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Vol. 30. Issue 5.
Pages 230-239 (September - October 2018)
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Vol. 30. Issue 5.
Pages 230-239 (September - October 2018)
Review article
DOI: 10.1016/j.artere.2018.09.001
Interplay between epicardial adipose tissue, metabolic and cardiovascular diseases
Interacción entre tejido adiposo epicárdico, enfermedades metabólicas y cardiovasculares
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Olga Bornacheaa,b, Angela Veaa, Vicenta Llorente-Cortesa,b,c,
Corresponding author
a Institute of Biomedical Research IIB-Sant Pau, Barcelona, Spain
b Institute of Biomedical Research of Barcelona (IibB)-CSIC, Barcelona, Spain
c CIBERCV, Instituto de Salud Carlos III, Madrid, Spain
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Table 1. Bioactive EAT-secreted molecules. Potential biomarkers have been marked in bold.
Abstract

Cardiovascular disease is the primary cause of death in obese and diabetic patients. In these groups of patients, the alterations of epicardial adipose tissue (EAT) contribute to both vascular and myocardial dysfunction. Therefore, it is of clinical interest to determine the mechanisms by which EAT influences cardiovascular disease. Two key factors contribute to the tight intercommunication among EAT, coronary arteries and myocardium. One is the close anatomical proximity between these tissues. The other is the capacity of EAT to secrete cytokines and other molecules with paracrine and vasocrine effects on the cardiovascular system. Epidemiological studies have demonstrated that EAT thickness is associated with not only metabolic syndrome but also atherosclerosis and heart failure. The evaluation of EAT using imaging modalities, although effective, presents several disadvantages including radiation exposure, limited availability and elevated costs. Therefore, there is a clinical interest in EAT as a source of new biomarkers of cardiovascular and endocrine alterations. In this review, we revise the mechanisms involved in the protective and pathological role of EAT and present the molecules released by EAT with greater potential to become biomarkers of cardiometabolic alterations.

Keywords:
Epicardial adipose tissue
Cytokines
Coronary arteries
Myocardium
Abbreviations:
CAD
CD40L
CRP
EAT
FFA
GLP-1
HbA1c
HMG-CoA
LDL
LRP1
MESA
MMP
NFLAD
NSTEMI
SAT
sCD40L
SFRP4
sLRP1
TGF-β
TIMI
TIMP-3
TNF-α
T1DM
T2DM
UCP-1
Resumen

Las enfermedades cardiovasculares son la primera causa de muerte en pacientes obesos y diabéticos. Las alteraciones del tejido adiposo epicárdico (TAE) contribuyen a la disfunción vascular y del miocardio en estos pacientes. Es por tanto de interés clínico determinar los mecanismos por los cuales el TAE influye en la enfermedad cardiovascular. Aquí resumimos los mecanismos que subyacen a la asociación entre TAE, síndrome metabólico y enfermedades cardiovasculares. Dos factores contribuyen a la estrecha intercomunicación entre el TAE, las arterias coronarias y el miocardio. Uno es la estrecha proximidad anatómica entre estos tejidos. El otro es la capacidad del TAE para secretar citocinas con efectos paracrinos y vasocrinos en el sistema cardiovascular. Estudios epidemiológicos han demostrado que el grosor del TAE está asociado no solo con el síndrome metabólico sino también con la aterosclerosis y la insuficiencia cardíaca. La evaluación del TAE utilizando técnicas de imagen, aunque eficaz presenta desventajas tales como la exposición a la radiación, la disponibilidad limitada y los costes elevados. Por lo tanto, existe un interés clínico en el TAE como fuente de nuevos biomarcadores de alteraciones cardiovasculares y endocrinas. En este artículo, revisamos los mecanismos implicados en el papel protector y patológico del TAE y presentamos las moléculas liberadas por el TAE con mayor potencial para convertirse en biomarcadores de alteraciones cardiometabólicas.

Palabras clave:
Tejido adiposo epicárdico
Citocinas
Arterias coronarias
Miocardio

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