Prognostic role of pulmonary hemodynamics before transcatheter aortic valve replacement among patients with severe aortic stenosis.


Journal

The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation
ISSN: 1557-3117
Titre abrégé: J Heart Lung Transplant
Pays: United States
ID NLM: 9102703

Informations de publication

Date de publication:
02 2023
Historique:
received: 21 03 2022
revised: 17 08 2022
accepted: 02 10 2022
pubmed: 28 11 2022
medline: 18 1 2023
entrez: 27 11 2022
Statut: ppublish

Résumé

Pulmonary hypertension (PH) frequently co-exists in patients with severe aortic stenosis (AS). In this study, we sought to identify the implications of invasive pulmonary hemodynamics on major adverse cardiac events (MACE), biventricular function and NYHA functional class after transcatheter aortic valve replacement (TAVR). Invasive hemodynamics via right heart catheterization (RHC) were performed pre-TAVR. Patients were stratified per mean PA pressure (mPAP), diastolic pulmonary gradient (DPG) and pulmonary vascular resistance (PVR), and followed at 1-month and 1-year intervals up to 6 years. MACE outcomes included cardiovascular death and heart failure hospitalizations post-TAVR. Among 215 patients, Kaplan-Meir estimates demonstrated an increased 1-year risk of MACE from 8% among those without pre-TAVR PH to 27% among patients with pre-existing PH. Specifically, the MACE risk was 32% among PH patients with PVR ≥ 3WU (p = .04) and 53% among PH patients with DPG ≥ 7 mm Hg (p < .01). On univariate Cox regression, RV stroke work index (RVSWI) (HR,1.02; p = .02), and pulmonary hemodynamic index (PHI) (HR,1.27; p = .047) were identified as additional predictors of MACE post-TAVR. On multivariable Cox regression analysis, SvO2 (HR, 0.95; p = .01) and PVR (HR, 1.2; p = .04) were demonstrated as predictive of MACE post-TAVR. A significant improvement in LVEF (2-Factor ANOVA, p < .01) and RV fractional area change (RVFAC%) (p < .01) was noted as assessed at baseline, 1-month and 1-year follow up post-TAVR. There was a significant interaction between pre-TAVR PH status and time post procedure with respect to NYHA functional class (p = .03), that is, the manner and degree of change in NYHA class over time depended on pre-TAVR PH status. Defining invasive pulmonary hemodynamics, such as mPAP, PVR, and DPG among patients with severe AS undergoing TAVR has significant prognostic implications. Routine risk stratification by utilizing invasive hemodynamics can better identify patients who will have functional improvement and improved outcomes post-TAVR.

Sections du résumé

BACKGROUND
Pulmonary hypertension (PH) frequently co-exists in patients with severe aortic stenosis (AS). In this study, we sought to identify the implications of invasive pulmonary hemodynamics on major adverse cardiac events (MACE), biventricular function and NYHA functional class after transcatheter aortic valve replacement (TAVR).
METHODS
Invasive hemodynamics via right heart catheterization (RHC) were performed pre-TAVR. Patients were stratified per mean PA pressure (mPAP), diastolic pulmonary gradient (DPG) and pulmonary vascular resistance (PVR), and followed at 1-month and 1-year intervals up to 6 years. MACE outcomes included cardiovascular death and heart failure hospitalizations post-TAVR.
RESULTS
Among 215 patients, Kaplan-Meir estimates demonstrated an increased 1-year risk of MACE from 8% among those without pre-TAVR PH to 27% among patients with pre-existing PH. Specifically, the MACE risk was 32% among PH patients with PVR ≥ 3WU (p = .04) and 53% among PH patients with DPG ≥ 7 mm Hg (p < .01). On univariate Cox regression, RV stroke work index (RVSWI) (HR,1.02; p = .02), and pulmonary hemodynamic index (PHI) (HR,1.27; p = .047) were identified as additional predictors of MACE post-TAVR. On multivariable Cox regression analysis, SvO2 (HR, 0.95; p = .01) and PVR (HR, 1.2; p = .04) were demonstrated as predictive of MACE post-TAVR. A significant improvement in LVEF (2-Factor ANOVA, p < .01) and RV fractional area change (RVFAC%) (p < .01) was noted as assessed at baseline, 1-month and 1-year follow up post-TAVR. There was a significant interaction between pre-TAVR PH status and time post procedure with respect to NYHA functional class (p = .03), that is, the manner and degree of change in NYHA class over time depended on pre-TAVR PH status.
CONCLUSIONS
Defining invasive pulmonary hemodynamics, such as mPAP, PVR, and DPG among patients with severe AS undergoing TAVR has significant prognostic implications. Routine risk stratification by utilizing invasive hemodynamics can better identify patients who will have functional improvement and improved outcomes post-TAVR.

Identifiants

pubmed: 36437170
pii: S1053-2498(22)02167-2
doi: 10.1016/j.healun.2022.10.001
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

275-282

Informations de copyright

Copyright © 2022 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.

Auteurs

Garima Dahiya (G)

Division of Cardiovascular Disease, Department of Medicine, University of Minnesota Medical Center, Minneapolis, Minnesota.

Andreas Kyvernitakis (A)

Division of Cardiovascular Disease, Department of Medicine, Allegheny Health Network Education Consortium, Pittsburgh, Pennsylvania.

Adee Elhamdani (A)

Department of Internal Medicine, Allegheny Health Network Education Consortium, Pittsburgh, Pennsylvania.

Andrew Begg (A)

Department of Internal Medicine, Allegheny Health Network Education Consortium, Pittsburgh, Pennsylvania.

Mark Doyle (M)

Division of Cardiovascular Disease, Department of Medicine, Allegheny Health Network Education Consortium, Pittsburgh, Pennsylvania.

Mahmoud Elsayed (M)

Division of Cardiovascular Disease, Department of Medicine, Allegheny Health Network Education Consortium, Pittsburgh, Pennsylvania.

Stephen Bailey (S)

Department of Thoracic and Cardiovascular Surgery, Allegheny Health Network Education Consortium, Pittsburgh, Pennsylvania.

Amresh Raina (A)

Division of Cardiovascular Disease, Department of Medicine, Allegheny Health Network Education Consortium, Pittsburgh, Pennsylvania.

Manreet Kanwar (M)

Division of Cardiovascular Disease, Department of Medicine, Allegheny Health Network Education Consortium, Pittsburgh, Pennsylvania.

Robert W W Biederman (RWW)

Division of Cardiovascular Disease, Department of Medicine, Allegheny Health Network Education Consortium, Pittsburgh, Pennsylvania.

Raymond L Benza (RL)

Division of Cardiovascular Medicine and Pulmonary Hypertension, Department of Medicine, Ohio State University Wexner Medical Center, Columbus, Ohio. Electronic address: raymond.benza@osumc.edu.

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