Inflammation and Cardiovascular Diseases in the Elderly: The Role of Epicardial Adipose Tissue.

aortic stenosis atrial fibrillation cardiovascular diseases coronary artery disease elderly epicardial adipose tissue heart failure inflammation

Journal

Frontiers in medicine
ISSN: 2296-858X
Titre abrégé: Front Med (Lausanne)
Pays: Switzerland
ID NLM: 101648047

Informations de publication

Date de publication:
2022
Historique:
received: 27 12 2021
accepted: 13 01 2022
entrez: 4 3 2022
pubmed: 5 3 2022
medline: 5 3 2022
Statut: epublish

Résumé

Human aging is a complex phenomenon characterized by a wide spectrum of biological changes which impact on behavioral and social aspects. Age-related changes are accompanied by a decline in biological function and increased vulnerability leading to frailty, thereby advanced age is identified among the major risk factors of the main chronic human diseases. Aging is characterized by a state of chronic low-grade inflammation, also referred as inflammaging. It recognizes a multifactorial pathogenesis with a prominent role of the innate immune system activation, resulting in tissue degeneration and contributing to adverse outcomes. It is widely recognized that inflammation plays a central role in the development and progression of numerous chronic and cardiovascular diseases. In particular, low-grade inflammation, through an increased risk of atherosclerosis and insulin resistance, promote cardiovascular diseases in the elderly. Low-grade inflammation is also promoted by visceral adiposity, whose accumulation is paralleled by an increased inflammatory status. Aging is associated to increase in epicardial adipose tissue (EAT), the visceral fat depot of the heart. Structural and functional changes in EAT have been shown to be associated with several heart diseases, including coronary artery disease, aortic stenosis, atrial fibrillation, and heart failure. EAT increase is associated with a greater production and secretion of pro-inflammatory mediators and neuro-hormones, so that thickened EAT can pathologically influence, in a paracrine and vasocrine manner, the structure and function of the heart and is associated to a worse cardiovascular outcome. In this review, we will discuss the evidence underlying the interplay between inflammaging, EAT accumulation and cardiovascular diseases. We will examine and discuss the importance of EAT quantification, its characteristics and changes with age and its clinical implication.

Identifiants

pubmed: 35242789
doi: 10.3389/fmed.2022.844266
pmc: PMC8887867
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

844266

Informations de copyright

Copyright © 2022 Conte, Petraglia, Poggio, Valerio, Cabaro, Campana, Comentale, Attena, Russo, Pilato, Formisano, Leosco and Parisi.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Maddalena Conte (M)

Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy.
Casa di Cura San Michele, Maddaloni, Italy.

Laura Petraglia (L)

Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy.

Paolo Poggio (P)

Centro Cardiologico Monzino IRCCS, Milan, Italy.

Vincenza Valerio (V)

Centro Cardiologico Monzino IRCCS, Milan, Italy.

Serena Cabaro (S)

Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy.

Pasquale Campana (P)

Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy.

Giuseppe Comentale (G)

Department of Advanced Biomedical Science, University of Naples Federico II, Naples, Italy.

Emilio Attena (E)

Department of Cardiology, Monaldi Hospital, Naples, Italy.

Vincenzo Russo (V)

Department of Medical Translational Sciences, Monaldi Hospital, University of Campania Luigi Vanvitelli, Campania, Italy.

Emanuele Pilato (E)

Department of Advanced Biomedical Science, University of Naples Federico II, Naples, Italy.

Pietro Formisano (P)

Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy.

Dario Leosco (D)

Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy.

Valentina Parisi (V)

Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy.

Classifications MeSH