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Nature Reviews. Cardiology Sep 2022Interest in epicardial adipose tissue (EAT) is growing rapidly, and research in this area appeals to a broad, multidisciplinary audience. EAT is unique in its anatomy... (Review)
Review
Interest in epicardial adipose tissue (EAT) is growing rapidly, and research in this area appeals to a broad, multidisciplinary audience. EAT is unique in its anatomy and unobstructed proximity to the heart and has a transcriptome and secretome very different from that of other fat depots. EAT has physiological and pathological properties that vary depending on its location. It can be highly protective for the adjacent myocardium through dynamic brown fat-like thermogenic function and harmful via paracrine or vasocrine secretion of pro-inflammatory and profibrotic cytokines. EAT is a modifiable risk factor that can be assessed with traditional and novel imaging techniques. Coronary and left atrial EAT are involved in the pathogenesis of coronary artery disease and atrial fibrillation, respectively, and it also contributes to the development and progression of heart failure. In addition, EAT might have a role in coronavirus disease 2019 (COVID-19)-related cardiac syndrome. EAT is a reliable potential therapeutic target for drugs with cardiovascular benefits such as glucagon-like peptide 1 receptor agonists and sodium-glucose co-transporter 2 inhibitors. This Review provides a comprehensive and up-to-date overview of the role of EAT in cardiovascular disease and highlights the translational nature of EAT research and its applications in contemporary cardiology.
Topics: Adipose Tissue; Atrial Fibrillation; COVID-19; Cardiology; Humans; Pericardium
PubMed: 35296869
DOI: 10.1038/s41569-022-00679-9 -
The American Journal of Clinical... Mar 2022Current global food systems threaten human health and environmental sustainability. In 2019, the EAT-Lancet Commission on healthy diets from sustainable food systems...
BACKGROUND
Current global food systems threaten human health and environmental sustainability. In 2019, the EAT-Lancet Commission on healthy diets from sustainable food systems defined the first global reference diet to improve both areas, but there is no consensus on how to quantify the EAT-Lancet reference diet as a diet index, and its relation to mortality has not been widely studied.
OBJECTIVES
We sought to develop a new dietary index to quantify adherence to the EAT-Lancet diet and assess its association with mortality in a large, population-based Swedish cohort. We also examined food components included in the index and their individual associations with mortality.
METHODS
We used the Malmö Diet and Cancer cohort (n = 22,421; 45-73 years old at baseline). Dietary data were collected using a modified diet history method. The EAT-Lancet index was developed based on intake levels and reference intervals of 14 food components defined in the EAT-Lancet diet (0-3 points per component; 0-42 points in total). Associations with mortality were examined based on registers during a mean of 20 years of follow-up and were adjusted for potential confounders.
RESULTS
Divided into 5 adherence groups, the highest adherence to the EAT-Lancet diet (≥23 points) was associated with lower all-cause mortality (HR, 0.75; 95% CI, 0.67-0.85), cancer mortality (HR, 0.76; 95% CI, 0.63-0.92), and cardiovascular mortality (HR, 0.68; 95% CI, 0.54-0.84) than the lowest adherence (≤13 points). Several food components included in the index contributed to the observed reductions in mortality.
CONCLUSIONS
We developed a new dietary index to investigate adherence to the EAT-Lancet diet. The findings indicate a 25% lower risk of mortality among those with the highest adherence to the EAT-Lancet diet, as defined using our index, which adds to the evidence base for the development of sustainable dietary guidelines.
Topics: Aged; Diet; Diet, Healthy; Humans; Middle Aged; Neoplasms; Nutrition Policy; Sweden
PubMed: 34791011
DOI: 10.1093/ajcn/nqab369 -
Metabolism: Clinical and Experimental Apr 2023In 2019, the EAT-Lancet Commission proposed a mainly plant-based diet that nurtures human health and supports environmental sustainability. However, its association with...
BACKGROUND AND AIMS
In 2019, the EAT-Lancet Commission proposed a mainly plant-based diet that nurtures human health and supports environmental sustainability. However, its association with type 2 diabetes (T2D) has not been widely studied, and it remains unclear whether genetic susceptibility for T2D can modify this association. The aim was therefore to investigate the association between the EAT-Lancet diet and risk of T2D and assess whether the association differs by the genetic predisposition to T2D.
METHODS
A total of 24,494 participants from the Malmö Diet and Cancer study were analyzed. Dietary intake was assessed using a modified diet history methodology, and an EAT-Lancet diet index (range from 0 to 42 points) was constructed based on the EAT-Lancet reference diet. National and local registers were used to identify T2D cases during follow-up. Cox proportional hazards regression model was applied to estimate the association between the EAT-Lancet diet index and risk of T2D. Genetic predisposition to T2D was captured based on 116 single nucleotide polymorphisms.
RESULTS
During a median of 24.3 years of follow-up, 4197 (17.1 %) T2D cases were documented. Compared with those with the lowest adherence to the EAT-Lancet diet (≤13 points), participants who had the highest adherence (≥23 points) showed an 18 % (95 % CI: 4 %-30 %) lower risk of T2D (P for trend <0.01). There was no significant multiplicative interaction between genetic predisposition to T2D and the EAT-Lancet diet index (P = 0.59). Also, no significant additive interaction between the genetic risk and the EAT-Lancet diet was seen (P = 0.44). The highest risk was observed among the 22.9 % of the individuals with high genetic risk and low EAT-Lancet diet score (HR = 1.79; 95 % CI: 1.63, 1.96).
CONCLUSIONS
Our findings indicate that high adherence to the EAT-Lancet diet was associated with decreased risk of incident T2D among people with different genetic risks.
Topics: Humans; Adult; Diabetes Mellitus, Type 2; Genetic Predisposition to Disease; Sweden; Prospective Studies; Diet; Risk Factors
PubMed: 36682448
DOI: 10.1016/j.metabol.2023.155401 -
Nutrients Oct 2023Several studies have explored the association between diabetes and the EAT-Lancet diet. Thus, the objective of our study was to conduct a systematic review to analyze... (Review)
Review
Several studies have explored the association between diabetes and the EAT-Lancet diet. Thus, the objective of our study was to conduct a systematic review to analyze and summarize all clinical studies concerning the association between diabetes and the EAT-Lancet diet. We undertook a comprehensive search of the Embase, Cochrane, and PubMed databases up to 15 August 2023. All clinical studies concerning the association between diabetes and the EAT-Lancet diet were summarized and analyzed. In total, our systematic review included five studies of four prospective studies and one cross-sectional study, encompassing 259,315 participants. All the included studies were evaluated as high quality. The outcomes from all studies indicated that adherence to the EAT-Lancet diet was correlated with a reduced risk of diabetes. In conclusion, the EAT-Lancet diet may be an effective dietary intervention for diabetes. Nevertheless, the number of studies examining the association between diabetes and the EAT-Lancet diet is limited. Further high-quality studies are required to expand our understanding of the benefits of the EAT-Lancet diet for patients with diabetes.
Topics: Humans; Cross-Sectional Studies; Prospective Studies; Diet; Diabetes Mellitus, Type 2
PubMed: 37892537
DOI: 10.3390/nu15204462 -
American Journal of Physiology. Heart... Feb 2022Obesity is associated with higher risks of cardiac arrhythmias. Although this may be partly explained by concurrent cardiometabolic ill-health, growing evidence suggests... (Review)
Review
Obesity is associated with higher risks of cardiac arrhythmias. Although this may be partly explained by concurrent cardiometabolic ill-health, growing evidence suggests that increasing adiposity independently confers risk for arrhythmias. Among fat depots, epicardial adipose tissue (EAT) exhibits a proinflammatory secretome and, given the lack of fascial separation, has been implicated as a transducer of inflammation to the underlying myocardium. The present review explores the mechanisms underpinning adverse electrophysiological remodeling as a consequence of EAT accumulation and the consequent inflammation. We first describe the physiological and pathophysiological function of EAT and its unique secretome and subsequently discuss the evidence for ionic channel and connexin expression modulation as well as fibrotic remodeling induced by cytokines and free fatty acids that are secreted by EAT. Finally, we highlight how weight reduction and regression of EAT volume may cause reverse remodeling to ameliorate arrhythmic risk.
Topics: Adipose Tissue; Animals; Arrhythmias, Cardiac; Cytokines; Humans; Ion Channels; Pericardium
PubMed: 34890279
DOI: 10.1152/ajpheart.00565.2021 -
Journal of Clinical Medicine Mar 2019Epicardial adipose tissue (EAT) is derived from splanchnic mesoderm, localized anatomically between the myocardium and pericardial visceral layer, and surrounds the... (Review)
Review
Epicardial adipose tissue (EAT) is derived from splanchnic mesoderm, localized anatomically between the myocardium and pericardial visceral layer, and surrounds the coronary arteries. Being a metabolically active organ, EAT secretes numerous cytokines, which moderate cardiovascular morphology and function. Through its paracrine and vasocrine secretions, EAT may play a prominent role in modulating cardiac function. EAT protects the heart in normal physiological conditions by secreting a variety of adipokines with anti-atherosclerotic properties, and in contrast, secretes inflammatory molecules in pathologic conditions that may play a dynamic role in the pathogenesis of cardiovascular diseases by promoting atherosclerosis. Considerable research has been focused on comparing the anatomical and biochemical features of EAT in healthy people, and a variety of disease conditions such as cardiovascular diseases and renal diseases. The global cardiovascular morbidity and mortality in renal disease are high, and there is a paucity of concrete evidence and societal guidelines to detect early cardiovascular disease (CVD) in this group of patients. Here we performed a clinical review on the existing evidence and knowledge on EAT in patients with renal disease, to evaluate its application as a reliable, early, noninvasive biomarker and indicator for CVD, and to assess its significance in cardiovascular risk stratification.
PubMed: 30832377
DOI: 10.3390/jcm8030299 -
Frontiers in Cardiovascular Medicine 2022Atrial Fibrillation (AF) is the most frequent cardiac arrhythmia and its prevalence increases with age. AF is strongly associated with an increased risk of stroke, heart... (Review)
Review
Atrial Fibrillation (AF) is the most frequent cardiac arrhythmia and its prevalence increases with age. AF is strongly associated with an increased risk of stroke, heart failure and cardiovascular mortality. Among the risk factors associated with AF onset and severity, obesity and inflammation play a prominent role. Numerous recent evidence suggested a role of epicardial adipose tissue (EAT), the visceral fat depot of the heart, in the development of AF. Several potential arrhythmogenic mechanisms have been attributed to EAT, including myocardial inflammation, fibrosis, oxidative stress, and fat infiltration. EAT is a local source of inflammatory mediators which potentially contribute to atrial collagen deposition and fibrosis, the anatomical substrate for AF. Moreover, the close proximity between EAT and myocardium allows the EAT to penetrate and generate atrial myocardium fat infiltrates that can alter atrial electrophysiological properties. These observations support the hypothesis of a strong implication of EAT in structural and electrical atrial remodeling, which underlies AF onset and burden. The measure of EAT, through different imaging methods, such as echocardiography, computed tomography and cardiac magnetic resonance, has been proposed as a useful prognostic tool to predict the presence, severity and recurrence of AF. Furthermore, EAT is increasingly emerging as a promising potential therapeutic target. This review aims to summarize the recent evidence exploring the potential role of EAT in the pathogenesis of AF, the main mechanisms by which EAT can promote structural and electrical atrial remodeling and the potential therapeutic strategies targeting the cardiac visceral fat.
PubMed: 35845044
DOI: 10.3389/fcvm.2022.932262 -
The British Journal of Radiology Sep 2020Epicardial adipose tissue (EAT) is a metabolically activated beige adipose tissue, non-homogeneously surrounding the myocardium. Physiologically, EAT regulates toxic... (Review)
Review
Epicardial adipose tissue (EAT) is a metabolically activated beige adipose tissue, non-homogeneously surrounding the myocardium. Physiologically, EAT regulates toxic fatty acids, protects the coronary arteries against mechanical strain, regulates proinflammatory cytokines, stimulates the production of nitric oxide, reduces oxidative stress, and works as a thermogenic source against hypothermia. Conversely, EAT has pathologic paracrine interactions with the surrounded vessels, and might favour the onset of atrial fibrillation. In addition, initial atherosclerotic lesions can promote inflammation and trigger the EAT production of cytokines increasing vascular inflammation, which, in turn, may help the development of collateral vessels but also of self-stimulating, dysregulated inflammatory process, increasing coronary artery disease severity. Variations in EAT were also linked to metabolic syndrome. Echocardiography first estimated EAT measuring its thickness on the free wall of the right ventricle but does not allow accurate volumetric EAT estimates. Cardiac CT (CCT) and cardiac MR (CMR) allow for three-dimensional EAT estimates, the former showing higher spatial resolution and reproducibility but being limited by radiation exposure and long segmentation times, the latter being radiation-free but limited by lower spatial resolution and reproducibility, higher cost, and difficulties for obese patients. EAT radiodensity at CCT could to be related to underlying metabolic processes. The correlation between EAT and response to certain pharmacological therapies has also been investigated, showing promising results. In the future, semi-automatic or fully automatic techniques, machine/deep-learning methods, if validated, will facilitate research for various EAT measures and may find a place in CCT/CMR reporting.
Topics: Adipose Tissue, Beige; Biomarkers; Coronary Artery Disease; Coronary Vessels; Cytokines; Echocardiography; Heart; Humans; Magnetic Resonance Imaging; Myocardium; Pericardium; Reproducibility of Results; Tomography, X-Ray Computed
PubMed: 31782934
DOI: 10.1259/bjr.20190770 -
Frontiers in Endocrinology 2022Ischemia with non-obstructive coronary artery (INOCA) is a blind spot of coronary artery disease (CAD). Such patients are often reassured but offered no specific care,... (Review)
Review
Ischemia with non-obstructive coronary artery (INOCA) is a blind spot of coronary artery disease (CAD). Such patients are often reassured but offered no specific care, that lead to a heightened risk of adverse cerebrovascular disease (CVD) outcomes. Epicardial adipose tissue (EAT) is proven to correlate independently with CAD and its severity, but it is unknown whether EAT is a specific and sensitive indicator of INOCA. This review focuses on the INOCA epidemiology and related factors, as well as the association between EAT.
Topics: Humans; Coronary Artery Disease; Pericardium; Ischemia; Adipose Tissue
PubMed: 36743934
DOI: 10.3389/fendo.2022.1028429 -
Biology Feb 2022Cardiovascular diseases (CVDs) are the leading causes of death worldwide. Epicardial adipose tissue (EAT) is defined as a fat depot localized between the myocardial... (Review)
Review
Cardiovascular diseases (CVDs) are the leading causes of death worldwide. Epicardial adipose tissue (EAT) is defined as a fat depot localized between the myocardial surface and the visceral layer of the pericardium and is a type of visceral fat. EAT is one of the most important risk factors for atherosclerosis and cardiovascular events and a promising new therapeutic target in CVDs. In health conditions, EAT has a protective function, including protection against hypothermia or mechanical stress, providing myocardial energy supply from free fatty acid and release of adiponectin. In patients with obesity, metabolic syndrome, or diabetes mellitus, EAT becomes a deleterious tissue promoting the development of CVDs. Previously, we showed an adverse modulation of gene expression in pericoronary adipose tissue in patients with coronary artery disease (CAD). Here, we summarize the currently available evidence regarding the role of EAT in the development of CVDs, including CAD, heart failure, and atrial fibrillation. Due to the rapid development of the COVID-19 pandemic, we also discuss data regarding the association between EAT and the course of COVID-19. Finally, we present the potential therapeutic possibilities aiming at modifying EAT's function. The development of novel therapies specifically targeting EAT could revolutionize the prognosis in CVDs.
PubMed: 35336728
DOI: 10.3390/biology11030355