University, Quebec, Quebec, Canada
- cUniversity of British Columbia and St. Paul’s Hospital, Vancouver, British Columbia, Canada
- dDuke University Medical Center, and Duke Clinical Research Institute, Durham, North Carolina
- eGeorgetown University School of Medicine, Medstar Health Research Institute, Washington, DC
- fCleveland Clinic, Cleveland, Ohio
- gUniversity of Pennsylvania, Philadelphia, Pennsylvania
- hCardiovascular Research Foundation, New York, New York
- ↵∗Address for correspondence:
Dr. Rebecca T. Hahn, Columbia University Medical Center, New York-Presbyterian Hospital, 177 Fort Washington Avenue, New York, New York 10032.
Objectives The purpose of this study was to understand the effects of balloon post-dilatation on outcomes following transcatheter aortic valve replacement with the SAPIEN 3 valve.
Background Hemodynamics and outcomes with balloon post-dilatation for the SAPIEN 3 valve have not been previously reported.
Methods The effects of balloon post-dilatation (BPD) in 1,661 intermediate (S3i cohort) and high surgical risk (S3HR cohort) patients with aortic stenosis enrolled in the PARTNER (Placement of Aortic Transcatheter Valves) 2, SAPIEN 3 observational study on outcomes, as well as procedural complications, were assessed.
Results 208 of 1,661 patients (12.5%) had BPD during the initial transcatheter aortic valve replacement. Baseline characteristics were similar except BPD had higher STS score (p < 0.001), significantly less % oversizing (p = 0.004), significantly more ≥moderate left ventricular outflow tract calcification (p = 0.005), and severe annular calcification (p = 0.006). BPD patients had no increase in permanent pacemaker, annular rupture, or valve embolization. Following transcatheter aortic valve replacement, BPD patients had significantly larger aortic valve area (1.72 ± 0.41 cm2 vs. 1.66 ± 0.37 cm2; p = 0.04) with no significant difference in prosthesis–patient mismatch (p = 0.08) or transvalvular aortic regurgitation (p = 0.65), but significantly more paravalvular regurgitation (p < 0.01). There was no significant difference in 30-day or 1-year outcomes of all-cause death (p = 0.65 to 0.76) or stroke (p = 0.28 to 0.72). However, at 1 year, there was a significantly higher incidence of minor stroke in BPD patients (p = 0.02). Adjusting for baseline differences, including calcium burden, minor strokes were no longer significantly different between the BPD and NoBPD groups (p = 0.21).
Conclusions BPD is performed more frequently in patients with lower % oversizing and greater calcium burden. BPD is not associated with procedural complications or an increase in 1-year adverse events of death, rehospitalization, or stroke.
The PARTNER 2 S3 trial was funded by Edwards Lifesciences. Drs. Hahn and Pibarot have had core lab contracts with Edwards Lifesciences for which they received no direct compensation. Dr. Leipsic has been a consultant for Edwards Lifesciences; and has had a core lab contract with Edwards Lifesciences, for which he received no direct compensation, Medtronic, and Abbott. Dr. Blanke has been a consultant for Edwards Lifesciences; and has had a core lab contract with Edwards Lifesciences, for which he received no direct compensation. Dr. Douglas has received grant funding from Edwards Lifesciences; and has had a core lab contract with Edwards Lifesciences, for which she received no direct compensation. Dr. Weissman has received research grants from Boston Scientific, Edwards, Medtronic, Abbott, and LivaNova; and has had a core lab contract with Edwards Lifesciences, for which he received no direct compensation. Dr. Thourani has been a consultant for Edwards Lifesciences. Dr. Herrmann has received grants to his institution from Edwards Lifesciences, Medtronic, St. Jude Medical, Boston Scientific, Bayer, Corvia, the University of Laval, and Abbott Vascular; and has been a consultant for Edwards Lifesciences. Dr. Webb has been a member of the PARTNER Trial Executive Committee for which he received no direct compensation; and has been a consultant for Edwards Lifesciences. Dr. Leon has been a member of the PARTNER Trial Executive Committee for which he received no direct compensation. Dr. Kodali has been a consultant for Edwards Lifesciences, Merrill Lifesciences, and Claret Medical; has served on the advisory boards of Abbott Vascular, Biotrace Medical, Dura Biotech, Thubrikar Aortic Valve, Duratech, and VS Medtech; and has equity in Thubrikar Aortic Valve, Dura Biotech, and Biotrace Medical. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received February 8, 2018.
- Revision received May 17, 2018.
- Accepted May 18, 2018.
- 2018 American College of Cardiology Foundation