Author + information
- Received January 2, 2018
- Revision received February 6, 2018
- Accepted February 15, 2018
- Published online December 12, 2018.
- Brunilda Alushi, MD, PhDa,b,
- Frederik Beckhoff, MDa,b,
- David Leistner, MDa,b,
- Marcus Franz, MDc,
- Markus Reinthaler, MDa,b,d,
- Barbara E. Stähli, MDa,b,
- Andreas Morguet, MDa,
- Hans R. Figulla, MDe,
- Torsten Doenst, MD, PhDf,
- Francesco Maisano, MDg,
- Volkmar Falk, MDa,b,h,
- Ulf Landmesser, MDa,b and
- Alexander Lauten, MDa,b,∗ ()
- aCharité–Universitätsmedizin Berlin, Germany
- bDeutsches Zentrum für Herz-Kreislauf-Forschung (DZHK), Partnersite Berlin, Berlin Institute of Health (BIH) Berlin, Germany
- cDepartment of Internal Medicine I, Jena University Hospital, Friedrich Schiller University Jena, Jena, Germany
- dUniversity College London, Department of Structural Heart Intervention, London, England
- eFriedrich-Schiller-Universität Jena, Jena, Germany
- fDepartment of Cardiothoracic Surgery, Jena University Hospital, Friedrich Schiller University Jena, Jena, Germany
- gUniversity Hospital of Zurich, University of Zurich, Zürich, Switzerland
- hDeutsches Herzzentrum Berlin, Berlin, Germany
- ↵∗Address for correspondence:
Prof. Dr. med. Alexander Lauten, Charité-Universitätsmedizin Berlin, Charité Campus Mitte and Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany.
Objectives The authors investigated the development of pulmonary hypertension (PH), predictors of PH regression, and its prognostic impact on short, mid-, and long-term outcomes in patients undergoing transcatheter aortic valve replacement (TAVR) for severe aortic stenosis (AS).
Background PH represents a common finding in patients with AS. Although TAVR is frequently associated with regression of PH, the predictors of reversible PH and its prognostic significance remain uncertain.
Methods In this study, 617 consecutive patients undergoing TAVR between 2009 and 2015 were stratified per baseline tertiles of pulmonary artery systolic pressure (PASP) as follows: normal (PASP <34 mm Hg), mild-to-moderate (34 mm Hg ≤ PASP <46 mm Hg), and severe PASP elevation (PASP ≥46 mm Hg). After TAVR, 520 patients with PH at discharge were stratified according to the presence or absence of PASP reduction. Primary outcome was all-cause mortality at 30 days, 1 year, and long-term follow-up at a maximum of 5.9 years.
Results In patients with both mild-to-moderate and severe PH at baseline, PASP decreased significantly at discharge (ΔPASP 3.0 ± 9.3 mm Hg and 12.0 ± 10.0 mm Hg, respectively) and 1 year (ΔPASP 5.0 ± 9.7 mm Hg and 18.0 ± 14.0 mm Hg, respectively). At a median follow-up of 370 days (interquartile range [IQR]: 84 to 500 days), the risk of all-cause mortality was similar among baseline PASP groups at all time intervals evaluated. After TAVR, a significant regression of PH was observed in 46% of patients. Contrarily, patients with residual PH had a higher risk of all-cause mortality at 30 days (hazard ratio [HR]: 3.49, 95% confidence interval [CI]: 1.74 to 6.99; p < 0.001), 1 year (HR: 3.12, 95% CI: 2.06 to 4.72; p < 0.001), and long-term (HR: 2.47, 95% CI: 1.74 to 3.49; p < 0.001). Left ventricular ejection fraction (LVEF) >40% (odds ratio [OR]: 3.56, 95% CI: 2.24 to 5.65; p < 0.001), baseline PASP ≥46 mm Hg (OR: 3.26, 95% CI: 2.07 to 5.12; p < 0.001), absence of concomitant tricuspid regurgitation (TR) ≥ moderate (OR: 0.53, 95% CI: 0.34 to 0.84; p < 0.001), and logistic EuroSCORE <25% (OR: 1.59, 95% CI: 1.04 to 2.45; p = 0.03) were independent predictors of PASP reduction.
Conclusions In most patients with PH and AS, TAVR is associated with a significant early and late reduction of PASP. Patients with reversible PH after TAVR are at lower risk of all-cause mortality at early, mid-, and long-term follow-up. Therefore, the presence of PH should not preclude treatment with TAVR.
- aortic stenosis
- aortic valve
- pulmonary hypertension
- right ventricular
- tricuspid regurgitation
Dr. Maisano has received grants from Medtronic, Biotronik, Edwards Lifesciences, and Abbott Vascular. Dr. Landmesser has received grants from Edwards Lifesciences; and personal fees from Abbott Vascular outside of the submitted work. Dr. Lauten has received grants from Edwards Lifesciences and Abbott Vascular outside the submitted work. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received January 2, 2018.
- Revision received February 6, 2018.
- Accepted February 15, 2018.
- 2018 American College of Cardiology Foundation
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