Impact of Left Ventricular Outflow Tract Calcification on Outcomes Following Transcatheter Aortic Valve Replacement.


Journal

Cardiovascular revascularization medicine : including molecular interventions
ISSN: 1878-0938
Titre abrégé: Cardiovasc Revasc Med
Pays: United States
ID NLM: 101238551

Informations de publication

Date de publication:
02 2022
Historique:
received: 07 07 2021
accepted: 07 07 2021
pubmed: 3 10 2021
medline: 26 3 2022
entrez: 2 10 2021
Statut: ppublish

Résumé

We aimed to determine left ventricular outflow tract (LVOT) calcification impact following transcatheter aortic valve replacement (TAVR) with contemporary transcatheter heart valves. Recent studies reported a higher rate of 2-year mortality with greater than moderate LVOT calcium, but they have not established a reliable and validated method to assess the degree of valve calcification and utilized first-generation valves for their analyses. We conducted a retrospective analysis of patients who underwent TAVR at our institution from 2013 through 2017 with available valves. LVOT calcification quantification was assessed as a continuous variable. We included 273 patients: 179 had a non-calcified LVOT (NOLVOTCA) and 96 had a calcified LVOT (LVOTCA). Balloon post-dilatation (BPD) was utilized in 31.3% of LVOTCA vs. 19% of NOLVOTCA (p = 0.029). The Evolut R valve was used in 40.6% vs. 23.4% (p = 0.002), while the Sapien 3 was used in 59.4% vs. 76.6% (p = 0.004), for the LVOTCA and NOLVOTCA, respectively. Paravalvular leak (PVL) at hospital discharge was higher in LVOTCA (47.5%) versus NOLVOTCA (29.1%; p = 0.004). All-cause mortality (11.5% vs. 10.1%; p = 0.5) and need for permanent pacemaker implantation were similar between the groups. There was a positive trend between LVOT calcification volume and the probability of any PVL (OR 1.012; 95% CI, 0.99-1.02). TAVR performed in patients with calcified LVOT is safe, but LVOT calcification adversely impacts TAVR outcomes, with a higher PVL rate despite greater usage of BPD. Calcium quantification did not predict any PVL degree post-TAVR.

Sections du résumé

BACKGROUND
We aimed to determine left ventricular outflow tract (LVOT) calcification impact following transcatheter aortic valve replacement (TAVR) with contemporary transcatheter heart valves. Recent studies reported a higher rate of 2-year mortality with greater than moderate LVOT calcium, but they have not established a reliable and validated method to assess the degree of valve calcification and utilized first-generation valves for their analyses.
MATERIALS/METHODS
We conducted a retrospective analysis of patients who underwent TAVR at our institution from 2013 through 2017 with available valves. LVOT calcification quantification was assessed as a continuous variable.
RESULTS
We included 273 patients: 179 had a non-calcified LVOT (NOLVOTCA) and 96 had a calcified LVOT (LVOTCA). Balloon post-dilatation (BPD) was utilized in 31.3% of LVOTCA vs. 19% of NOLVOTCA (p = 0.029). The Evolut R valve was used in 40.6% vs. 23.4% (p = 0.002), while the Sapien 3 was used in 59.4% vs. 76.6% (p = 0.004), for the LVOTCA and NOLVOTCA, respectively. Paravalvular leak (PVL) at hospital discharge was higher in LVOTCA (47.5%) versus NOLVOTCA (29.1%; p = 0.004). All-cause mortality (11.5% vs. 10.1%; p = 0.5) and need for permanent pacemaker implantation were similar between the groups. There was a positive trend between LVOT calcification volume and the probability of any PVL (OR 1.012; 95% CI, 0.99-1.02).
CONCLUSIONS
TAVR performed in patients with calcified LVOT is safe, but LVOT calcification adversely impacts TAVR outcomes, with a higher PVL rate despite greater usage of BPD. Calcium quantification did not predict any PVL degree post-TAVR.

Identifiants

pubmed: 34598904
pii: S1553-8389(21)00515-7
doi: 10.1016/j.carrev.2021.07.010
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1-7

Informations de copyright

Copyright © 2021. Published by Elsevier Inc.

Auteurs

Anees Musallam (A)

Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, DC, USA.

Kyle D Buchanan (KD)

Section of Interventional Cardiology, St. Clair Hospital, Pittsburgh, PA, USA.

Charan Yerasi (C)

Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, DC, USA.

Aaphtaab Dheendsa (A)

Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, DC, USA.

Cheng Zhang (C)

Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, DC, USA.

Corey Shea (C)

Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, DC, USA.

Brian C Case (BC)

Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, DC, USA.

Brian J Forrestal (BJ)

Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, DC, USA.

Lowell F Satler (LF)

Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, DC, USA.

Itsik Ben-Dor (I)

Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, DC, USA.

Rebecca Torguson (R)

The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Toby Rogers (T)

Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, DC, USA; Cardiovascular Branch, Division of Intramural Research, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.

Ron Waksman (R)

Section of Interventional Cardiology, MedStar Washington Hospital Center, Washington, DC, USA. Electronic address: ron.waksman@medstar.net.

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