Abstract
Background
Although epicardial adipose tissue (EAT) volume is associated with increased incidence
of coronary artery disease (CAD), its role in myocardial systolic dysfunction is unclear.
The present study aimed to identify independent determinants of EAT volume in patients
without obstructive CAD, and to evaluate the association between EAT volume (vs other
measures of obesity) and myocardial systolic strain analysis.
Methods
We prospectively recruited 130 patients without obstructive CAD on contrast-enhanced
cardiac computed tomography imaging and normal left ventricular ejection fraction
on 3-dimensional (3D) echocardiography. EAT volume was quantified from cardiac computed
tomography imaging, and 3D multidirectional (longitudinal, circumferential, radial,
and area) strain were measured.
Results
The mean EAT volume was 97.5 ± 43.7 cm3. In multivariable analysis, measures of obesity (body mass index [P = 0.007] and waist/hip ratio [P = 0.001]) were independently associated with larger EAT volume. EAT volume was correlated
with 3D global longitudinal (r = 0.601; P < 0.001), circumferential (r = 0.375; P < 0.001), radial (r = −0.546; P < 0.001), and area (r = 0.558; P < 0.001) strain. In multivariable analyses, epicardial fat volume was the strongest
predictor of 3D global longitudinal (standardized β = 0.512; P < 0.001), circumferential (standardized β = 0.242; P = 0.006), radial (standardized β = −0.422; P < 0.001), and area (standardized β = 0.428; P < 0.001) strain. In contrast, other measures of obesity including body mass index
and waist/hip ratio were not independent determinants of 3D multidirectional global
strain (all P > 0.05).
Conclusions
EAT volume is independently associated with impaired myocardial systolic function
despite preserved 3D left ventricular ejection fraction and absence of obstructive
CAD, and might play a significant role in the pathophysiology of diabetic, obesity,
and metabolic heart disease.
Résumé
Introduction
Bien que le volume du tissu adipeux de l’épicarde (TAE) soit associé à une fréquence
accrue de coronaropathie, son rôle dans la dysfonction systolique myocardique est
incertain. La présente étude visait à cerner les déterminants indépendants du volume
du TAE chez des patients exempts de coronaropathie obstructive, et à évaluer le lien
entre le volume du TAE (par rapport à d’autres mesures de l’obésité) et l’analyse
de la déformation systolique myocardique.
Méthodes
Nous avons recruté de façon prospective 130 patients chez qui la tomodensitométrie
cardiaque avec injection d’un produit de contraste n’avait pas révélé de coronaropathie
obstructive, et dont la fraction d’éjection ventriculaire gauche (FEVG) était normale
selon l’échocardiographie tridimensionnelle (3D). Le volume du TAE a été quantifié
par tomodensitométrie cardiaque, et la déformation a fait l’objet de mesures 3D et
multidirectionnelles (longitudinale, circonférentielle, radiale et de l’espace).
Résultats
Le volume moyen du TAE était de 97,5 ± 43,7 cm3. Lors de l’analyse multivariée, les mesures de l’obésité (indice de masse corporelle
[IMC; P = 0,007] et rapport taille/hanches [RTH; P = 0,001]) étaient associées de façon indépendante à un volume plus grand. Le volume
du TAE était en corrélation avec la déformation globale selon les mesures 3D et les
mesures longitudinale (r = 0,601; P < 0,001), circonférentielle (r = 0,375; P < 0,001), radiale (r = -0,546; P < 0,001) et de l’espace (r = 0,558; P < 0,001). Dans le cadre des analyses multivariées, le volume du TAE était l’indicateur
le plus fiable d’une déformation globale selon les mesures 3D et longitudinale (β
standardisé = 0,512; P < 0,001), circonférentielle (β standardisé = 0,242; P = 0,006), radiale (β standardisé = -0,422; P < 0,001) et de l’espace (β standardisé = 0,428; P < 0,001). En revanche, les autres mesures de l’obésité dont l’IMC et le RTH n’étaient
pas des déterminants indépendants de la déformation globale selon les mesures 3D et
multidirectionnelles (P > 0,05 dans tous les cas).
Conclusions
Le volume du TAE est associé de façon indépendante à une dysfonction systolique myocardique,
et ce, malgré l’absence d’altération de la FEVG, selon les mesures 3D, et de coronaropathie
obstructive, et pourrait être un facteur important de la physiopathologie de la maladie
cardiaque liée au diabète, à l’obésité et au métabolisme.
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Article info
Publication history
Published online: June 23, 2016
Accepted:
June 19,
2016
Received:
February 3,
2016
Footnotes
See page 1491 for disclosure information.
Identification
Copyright
© 2016 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
