Epicardial Adipose Tissue Attenuation and Fat Attenuation Index: Phantom Study and In-Vivo Measurements With Photon-Counting CT

Obesity is associated with elevated inflammatory signals from various adipose tissue depots. This study aimed to evaluate release of regulated on activation, normal T cell expressed and secreted (RANTES) by human adipose tissue in vivo and ex vivo, in reference to monocyte chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6) release. Arteriovenous differences of RANTES, MCP-1, and IL-6 were studied in vivo across the abdominal subcutaneous adipose tissue in healthy Caucasian subjects with a wide range of adiposity. Systemic levels and ex vivo RANTES release were studied in abdominal subcutaneous, gastric fat pad, and omental adipose tissue from morbidly obese bariatric surgery patients and in thoracic subcutaneous and epicardial adipose tissue from cardiac surgery patients without coronary artery disease. Arteriovenous studies confirmed in vivo RANTES and IL-6 release in adipose tissue of lean and obese subjects and release of MCP-1 in obesity. However, in vivo release of MCP-1 and RANTES, but not IL-6, was lower than circulating levels. Ex vivo release of RANTES was greater from the gastric fat pad compared with omental ( P = 0.01) and subcutaneous ( P = 0.001) tissue. Epicardial adipose tissue released less RANTES than thoracic subcutaneous adipose tissue in lean ( P = 0.04) but not obese subjects. Indexes of obesity correlated with epicardial RANTES but not with systemic RANTES or its release from other depots. In conclusion, RANTES is released by human subcutaneous adipose tissue in vivo and in varying amounts by other depots ex vivo. While it appears unlikely that the adipose organ contributes significantly to circulating levels, local implications of this chemokine deserve further investigation.

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Editorial Comment: New Photon-Counting Detector CT Technology May Improve Quantitative Evaluation of Epicardial Adipose Tissue, an Important Marker of Coronary Artery Inflammation

American Journal of Roentgenology ◽

10.2214/ajr.21.27233 ◽

2021 ◽

Author(s):

David J. Murphy

Keyword(s):

Adipose Tissue ◽

Coronary Artery ◽

Editorial Comment ◽

Quantitative Evaluation ◽

Epicardial Adipose Tissue ◽

Photon Counting ◽

Photon Counting Detector ◽

Ct Technology ◽

Important Marker

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Adiponectin expression in human epicardial adipose tissue in vivo is lower in patients with coronary artery disease

Cytokine ◽

10.1016/j.cyto.2004.11.002 ◽

2005 ◽

Cited By ~ 30

Author(s):

G IACOBELLIS ◽

D PISTILLI ◽

M GUCCIARDO ◽

F LEONETTI ◽

F MIRALDI ◽

...

Keyword(s):

Coronary Artery Disease ◽

Adipose Tissue ◽

Coronary Artery ◽

Epicardial Adipose Tissue ◽

Artery Disease

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155 In vivo measurements of urethral dose using the MOSFET dosimeter post-LDR prostate brachy-therapy: A phantom study

Radiotherapy and Oncology ◽

10.1016/s0167-8140(06)80896-0 ◽

2006 ◽

Vol 80 ◽

pp. S45-S46

Author(s):

A. Ng ◽

C. Cummins-Holder ◽

J. Crook ◽

I. Yeung

Keyword(s):

Phantom Study ◽

In Vivo Measurements ◽

Urethral Dose ◽

Brachy Therapy

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Adipogenesis and epicardial adipose tissue: A novel fate of the epicardium induced by mesenchymal transformation and PPARγ activation

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1417232112 ◽

2015 ◽

Vol 112 (7) ◽

pp. 2070-2075 ◽

Cited By ~ 82

Author(s):

Yukiko Yamaguchi ◽

Susana Cavallero ◽

Michaela Patterson ◽

Hua Shen ◽

Jian Xu ◽

...

Keyword(s):

Adipose Tissue ◽

Epicardial Adipose Tissue ◽

Cardiac Fibroblasts ◽

Mammalian Species ◽

Model Organisms ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

Coronary Smooth Muscle ◽

Mesenchymal Transformation

The hearts of many mammalian species are surrounded by an extensive layer of fat called epicardial adipose tissue (EAT). The lineage origins and determinative mechanisms of EAT development are unclear, in part because mice and other experimentally tractable model organisms are thought to not have this tissue. In this study, we show that mouse hearts have EAT, localized to a specific region in the atrial–ventricular groove. Lineage analysis indicates that this adipose tissue originates from the epicardium, a multipotent epithelium that until now is only established to normally generate cardiac fibroblasts and coronary smooth muscle cells. We show that adoption of the adipocyte fate in vivo requires activation of the peroxisome proliferator activated receptor gamma (PPARγ) pathway, and that this fate can be ectopically induced in mouse ventricular epicardium, either in embryonic or adult stages, by expression and activation of PPARγ at times of epicardium–mesenchymal transformation. Human embryonic ventricular epicardial cells natively express PPARγ, which explains the abundant presence of fat seen in human hearts at birth and throughout life.

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Are Interactions between Epicardial Adipose Tissue, Cardiac Fibroblasts and Cardiac Myocytes Instrumental in Atrial Fibrosis and Atrial Fibrillation?

Cells ◽

10.3390/cells10092501 ◽

2021 ◽

Vol 10 (9) ◽

pp. 2501

Author(s):

Anirudh Krishnan ◽

Emily Chilton ◽

Jaishankar Raman ◽

Pankaj Saxena ◽

Craig McFarlane ◽

...

Keyword(s):

Atrial Fibrillation ◽

Adipose Tissue ◽

Epicardial Adipose Tissue ◽

Cardiac Fibroblasts ◽

Reactive Oxygen Species Generation ◽

The Elderly ◽

Intimate Contact ◽

Electrotonic Interactions

Atrial fibrillation is very common among the elderly and/or obese. While myocardial fibrosis is associated with atrial fibrillation, the exact mechanisms within atrial myocytes and surrounding non-myocytes are not fully understood. This review considers the potential roles of myocardial fibroblasts and myofibroblasts in fibrosis and modulating myocyte electrophysiology through electrotonic interactions. Coupling with (myo)fibroblasts in vitro and in silico prolonged myocyte action potential duration and caused resting depolarization; an optogenetic study has verified in vivo that fibroblasts depolarized when coupled myocytes produced action potentials. This review also introduces another non-myocyte which may modulate both myocardial (myo)fibroblasts and myocytes: epicardial adipose tissue. Epicardial adipocytes are in intimate contact with myocytes and (myo)fibroblasts and may infiltrate the myocardium. Adipocytes secrete numerous adipokines which modulate (myo)fibroblast and myocyte physiology. These adipokines are protective in healthy hearts, preventing inflammation and fibrosis. However, adipokines secreted from adipocytes may switch to pro-inflammatory and pro-fibrotic, associated with reactive oxygen species generation. Pro-fibrotic adipokines stimulate myofibroblast differentiation, causing pronounced fibrosis in the epicardial adipose tissue and the myocardium. Adipose tissue also influences myocyte electrophysiology, via the adipokines and/or through electrotonic interactions. Deeper understanding of the interactions between myocytes and non-myocytes is important to understand and manage atrial fibrillation.

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Functional characterization of human brown adipose tissue metabolism

Biochemical Journal ◽

10.1042/bcj20190464 ◽

2020 ◽

Vol 477 (7) ◽

pp. 1261-1286 ◽

Cited By ~ 3

Author(s):

Marie Anne Richard ◽

Hannah Pallubinsky ◽

Denis P. Blondin

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Functional Characterization ◽

Human Infants ◽

Positron Emission ◽

Brown Adipose ◽

Treatment Of Obesity ◽

And Function

Brown adipose tissue (BAT) has long been described according to its histological features as a multilocular, lipid-containing tissue, light brown in color, that is also responsive to the cold and found especially in hibernating mammals and human infants. Its presence in both hibernators and human infants, combined with its function as a heat-generating organ, raised many questions about its role in humans. Early characterizations of the tissue in humans focused on its progressive atrophy with age and its apparent importance for cold-exposed workers. However, the use of positron emission tomography (PET) with the glucose tracer [18F]fluorodeoxyglucose ([18F]FDG) made it possible to begin characterizing the possible function of BAT in adult humans, and whether it could play a role in the prevention or treatment of obesity and type 2 diabetes (T2D). This review focuses on the in vivo functional characterization of human BAT, the methodological approaches applied to examine these features and addresses critical gaps that remain in moving the field forward. Specifically, we describe the anatomical and biomolecular features of human BAT, the modalities and applications of non-invasive tools such as PET and magnetic resonance imaging coupled with spectroscopy (MRI/MRS) to study BAT morphology and function in vivo, and finally describe the functional characteristics of human BAT that have only been possible through the development and application of such tools.

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