Differential Peripheral Inflammatory Factors Associated with Cognitive Function in Patients with Heart Failure

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Abstract

Objective: Cognitive deficits are common in patients with heart failure (HF), and can negatively affect self-care, predict rehospitalizations, and increase mortality rates 5-fold. Inflammation can produce vascular pathology, reducing cerebral blood flow to brain regions necessary for optimal cognitive function. The purpose of the investigation was to identify a pattern of peripheral blood inflammation-related biomarkers associated with cognitive impairment in patients with HF. Methods: Forty-five outpatients (median age = 67 years, SD = 9.9) were recruited from University of California, San Diego (UCSD) and Veterans Affairs San Diego Healthcare Systems (VASDHS), diagnosed with New York Heart Association Stages I–III HF. Participants were administered the Montreal Cognitive Assessment (MoCA) as a measure of global cognitive impairment, and blood was analyzed for plasma biomarkers, interferon-γ, tumor necrosis factor-α (TNFα), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), brain-derived neurotrophic factor (BDNF), interleukin-8 (IL-8), matrix metallopeptidase-9 (MMP-9), IL-6, C-reactive protein (CRP), and serum amyloid-A (SAA). Results: Almost half the patients scored below the threshold on the MoCA, indicating at least mild cognitive impairment. A factor analysis produced three biomarker factors: vascular inflammatory factor-1: TNFα, sICAM1, sVCAM1; neuroinflammatory factor-2: BDNF, MMP-9, IL-8; peripheral inflammatory factor-3: IL-6, CRP, SAA. Only vascular inflammatory factor-1 was significantly associated with cognitive function (MoCA) (Δ R<sup>2</sup> = 0.214, beta = –0.468, p = 0.008). Conclusions: In this cohort with HF, vascular inflammation appears related to poorer cognitive function. This could indicate targets for treatment to reduce cognitive deficits in HF. However, this is a preliminary study, and further research is needed.

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Most cited references 35

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TNF-mediated inflammatory disease.

JR Bradley (2008)

TNF was originally described as a circulating factor that can cause necrosis of tumours, but has since been identified as a key regulator of the inflammatory response. This review describes the known signalling pathways and cell biological effects of TNF, and our understanding of the role of TNF in human disease. TNF interacts with two different receptors, designated TNFR1 and TNFR2, which are differentially expressed on cells and tissues and initiate both distinct and overlapping signal transduction pathways. These diverse signalling cascades lead to a range of cellular responses, which include cell death, survival, differentiation, proliferation and migration. Vascular endothelial cells respond to TNF by undergoing a number of pro-inflammatory changes, which increase leukocyte adhesion, transendothelial migration and vascular leak and promote thrombosis. The central role of TNF in inflammation has been demonstrated by the ability of agents that block the action of TNF to treat a range of inflammatory conditions, including rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease and psoriasis. The increased incidence of infection in patients receiving anti-TNF treatment has highlighted the physiological role of TNF in infectious diseases. 2007 Pathological Society of Great Britain and Ireland

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Circulating adhesion molecules VCAM-1, ICAM-1, and E-selectin in carotid atherosclerosis and incident coronary heart disease cases: the Atherosclerosis Risk In Communities (ARIC) study.

Shih-Jen Hwang, Christie Ballantyne, A. Richey Sharrett … (1997)

Recruitment of circulating leukocytes at sites of atherosclerosis is mediated through a family of adhesion molecules. The function of circulating forms of these adhesion molecules remains unknown, but their levels may serve as molecular markers of subclinical coronary heart disease (CHD). To determine the ability of circulating vascular cell adhesion molecule-1 (VCAM-1), endothelial-leukocyte adhesion molecule-1 (E-selectin), and intercellular adhesion molecule-1 (ICAM-1) to serve as molecular markers of atherosclerosis and predictors of incident CHD, we studied 204 patients with incident CHD, 272 patients with carotid artery atherosclerosis (CAA), and 316 control subjects from the large, biracial Atherosclerosis Risk In Communities (ARIC) study. Levels of VCAM-1 were not significantly different among the patients with incident CHD, those with CAA, and control subjects. Higher levels of E-selectin and ICAM-1 were observed for the patients with CHD (means [ng/mL]: E-selectin, 38.4; ICAM-1, 288.7) and those with CAA (E-selectin, 41.5; ICAM-1, 283.6) compared with the control subjects (E-selectin, 32.8; ICAM-1, 244.2), but the distributions were not notably different between the patients with CHD and CAA. Results of logistic regression analyses indicated that the relationship of ICAM-1 and E-selectin with CHD and CAA was independent of other known CHD risk factors and was most pronounced in the highest quartile. The odds of CHD and CAA were 5.53 (95% CI, 2.51-12.21) and 2.64 (95% CI, 1.40-5.01), respectively, for those with levels of ICAM-1 in the highest quartile compared with those in the lowest quartile. Odds of CAA were 2.03 (95% CI, 1.14-3.62) for those with levels of E-selectin in the highest quartile compared with those in the lowest quartile. These data indicate that plasma levels of ICAM-1 and E-selectin may serve as molecular markers for atherosclerosis and the development of CHD.

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Exploratory Factor Analysis With Small Sample Sizes.

J. de Winter*, D. Dodou*, P Wieringa (2009)

Exploratory factor analysis (EFA) is generally regarded as a technique for large sample sizes (N), with N = 50 as a reasonable absolute minimum. This study offers a comprehensive overview of the conditions in which EFA can yield good quality results for N below 50. Simulations were carried out to estimate the minimum required N for different levels of loadings (λ), number of factors (f), and number of variables (p) and to examine the extent to which a small N solution can sustain the presence of small distortions such as interfactor correlations, model error, secondary loadings, unequal loadings, and unequal p/f. Factor recovery was assessed in terms of pattern congruence coefficients, factor score correlations, Heywood cases, and the gap size between eigenvalues. A subsampling study was also conducted on a psychological dataset of individuals who filled in a Big Five Inventory via the Internet. Results showed that when data are well conditioned (i.e., high λ, low f, high p), EFA can yield reliable results for N well below 50, even in the presence of small distortions. Such conditions may be uncommon but should certainly not be ruled out in behavioral research data. ∗ These authors contributed equally to this work.

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Journal

Journal ID (publisher-id): NIM

Journal ID (nlm-ta): Neuroimmunomodulation

Journal ID (doi): 10.1159/issn.1021-7401

Title: Neuroimmunomodulation

Publisher: S. Karger AG

ISSN (Print): 1021-7401

ISSN (Electronic): 1423-0216

Publication date Subscription-year: 2018

Publication date (Print): December 2018

Publication date (Electronic): 23 October 2018

Volume: 25

Issue: 3

Pages: 146-152

Affiliations

[_a] _aDepartment of Psychiatry, University of California San Diego, San Diego, California, USA

[_b] _bDepartment of Family Medicine and Public Health, University of California San Diego, San Diego, California, USA

[_c] _cCollege of Nursing, University of South Florida, Tampa, Florida, USA

Author notes

*Laura S. Redwine, PhD, College of Nursing, University of South Florida, 12901 Bruce B. Downs Blvd., MDC22, Tampa, FL 33612-4766 (USA), E-Mail lredwine@health.usf.edu

Author information

Laura S. Redwine https://orcid.org/0000-0001-7633-2034

Article

Publisher ID: 493142 Other ID: Neuroimmunomodulation 2018;25:146–152

DOI: 10.1159/000493142

PubMed ID: 30352444

SO-VID: 0c7292ba-c9fd-463d-ace4-b7c74e0bd0dc

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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 16 May 2018

Date accepted : 19 August 2018

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Figures: 1, Tables: 3, Pages: 7

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Differential Peripheral Inflammatory Factors Associated with Cognitive Function in Patients with Heart Failure

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Karger: Endocrinology

Most cited references 35

TNF-mediated inflammatory disease.

Circulating adhesion molecules VCAM-1, ICAM-1, and E-selectin in carotid atherosclerosis and incident coronary heart disease cases: the Atherosclerosis Risk In Communities (ARIC) study.

Exploratory Factor Analysis With Small Sample Sizes.

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