Impacts of hippocampal blood flow on changes in left ventricular wall thickness in patients with chronic heart failure.


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 07 2020
Historique:
received: 03 09 2019
revised: 04 01 2020
accepted: 09 01 2020
pubmed: 21 1 2020
medline: 15 5 2021
entrez: 21 1 2020
Statut: ppublish

Résumé

Although depressive symptoms increased mortality and hospitalization in chronic heart failure (CHF) patients, the underlying mechanism remains unclear. The aim of this study was to investigate whether an alteration in hippocampal perfusion, which is the neural substrate of depressive symptoms, is associated with changes in cardiac structures and/or functions in CHF patients. We used baseline data of 70 CHF patients (66.8 ± 8.9 yrs, 32.5% women), including cerebral blood flow (CBF) in the hippocampus, geriatric depression scale (GDS) scores and echocardiographic parameters, in the Brain Assessment and Investigation in Heart Failure Trial (B-HeFT) (UMIN000008584). Echocardiography was repeated at 3.1 ± 0.5 years after the baseline evaluation. We first tested voxel-wise regression model with hippocampal CBF as dependent variable and each of echocardiographic parameter change as independent variable, adjusted for age and sex. Structural equation modeling was used to test a mediation effect of cognitive test scores on associations between hippocampal perfusion and changes in cardiac structures and/or functions. Baseline anterior hippocampal CBF was negatively correlated with changes in left ventricular posterior wall thickness (PWT) (P < 0.05 with family-wise error corrections). An existence of depressive symptoms was positively correlated with the baseline anterior CBF and negatively with the PWT changes (P < 0.05, both). There were both direct effects of the baseline anterior hippocampal CBF on PWT thinning and effects mediated through the depressive symptoms (P < 0.05, both). This study provides the first evidence that the alteration in hippocampal perfusion may lead to changes in cardiac structures via increase in depressive symptoms in CHF patients.

Sections du résumé

BACKGROUND
Although depressive symptoms increased mortality and hospitalization in chronic heart failure (CHF) patients, the underlying mechanism remains unclear. The aim of this study was to investigate whether an alteration in hippocampal perfusion, which is the neural substrate of depressive symptoms, is associated with changes in cardiac structures and/or functions in CHF patients.
METHODS
We used baseline data of 70 CHF patients (66.8 ± 8.9 yrs, 32.5% women), including cerebral blood flow (CBF) in the hippocampus, geriatric depression scale (GDS) scores and echocardiographic parameters, in the Brain Assessment and Investigation in Heart Failure Trial (B-HeFT) (UMIN000008584). Echocardiography was repeated at 3.1 ± 0.5 years after the baseline evaluation. We first tested voxel-wise regression model with hippocampal CBF as dependent variable and each of echocardiographic parameter change as independent variable, adjusted for age and sex. Structural equation modeling was used to test a mediation effect of cognitive test scores on associations between hippocampal perfusion and changes in cardiac structures and/or functions.
RESULTS
Baseline anterior hippocampal CBF was negatively correlated with changes in left ventricular posterior wall thickness (PWT) (P < 0.05 with family-wise error corrections). An existence of depressive symptoms was positively correlated with the baseline anterior CBF and negatively with the PWT changes (P < 0.05, both). There were both direct effects of the baseline anterior hippocampal CBF on PWT thinning and effects mediated through the depressive symptoms (P < 0.05, both).
CONCLUSIONS
This study provides the first evidence that the alteration in hippocampal perfusion may lead to changes in cardiac structures via increase in depressive symptoms in CHF patients.

Identifiants

pubmed: 31955976
pii: S0167-5273(19)34386-4
doi: 10.1016/j.ijcard.2020.01.019
pii:
doi:

Types de publication

Clinical Trial Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

103-107

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

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

Déclaration de conflit d'intérêts

Declaration of competing interest None declared.

Auteurs

Hideaki Suzuki (H)

Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.

Yasuharu Matsumoto (Y)

Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.

Koichiro Sugimura (K)

Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.

Jun Takahashi (J)

Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.

Satoshi Miyata (S)

Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.

Yoshihiro Fukumoto (Y)

Division of Cardiovascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan.

Yasuyuki Taki (Y)

Department of Nuclear Medicine and Radiology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.

Hiroaki Shimokawa (H)

Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan. Electronic address: shimo@cardio.med.tohoku.ac.jp.

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Classifications MeSH