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

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Native T1 and T2 provide distinctive signatures in hypertrophic cardiac conditions - Comparison of uremic, hypertensive and hypertrophic cardiomyopathy. / Arcari, L; Hinojar, R; Engel, J; Freiwald, T; Platschek, S; Zainal, H; Zhou, H; Vasquez, M; Keller, T; Rolf, A; Geiger, H; Hauser, I; Vogl, TJ; Zeiher, AM; Puntmann, VO.

In: INT J CARDIOL, Vol. 306, 03.2020, p. 102-108.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Arcari, L, Hinojar, R, Engel, J, Freiwald, T, Platschek, S, Zainal, H, Zhou, H, Vasquez, M, Keller, T, Rolf, A, Geiger, H, Hauser, I, Vogl, TJ, Zeiher, AM & Puntmann, VO 2020, 'Native T1 and T2 provide distinctive signatures in hypertrophic cardiac conditions - Comparison of uremic, hypertensive and hypertrophic cardiomyopathy', INT J CARDIOL, vol. 306, pp. 102-108. https://doi.org/10.1016/j.ijcard.2020.03.002

APA

Arcari, L., Hinojar, R., Engel, J., Freiwald, T., Platschek, S., Zainal, H., Zhou, H., Vasquez, M., Keller, T., Rolf, A., Geiger, H., Hauser, I., Vogl, TJ., Zeiher, AM., & Puntmann, VO. (2020). Native T1 and T2 provide distinctive signatures in hypertrophic cardiac conditions - Comparison of uremic, hypertensive and hypertrophic cardiomyopathy. INT J CARDIOL, 306, 102-108. https://doi.org/10.1016/j.ijcard.2020.03.002

Vancouver

Arcari L, Hinojar R, Engel J, Freiwald T, Platschek S, Zainal H et al. Native T1 and T2 provide distinctive signatures in hypertrophic cardiac conditions - Comparison of uremic, hypertensive and hypertrophic cardiomyopathy. INT J CARDIOL. 2020 Mar;306:102-108. https://doi.org/10.1016/j.ijcard.2020.03.002

Bibtex

@article{b8ab5d42fd694b18b5559f700b8175f1,
title = "Native T1 and T2 provide distinctive signatures in hypertrophic cardiac conditions - Comparison of uremic, hypertensive and hypertrophic cardiomyopathy",
abstract = "AimsProfound 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.MethodsIn 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).ResultsNative 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.ConclusionsOur 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.",
author = "L Arcari and R Hinojar and J Engel and T Freiwald and S Platschek and H Zainal and H Zhou and M Vasquez and T Keller and A Rolf and H Geiger and I Hauser and TJ Vogl and AM Zeiher and VO Puntmann",
year = "2020",
month = mar,
doi = "10.1016/j.ijcard.2020.03.002",
language = "English",
volume = "306",
pages = "102--108",
journal = "INT J CARDIOL",
issn = "0167-5273",
publisher = "Elsevier Ireland Ltd",

}

RIS

TY - JOUR

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

AU - Arcari, L

AU - Hinojar, R

AU - Engel, J

AU - Freiwald, T

AU - Platschek, S

AU - Zainal, H

AU - Zhou, H

AU - Vasquez, M

AU - Keller, T

AU - Rolf, A

AU - Geiger, H

AU - Hauser, I

AU - Vogl, TJ

AU - Zeiher, AM

AU - Puntmann, VO

PY - 2020/3

Y1 - 2020/3

N2 - AimsProfound 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.MethodsIn 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).ResultsNative 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.ConclusionsOur 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.

AB - AimsProfound 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.MethodsIn 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).ResultsNative 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.ConclusionsOur 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.

UR - http://europepmc.org/abstract/med/32169347

U2 - 10.1016/j.ijcard.2020.03.002

DO - 10.1016/j.ijcard.2020.03.002

M3 - SCORING: Journal article

C2 - 32169347

VL - 306

SP - 102

EP - 108

JO - INT J CARDIOL

JF - INT J CARDIOL

SN - 0167-5273

ER -