The aortic root in repaired tetralogy of Fallot: Serial measurements and impact of losartan treatment.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
01 03 2021
Historique:
received: 16 06 2020
revised: 01 09 2020
accepted: 07 10 2020
pubmed: 26 10 2020
medline: 29 5 2021
entrez: 25 10 2020
Statut: ppublish

Résumé

Aortic root dilatation is common in adults with repaired tetralogy of Fallot (rTOF) and might lead to aortic dissection. However, little is known on progression of aortic dilatation and the effect of pharmaceutical treatment. This study aims to determine factors associated with aortic growth and investigate effects of losartan. We performed a prespecified analysis from the 1:1 randomized, double-blind REDEFINE trial. Aortic root diameters were measured at baseline and after 2.0 ± 0.3 years of follow-up using cardiovascular magnetic resonance (CMR) imaging. A total of 66 patients were included (68% men, age 40 ± 12 years, baseline aortic root 37 ± 6 mm, 32% aortic dilatation (>40 mm)). There was a trend towards slow aortic root growth (+0.6 ± 2.3 mm after two years, p = 0.06) (n = 60). LV stroke volume was the only factor associated with both a larger baseline aortic root (β: 0.09 mm/ml (95% C.I.:0.02, 0.15), p = 0.010) and with aortic growth during follow-up (β: 0.04 mm/ml (95% C.I.:0.005, 0.066), p = 0.024), after correction for age, sex, and body surface area using linear regression analysis. No treatment effect of losartan was found (p = 0.17). Aortic root dilatation was present in about one-third of rTOF patients. A larger LV stroke volume was associated with both a larger baseline aortic root and ongoing growth. Our findings provide no arguments for lower aortic diameter thresholds for prophylactic surgery compared to the general population.

Sections du résumé

BACKGROUND
Aortic root dilatation is common in adults with repaired tetralogy of Fallot (rTOF) and might lead to aortic dissection. However, little is known on progression of aortic dilatation and the effect of pharmaceutical treatment. This study aims to determine factors associated with aortic growth and investigate effects of losartan.
METHODS AND RESULTS
We performed a prespecified analysis from the 1:1 randomized, double-blind REDEFINE trial. Aortic root diameters were measured at baseline and after 2.0 ± 0.3 years of follow-up using cardiovascular magnetic resonance (CMR) imaging. A total of 66 patients were included (68% men, age 40 ± 12 years, baseline aortic root 37 ± 6 mm, 32% aortic dilatation (>40 mm)). There was a trend towards slow aortic root growth (+0.6 ± 2.3 mm after two years, p = 0.06) (n = 60). LV stroke volume was the only factor associated with both a larger baseline aortic root (β: 0.09 mm/ml (95% C.I.:0.02, 0.15), p = 0.010) and with aortic growth during follow-up (β: 0.04 mm/ml (95% C.I.:0.005, 0.066), p = 0.024), after correction for age, sex, and body surface area using linear regression analysis. No treatment effect of losartan was found (p = 0.17).
CONCLUSIONS
Aortic root dilatation was present in about one-third of rTOF patients. A larger LV stroke volume was associated with both a larger baseline aortic root and ongoing growth. Our findings provide no arguments for lower aortic diameter thresholds for prophylactic surgery compared to the general population.

Identifiants

pubmed: 33098953
pii: S0167-5273(20)33990-5
doi: 10.1016/j.ijcard.2020.10.037
pii:
doi:

Substances chimiques

Losartan JMS50MPO89

Types de publication

Journal Article Randomized Controlled Trial

Langues

eng

Sous-ensembles de citation

IM

Pagination

88-91

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest None.

Auteurs

O I Woudstra (OI)

Heart Center; Department of Clinical and Experimental Cardiology, Amsterdam UMC, University of Amsterdam, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands; Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.

A Ghanam (A)

Heart Center; Department of Clinical and Experimental Cardiology, Amsterdam UMC, University of Amsterdam, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands.

H W Vliegen (HW)

Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.

A P J van Dijk (APJ)

Department of Cardiology, Radboud University Medical Center, Nijmegen, the Netherlands.

J P van Melle (JP)

Department of Cardiology, Groningen University Medical Center, Groningen, the Netherlands.

M Groenink (M)

Heart Center; Department of Clinical and Experimental Cardiology, Amsterdam UMC, University of Amsterdam, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands.

F J Meijboom (FJ)

Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.

M C Post (MC)

Department of Cardiology, St. Antonius Hospital, Nieuwegein, the Netherlands.

B J M Mulder (BJM)

Heart Center; Department of Clinical and Experimental Cardiology, Amsterdam UMC, University of Amsterdam, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands; Netherlands Heart Institute, Utrecht, the Netherlands.

B J Bouma (BJ)

Heart Center; Department of Clinical and Experimental Cardiology, Amsterdam UMC, University of Amsterdam, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands.

J P Bokma (JP)

Heart Center; Department of Clinical and Experimental Cardiology, Amsterdam UMC, University of Amsterdam, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands. Electronic address: j.p.bokma@amsterdamumc.nl.

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