Native T1 and T2 provide distinctive signatures in hypertrophic cardiac conditions - Comparison of uremic, hypertensive and hypertrophic cardiomyopathy.


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 05 2020
Historique:
received: 29 09 2019
revised: 26 02 2020
accepted: 02 03 2020
pubmed: 15 3 2020
medline: 20 5 2021
entrez: 15 3 2020
Statut: ppublish

Résumé

Profound left ventricular (LV) hypertrophy with diastolic dysfunction and heart failure is the cardinal manifestation of heart remodelling in chronic kidney disease (CKD). Previous studies related increased T1 mapping values in CKD with diffuse fibrosis. Native T1 is a non-specific readout that may also relate to increased intramyocardial fluid. We examined concomitant T1 and T2 mapping signatures and undertook comparisons with other hypertrophic conditions. In this prospective multicentre study, consecutive CKD patients (n = 154) undergoing routine clinical cardiac magnetic resonance (CMR) imaging were compared with patients with hypertensive (HTN, n = 163) and hypertrophic cardiomyopathy (HCM, n = 158), and normotensive controls (n = 133). Native T1 was significantly higher in all patient groups, whereas native T2 in CKD only (p < 0.001 vs. all groups). Native T1 and T2 were interrelated in patient groups and the strength of association was condition-specific (CKD r = 0.558, HTN r = 0.324, both p < 0.001; HCM r = 0.157, p = 0.05). Native T1 and T2 were similarly correlated in all CKD stages (S3 r = 0.501, S4 0.586, S5 r = 0.424, p < 0.001 for all). Native T1 was the strongest myocardial discriminator between patients and controls (area under the curve, AUC HCM: 0.97; CKD: 0.97, HTN 0.98), native T2 between CKD vs HCM (AUC 0.90) and native T1 and T2 between CKD vs HTN (AUC: 0.83 and 0.80 respectively), p < 0.001 for all. Our findings reveal different CMR signatures of common hypertrophic cardiac phenotypes. Native T1 was raised in all conditions, indicating the presence of pathologic hypertrophic remodelling. Markedly raised native T2 was CKD-specific, suggesting a prominent role of intramyocardial fluid.

Identifiants

pubmed: 32169347
pii: S0167-5273(19)34753-9
doi: 10.1016/j.ijcard.2020.03.002
pii:
doi:

Substances chimiques

Contrast Media 0

Types de publication

Journal Article Multicenter Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

102-108

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors report no relationships that could be construed as a conflict of interest.

Auteurs

Luca Arcari (L)

Institute of Experimental and Translational Cardiac Imaging, DZHK Centre for Cardiovascular Imaging, Goethe University Hospital Frankfurt, Frankfurt am Main, Germany; Cardiology Unit, Clinical and Molecular Medicine Department, Faculty of Medicine and Psychology, "Sapienza" University of Rome, Rome, Italy.

Rocio Hinojar (R)

Institute of Experimental and Translational Cardiac Imaging, DZHK Centre for Cardiovascular Imaging, Goethe University Hospital Frankfurt, Frankfurt am Main, Germany; Department of Cardiology, University Hospital Ramón y Cajal, Madrid, Spain.

Juergen Engel (J)

Department of Nephrology, Goethe University Hospital Frankfurt, Frankfuret-am Main, Germany.

Tilo Freiwald (T)

Department of Nephrology, Goethe University Hospital Frankfurt, Frankfuret-am Main, Germany.

Steffen Platschek (S)

Department of Nephrology, Goethe University Hospital Frankfurt, Frankfuret-am Main, Germany.

Hafisyatul Zainal (H)

Institute of Experimental and Translational Cardiac Imaging, DZHK Centre for Cardiovascular Imaging, Goethe University Hospital Frankfurt, Frankfurt am Main, Germany; Department of Cardiology, Universiti Teknologi MARA (UiTM), Sg. Buloh, Malaysia.

Hui Zhou (H)

Institute of Experimental and Translational Cardiac Imaging, DZHK Centre for Cardiovascular Imaging, Goethe University Hospital Frankfurt, Frankfurt am Main, Germany; Department of Radiology, XiangYa Hospital, Central South University, Changsha, Hunan, China.

Moises Vasquez (M)

Institute of Experimental and Translational Cardiac Imaging, DZHK Centre for Cardiovascular Imaging, Goethe University Hospital Frankfurt, Frankfurt am Main, Germany; Department of Cardiology, Enrique Baltodano Briceño Hospital, Liberia, Costa Rica.

Till Keller (T)

Department of Cardiology, Kerckhoff Hospital, University Giessen, Bad Nauheim, Germany.

Andreas Rolf (A)

Department of Cardiology, Kerckhoff Hospital, University Giessen, Bad Nauheim, Germany.

Helmut Geiger (H)

Department of Nephrology, Goethe University Hospital Frankfurt, Frankfuret-am Main, Germany.

Ingeborg Hauser (I)

Department of Nephrology, Goethe University Hospital Frankfurt, Frankfuret-am Main, Germany.

Thomas J Vogl (TJ)

Department of Radiology, Goethe University Hospital Frankfurt, Frankfurt-am Main, Germany.

Andreas M Zeiher (AM)

Department of Radiology, Goethe University Hospital Frankfurt, Frankfurt-am Main, Germany.

Massimo Volpe (M)

Cardiology Unit, Clinical and Molecular Medicine Department, Faculty of Medicine and Psychology, "Sapienza" University of Rome, Rome, Italy; IRCCS Neuromed, Pozzilli, Italy.

Eike Nagel (E)

Institute of Experimental and Translational Cardiac Imaging, DZHK Centre for Cardiovascular Imaging, Goethe University Hospital Frankfurt, Frankfurt am Main, Germany.

Valentina O Puntmann (VO)

Institute of Experimental and Translational Cardiac Imaging, DZHK Centre for Cardiovascular Imaging, Goethe University Hospital Frankfurt, Frankfurt am Main, Germany; Department of Cardiology, Goethe University Hospital Frankfurt, Frankfurt-am Main, Germany. Electronic address: vppapers@icloud.com.

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