Serum resistin as an independent marker of aortic stiffness in patients with coronary artery disease

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Abstract

Background

Subjects with higher carotid–femoral pulse wave velocity (cfPWV) will be at an increased risk for cardiovascular (CV) events in future. Resistin is an inflammatory mediator and a biomarker of CV diseases. We evaluated the association between serum resistin and aortic stiffness in patients with coronary artery disease (CAD).

Methods

A total of 104 patients with CAD were enrolled in this study. cfPWV was measured using the SphygmoCor system. Patients with cfPWV >10 m/s were defined as the high aortic stiffness group.

Results

Thirty-seven patients (35.6%) had high aortic stiffness and higher percentages of diabetes ( p = 0.001), were of older age ( p = 0.001) and had higher waist circumference ( p < 0.001), systolic blood pressure ( p = 0.027), pulse pressure ( p = 0.013), high-sensitivity C-reactive protein ( p < 0.001) and resistin levels ( p < 0.001) but lower estimated glomerular filtration rate ( p = 0.009) compared to subjects with low aortic stiffness. After adjusting for factors significantly associated with aortic stiffness by multivariate logistic regression analysis, serum resistin (odds ratio = 1.275, 95% confidence interval: 1.065–1.527, p = 0.008) was also found to be an independent predictor of aortic stiffness in patients with CAD.

Conclusions

Serum resistin level is a biomarker for aortic stiffness in patients with CAD.

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Most cited references 28

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Inflammation, immunity, and hypertensive end-organ damage.

William G McMaster, Annet Kirabo, Meena S Madhur … (2015)

For >50 years, it has been recognized that immunity contributes to hypertension. Recent data have defined an important role of T cells and various T cell-derived cytokines in several models of experimental hypertension. These studies have shown that stimuli like angiotensin II, deoxycorticosterone acetate-salt, and excessive catecholamines lead to formation of effector like T cells that infiltrate the kidney and perivascular regions of both large arteries and arterioles. There is also accumulation of monocyte/macrophages in these regions. Cytokines released from these cells, including interleukin-17, interferon-γ, tumor necrosis factorα, and interleukin-6 promote both renal and vascular dysfunction and damage, leading to enhanced sodium retention and increased systemic vascular resistance. The renal effects of these cytokines remain to be fully defined, but include enhanced formation of angiotensinogen, increased sodium reabsorption, and increased renal fibrosis. Recent experiments have defined a link between oxidative stress and immune activation in hypertension. These have shown that hypertension is associated with formation of reactive oxygen species in dendritic cells that lead to formation of gamma ketoaldehydes, or isoketals. These rapidly adduct to protein lysines and are presented by dendritic cells as neoantigens that activate T cells and promote hypertension. Thus, cells of both the innate and adaptive immune system contribute to end-organ damage and dysfunction in hypertension. Therapeutic interventions to reduce activation of these cells may prove beneficial in reducing end-organ damage and preventing consequences of hypertension, including myocardial infarction, heart failure, renal failure, and stroke.

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Vascular Fibrosis in Aging and Hypertension: Molecular Mechanisms and Clinical Implications

Adam Harvey, Augusto C. Montezano, Rhéure Alves Moreira Lopes … (2016)

Aging is the primary risk factor underlying hypertension and incident cardiovascular disease. With aging, the vasculature undergoes structural and functional changes characterized by endothelial dysfunction, wall thickening, reduced distensibility, and arterial stiffening. Vascular stiffness results from fibrosis and extracellular matrix (ECM) remodelling, processes that are associated with aging and are amplified by hypertension. Some recently characterized molecular mechanisms underlying these processes include increased expression and activation of matrix metalloproteinases, activation of transforming growth factor-β1/SMAD signalling, upregulation of galectin-3, and activation of proinflammatory and profibrotic signalling pathways. These events can be induced by vasoactive agents, such as angiotensin II, endothelin-1, and aldosterone, which are increased in the vasculature during aging and hypertension. Complex interplay between the “aging process” and prohypertensive factors results in accelerated vascular remodelling and fibrosis and increased arterial stiffness, which is typically observed in hypertension. Because the vascular phenotype in a young hypertensive individual resembles that of an elderly otherwise healthy individual, the notion of “early” or “premature” vascular aging is now often used to describe hypertension-associated vascular disease. We review the vascular phenotype in aging and hypertension, focusing on arterial stiffness and vascular remodelling. We also highlight the clinical implications of these processes and discuss some novel molecular mechanisms of fibrosis and ECM reorganization.

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Human resistin: found in translation from mouse to man.

Mark D Schwartz, Aurel A. Lazar (2011)

The discovery of resistin 10 years ago as a fat cell-secreted factor that modulates insulin resistance suggested a link to the current obesity-associated epidemics of diabetes and cardiovascular disease, which are major human health concerns. Although adipocyte-derived resistin is indisputably linked to insulin resistance in rodent models, the relevance of human resistin is complicated because human resistin is secreted by macrophages rather than adipocytes, and because of the descriptive nature of human epidemiology. In this review, we examine the recent and growing evidence that human resistin is an inflammatory biomarker and a potential mediator of diabetes and cardiovascular disease. Copyright © 2011 Elsevier Ltd. All rights reserved.

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Author and article information

Contributors

Ji-Hung Wang: Role: ConceptualizationRole: Data curationRole: Writing – original draft

Chung-Jen Lee: Role: Data curationRole: Formal analysis

Chiu-Fen Yang: Role: Data curationRole: Formal analysis

Yu-Chih Chen: Role: Data curationRole: Formal analysis

Bang-Gee Hsu:

ORCID: http://orcid.org/0000-0001-9364-4558

Role: ConceptualizationRole: Formal analysisRole: Funding acquisitionRole: SupervisionRole: Writing – original draftRole: Writing – review & editing

Yan Chen: Role: Editor

Journal

Journal ID (nlm-ta): PLoS One

Journal ID (iso-abbrev): PLoS ONE

Journal ID (publisher-id): plos

Journal ID (pmc): plosone

Title: PLoS ONE

Publisher: Public Library of Science (San Francisco, CA USA )

ISSN (Electronic): 1932-6203

Publication date (Electronic): 14 August 2017

Publication date Collection: 2017

Volume: 12

Issue: 8

Electronic Location Identifier: e0183123

Affiliations

[1 ] Division of Cardiology, Buddhist Tzu Chi General Hospital, Hualien, Taiwan

[2 ] School of Medicine, Tzu Chi University, Hualien, Taiwan

[3 ] Department of Nursing, Tzu Chi University of Science and Technology, Hualien, Taiwan

[4 ] Division of Nephrology, Buddhist Tzu Chi General Hospital, Hualien, Taiwan

Institute for Nutritional Sciences, CHINA

Author notes

Competing Interests: The authors have declared that no competing interests exist.

* E-mail: gee.lily@ 123456msa.hinet.net

Author information

Bang-Gee Hsu http://orcid.org/0000-0001-9364-4558

Article

Publisher ID: PONE-D-17-09685

DOI: 10.1371/journal.pone.0183123

PMC ID: 5555662

PubMed ID: 28806778

SO-VID: 2f26586f-3b15-4b4b-bc75-4c59159cacfe

License:

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

History

Date received : 11 March 2017

Date accepted : 31 July 2017

Page count

Figures: 0, Tables: 4, Pages: 11

Funding

Funded by: This work was supported by grants from Tzu Chi Hospital in Taiwan

Award ID: TCRD 101-03

Award Recipient :

ORCID: http://orcid.org/0000-0001-9364-4558

Bang-Gee Hsu

This work was supported by Grant TCRD 101-03 from Tzu Chi Hospital in Taiwan. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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Serum resistin as an independent marker of aortic stiffness in patients with coronary artery disease

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Abstract

Background

Methods

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Conclusions

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Most cited references 28

Inflammation, immunity, and hypertensive end-organ damage.

Vascular Fibrosis in Aging and Hypertension: Molecular Mechanisms and Clinical Implications

Human resistin: found in translation from mouse to man.

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