Quantification of epicardial fat by computed tomography: Why, when and how?

doi:10.1016/j.jcct.2013.01.002

Journal of Cardiovascular Computed Tomography

Volume 7, Issue 1, January–February 2013, Pages 3-10

https://doi.org/10.1016/j.jcct.2013.01.002 Get rights and content

Abstract

In the past decade, interest has grown in the relation between epicardial fat and cardiovascular disease. Several imaging modalities such as echocardiography, computed tomography, and magnetic resonance imaging can be used to quantify epicardial adipose tissue. Computed tomography provides high spatial resolution and true volume coverage of the heart; therefore, it constitutes an attractive approach to quantifying epicardial fat. An increasing body of evidence has been accumulated which shows a relation between epicardial fat volume and coronary atherosclerosis, cardiovascular outcomes, and even non–atherosclerotic heart disease such as atrial fibrillation. The association of increased epicardial fat volume with cardiac disease remains significant even after correction for weight, body mass index, and traditional cardiovascular risk factors. The mechanisms have not been reliably identified, but metabolic properties of epicardial fat may play a role. At the present time, epicardial fat quantification is not included in recommended algorithms for risk stratification. However, the available data are intriguing enough to warrant further research.

Introduction

Within the pericardial sac, adipose tissue surrounds the myocardium. Epicardial fat creates a smooth surface and, along with the pericardial fluid, facilitates motion of the heart relative to the pericardium. Interestingly, the amount and distribution of epicardial fat varies widely between persons and are not strictly related to body mass index (BMI) or obesity. The coronary arteries are embedded in epicardial fat over most of their course. In fact, a growing body of evidence indicates that there is a significant relation between epicardial fat and coronary artery disease (CAD).1, 2, 3, 4, 5, 6 Even for non–atherosclerotic diseases, such as atrial fibrillation, a correlation to epicardial fat has been proposed.⁷ This review provides an overview of the current literature about epicardial fat, its quantification, and its relation to cardiac disease.

Section snippets

Definition of epicardial fat

The terminology used to define fat deposits surrounding the heart in the current literature is diverse and, to some extent, confusing. It includes terms such as “epicardial,” “pericardial,” “paracardiac,” and “intrathoracic” fat.2, 3, 5, 8, 9, 10, 11, 12, 13 The term pericardial fat is frequently used in most of the published literature and refers to adipose tissue enclosed within the pericardial sac. It is hence the fat contained in the pericardial space, between the serous epicardium and the

Epicardial fat: A metabolically active fat depot?

The importance of differentiating adipose tissue within and outside the pericardium lies in the fact that they are anatomically, embryologically, and biochemically different.11, 12 Furthermore, convincing data indicate that epicardial fat is metabolically active and functions as a source of several adipokines, which leads some researchers to assume that, through paracrine or vasocrine mechanisms, there may be a direct interaction between epicardial fat on the one hand and the closely related

Epicardial fat and relation to coronary atherosclerosis

Because of the close proximity of epicardial fat to the coronary arteries, the hypothesis of a direct mediator-related role in the development and progression of coronary atherosclerosis has been generated, and it has received increasing support over the past decade through 2 lines of evidence. First, the amount of epicardial fat seems to be relatively independent from overall adipose body tissue but, like intra-abdominal visceral fat, shows an association to atherosclerosis. Second,

Epicardial fat and cardiovascular outcome

Analysis of cardiovascular events in follow-up studies represents the true “gold standard” for risk stratification measures. In a case–cohort study by Ding et al,³⁸ intrathoracic fat volume (15 mm above and 30 mm below the superior extent of the left main coronary artery) quantified in a baseline CT of 972 persons with no incident CAD (myocardial infarction, resuscitated cardiac arrest, angina, or fatal coronary heart disease) randomly selected from 6814 Multi-Ethnic Study of Atherosclerosis

Epicardial fat and non–atherosclerotic heart disease

A number of studies have shown associations of epicardial fat with non–coronary heart disease, including striking associations to atrial fibrillation. Recently Al Chekakie et al⁷ demonstrated that epicardial fat as quantified by CT was highly associated with paroxysmal and persistent atrial fibrillation independent of traditional risk factors, including left atrial enlargement. Patients with atrial fibrillation had significantly larger epicardial fat volumes than patients in sinus rhythm, and

Quantification of epicardial fat

Several imaging modalities, including echocardiography, magnetic resonance, and CT, have been used over the past decade for in vivo quantification of epicardial fat. Surrogate parameters to estimate the true volume of epicardial fat include epicardial fat thickness, pericoronary fat thickness, and epicardial fat areas in single cross sections. However, given the considerable interindividual differences in the distribution of epicardial fat, it is questionable whether such surrogate parameters

Epicardial fat: What is normal and what is abnormal?

The absence of standardized reference values for epicardial fat volumes is a main limitation for a widespread use in clinical routine. Little data are available to determine cut-off values for what should be considered abnormally high epicardial fat or cardiac adipostiy. In a community-based sample of >3000 middle-aged persons, Thanassouslis et al⁸ quantified epicardial and paracardiac fat volumes in participants from the Framingham Heart study. For the overall sample, the median values for

Clinical implications: When to quantify epicardial fat?

With the current body of evidence, epicardial fat assessment cannot yet be recommended to use in clinical routine. No uniform algorithms are available for data acquisition, interpretation, and epicardial fat quantification, and data are insufficient about the normal distribution of fat volumes in the population. Available data about the prognostic benefit are not sufficiently strong to justify performing a cardiac CT examination for the sole purpose of quantifying epicardial fat, and it is

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The expansion rate of AAA correlated positively with the EATV index (R = 0.237; P < .001). The initial aneurysm diameter (P < .001) and EATV index (P = .009) differed significantly between the two groups. The cutoff for the EATV index was 60.3 cm³/m² (area under the curve, 0.658; 95% confidence interval [CI], 0.568–0.749; sensitivity, 1.000; specificity, 0.309). Multivariate analysis revealed that the initial aneurysm diameter and an EATV index of >60.3 cm³/m² were significantly associated with the AAA expansion rate.
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Epicardial fat tissue, coronary arterial calcification and mortality in patients with advanced chronic kidney disease and hemodialysis
2021, Nefrologia
Citation Excerpt :
The distinction between the different locations of fat deposits is important, since pericardial fat has specific metabolic characteristics and different blood drainage.13–17 The quantification of EAT is not standardized, the studies are heterogeneous in terms of radiological technique and the location of the fat, and there is no consensus on the reference ranges.13,18 In patients with advanced CKD or undergoing renal replacement therapy, the volume of EAT has been linked to coronary artery calcification (CaC), atherosclerosis, inflammation and malnutrition.12,19–22
Epicardial and mediastinal adipose tissue (EAT, MAT) are linked to metabolic syndrome and coronary artery disease. Patients with chronic kidney disease (CKD) have thicker EAT. We assessed if EAT and MAT could be associated with increased mortality and cardiovascular events in patients with advanced CKD and haemodialysis therapy.
A post-hoc study was performed. We analyzed a prospective series of 104 cases. EAT thickness was quantified by a multislice synchronized computed tomography (MSCT).
The follow-up period was 112.68 (109.94–115.42) months. The optimal cut-off point of EAT for prediction of total mortality was 11.45 mm (92.86% and 43.75%). EAT thickness was associated with serum albumin levels, serum triglyceride levels, phosphorus and calcium phosphate product. The EAT was greater in haemodialysis patients compared to those with advanced CKD (P < .001). Patients with diabetes mellitus had greater EAT and MAT thickness (P = .018). At the end of follow up, the survival average time of patients with EAT thickness <11.45 mm was 97.48 months vs. 76.65 months for thickness > 11.45 mm (P = .007).
A higher EAT and MAT thickness was associated with increased mortality. Furthermore, EAT was associated with lower free survival time to fatal and non-fatal cardiovascular events. The measurement of EAT and MAT by MSCT could be a prognostic tool to predict cardiovascular events and mortality risk in advanced CKD patients.
El tejido graso epicardico (EAT) y mediastínico (MAT) se relaciona con el síndrome metabólico y la enfermedad arterial coronaria. Los pacientes con enfermedad renal crónica (ERC) tienen mayor volumen de EAT. El objetivo de nuestro estudio fue determinar si estos depósitos adiposos podrían estar relacionados con un aumento de mortalidad y eventos cardiovasculares en pacientes con ERC avanzada y en hemodiálisis.
Se realizó un análisis post hoc de una serie prospectiva, de 104 casos, con una tomografía computarizada sincronizada multicorte (MSCT) que permitiera cuantificar el grosor EAT.
El periodo de seguimiento fue de 112,68 (109,94-115,42) meses. El punto de corte de EAT con mayor sensibilidad y especificidad para predecir mortalidad total fue 11,45 mm (el 92,86 y el 43,75%, respectivamente). Las variables que se correlacionaron con el EAT fueron la albúmina, el nivel sérico de triglicéridos, de fósforo y el producto fosfo-cálcico. El EAT fue mayor en pacientes en hemodiálisis respecto aquellos con ERC avanzada (p < 0,001). Los pacientes con diabetes mellitus tenían mayor grosor de EAT y MAT (p = 0,018). La supervivencia media de los pacientes con EAT < 11,45 mm fue de 97,48 meses vs. 76,65 meses para un grosor > 11,45 mm (p = 0,007).
Un mayor grosor de EAT y MAT se relacionó con un incremento de mortalidad total. Además, el EAT se asoció con una menor supervivencia libre de eventos cardiovasculares fatales y no fatales. La cuantificación de EAT y MAT mediante MSCT podría tener valor pronóstico para pacientes con ERC avanzada y hemodiálisis.

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: Conflict of interest: Stephan Achenbach received research support from Bayer Schering Pharma and Siemens.

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Review ArticleQuantification of epicardial fat by computed tomography: Why, when and how?

Abstract

Introduction

Section snippets

Definition of epicardial fat

Epicardial fat: A metabolically active fat depot?

Epicardial fat and relation to coronary atherosclerosis

Epicardial fat and cardiovascular outcome

Epicardial fat and non–atherosclerotic heart disease

Quantification of epicardial fat

Epicardial fat: What is normal and what is abnormal?

Clinical implications: When to quantify epicardial fat?

Atherosclerosis

Atherosclerosis

J Am Coll Cardiol

Atherosclerosis

Am J Cardiol

Am Heart J

Atherosclerosis

Metabolism

Cardiovasc Pathol

Atherosclerosis

J Am Coll Cardiol

Atherosclerosis

Atherosclerosis

Atherosclerosis

Nutr Metab Cardiovasc Dis

JACC Cardiovasc Imaging

J Nucl Cardiol

Am J Clin Nutr

JACC Cardiovasc Imaging

J Am Coll Cardiol

Am J Cardiol

Atherosclerosis

Review Article
Quantification of epicardial fat by computed tomography: Why, when and how?