Increased Epicardial Adipose Tissue Thickness Research Articles

Evaluation of epicardial adipose tissue thickness and carotid intima-media thickness in children with Behçet's disease.

Behçet's disease (BD) is a systemic vasculitis affecting all sizes of arteries and veins. Approximately 5-10% of patients with BD are present during childhood. The chronic nature of the disease may lead to serious cardiovascular complications over time including early atherosclerosis. Increased levels of epicardial adipose tissue (EAT) and carotid intima-media thickness (CIMT) are considered early signs of subclinical atherosclerosis. Ongoing chronic inflammation may cause to increase in both EAT and CIMT. In this study, we aimed to evaluate CIMT and EAT in children with BD and determine their relationship with the clinical manifestations and course of the disease. This cross-sectional study evaluated 30 patients with juvenile-onset BD and age-sex-matched 20 healthy controls. The CIMT and EAT thickness were measured by the same paediatric cardiologist. The association between clinical features, baseline disease activity, disease duration, EAT thickness and CIMT was also evaluated. Thirty children with BD and 20 age-sex-matched healthy volunteers enrolled in the study. The most common BD-related feature was oral aphthous (n=30), followed by mucocutaneous findings (n=22). Uveitis was observed in 5 patients, vascular involvement in 4, neurological involvement in 4, and gastrointestinal involvement in 2. All patients were inactive at the time of evaluation. The EAT thickness was significantly higher in patients while CIMT levels revealed no significant differences. However, there was no correlation between disease duration, baseline disease activity, and EAT thickness. Increased EAT thickness may be a risk factor for early atherosclerosis in patients with BD. The EAT thickness was found to be significantly higher in paediatric BD patients. Confirmation of results in larger series may provide better insight into early screening for risk factors in these patients.

Epicardial Adipose Tissue and Psoriasis: A Systematic Review and Meta-Analysis.

Background: As a novel biomarker for cardiovascular diseases, epicardial adipose tissue (EAT) has been linked to psoriasis. We conducted an updated systematic review, building upon a previous report on the relationship between EAT and psoriasis. Methods: We searched Medline, Embase, and the Cochrane Central Register of Controlled Trials. The methodological quality of each study was assessed using the Newcastle-Ottawa Scale. The pooled mean difference (MD) or standardized mean difference (SMD) and the corresponding confidence interval (CIs) were calculated. Results: We included 10 studies with 1287 participants. Five of the included studies were of high methodological quality, while the other five were of moderate quality. The pooled data indicated that psoriasis patients had significantly increased EAT compared to individuals in the control group (SMD 1.53, 95% CI 0.61 to 2.45, 9 studies, 1195 participants). The subgroup analysis showed that psoriasis patients had significantly increased EAT thickness compared with the controls (SMD 2.45, 95% CI 0.73 to 4.17, 5 studies, 657 participants). Similarly, EAT area in single-slice CT images was significantly higher in the psoriasis group than in the control group (SMD 0.45, 95% CI 0.14 to 0.76, 2 studies, 195 participants). The EAT volume based on CT images appeared to be higher in the psoriasis group than in the control group, but the difference was not statistically significant (SMD 0.32, 95% CI -0.06 to 0.70, 2 studies, 343 participants). Conclusions: EAT, especially echocardiographic EAT thickness and CT-determined EAT area, was significantly associated with psoriasis, but CT-determined EAT volume was not.

Exploring the interplay between epicardial fat, coronary artery calcium score, and nonalcoholic fatty liver disease through non-ECG-gated chest computed tomography: A cross-sectional study.

This study examines the relationships between epicardial adipose tissue (EAT), nonalcoholic fatty liver disease (NAFLD), and coronary artery calcium score (CACS) using non-ECG-gated CT scans. It aims to determine the effectiveness of EAT measurements and NAFLD as predictors for coronary artery disease (CAD). This cross-sectional study was conducted at a specialized center, focusing on individuals who underwent non-ECG-gated chest CT scans without contrast. We evaluated EAT thickness and density in three areas: the right atrioventricular groove, the free wall of the right ventricle, and the central area of the right anterior interventricular groove. Additionally, we measured CACS and determined the presence of NAFLD by comparing liver-to-spleen density ratios. Statistical analyses, including regression models, were performed using SPSS (version 26). In this study, we enrolled 365 participants, including 203 males with an average age of 47 ± 17.93 years. EAT thickness was 6.28 ± 1.62 mm, and EAT density was -96.07 ± 12.47 Hounsfield units (HU). The mean CACS was 22.27 ± 79.01, and the mean liver density was 50.01 ± 10.76 HU. A significant positive correlation was observed between EAT thickness and CACS (r = 0.208, p < 0.001). EAT density showed a significant negative correlation with CACS (r = -0.155, p = 0.003). No correlation was found between NAFLD and CACS. Univariate logistic regression analysis identified significant predictors of increased CACS, including EAT thickness (OR: 1.803), EAT density (OR: 0.671), diabetes mellitus (DM) (OR: 5.921), and hypertension (HTN) (OR: 7.414). Multivariate analysis confirmed the significance of EAT thickness (OR: 0.682), DM (OR: 3.66), and HTN (OR: 2.79) as predictors of elevated CACS. Our findings demonstrate that increased EAT thickness and decreased density are associated with higher CACS. Also, both DM and HTN significantly contribute to increased CACS. These results support the inclusion of EAT measurements in cardiovascular risk assessment models to enhance diagnostic accuracy.

The adipose-neural axis is involved in epicardial adipose tissue-related cardiac arrhythmias

Dysfunction of the sympathetic nervous system and increased epicardial adipose tissue (EAT) have been independently associated with the occurrence of cardiac arrhythmia. However, their exact roles in triggering arrhythmia remain elusive. Here, using an invitro coculture system with sympathetic neurons, cardiomyocytes, and adipocytes, we show that adipocyte-derived leptin activates sympathetic neurons and increases the release of neuropeptide Y (NPY), which in turn triggers arrhythmia in cardiomyocytes by interacting with the Y1 receptor (Y1R) and subsequently enhancing the activity of the Na+/Ca2+ exchanger (NCX) and calcium/calmodulin-dependent protein kinase II (CaMKII). The arrhythmic phenotype can be partially blocked by a leptin neutralizing antibody or an inhibitor of Y1R, NCX, or CaMKII. Moreover, increased EAT thickness and leptin/NPY blood levels are detected in atrial fibrillation patients compared with the control group. Our study provides robust evidence that the adipose-neural axis contributes to arrhythmogenesis and represents a potential target for treating arrhythmia.

Impact of epicardial adipose tissue thickness on coronary artery thrombus burden in patients with ST segment elevation myocardial infarction treated by primary percutaneous coronary interventions

ABSTRACT Objectives Coronary artery thrombus burden (TB) is one of the risk factors for major adverse cardiovascular events (MACE) in patients with acute ST segment elevation myocardial infarction (STEMI). It was discovered that there is a strong relationship between epicardial adipose tissue (EAT) thickness and the incidence of coronary atherosclerosis. The aim of our study is to evaluate the relationship between EAT thickness and coronary TB in patients with STEMI treated with primary percutaneous coronary interventions (PPCI). Methods The study included 80 patients presented with acute STEMI and treated by PPCI; their mean age was 54.35 ± 8.80 years, and 70 (87.5%) were males. Patients were divided into 2 groups according to the degree of TB: group I (25 patients) with low TB and group II (55 patients) with high TB. The EAT thickness was measured by 2D-echocardiography in all patients. Results We found that EAT thickness was significantly higher in group II compared to group I (p < 0.001), and theROC curve cutoff point value of EAT thickness equal to or greater than 2.48 mm could predict high TB in patients with STEMI (p < 0.001), and by multivariate analysis, EAT thickness was the most significant predictor of high TB. Conclusions In STEMI patients undergoing primary PCI, the increased EAT thickness measured by 2D echocardiography is significantly associated with a high coronary artery thrombus burden.

Association between epicardial adipose tissue and cardiac dysfunction in subjects with severe obesity.

Epicardial adipose tissue (EAT) plays a role in obesity-related heart failure with preserved ejection fraction. However, the association of EAT thickness with the development of cardiac dysfunction in subjects with severe obesity without known cardiovascular disease is unclear. Determine the association between EAT thickness and cardiac dysfunction and describe the potential value of EAT as an early marker of cardiac dysfunction. Subjects with BMI ≥35 kg/m2 aged 35 to 65 years, who were referred for bariatric surgery, without suspicion of or known cardiac disease, were enrolled. Conventional transthoracic echocardiography and strain analyses were performed. A total of 186 subjects were divided into tertiles based on EAT thickness, of whom 62 were in EAT-1 (EAT <3.8 mm), 63 in EAT-2 (EAT 3.8-5.4 mm), and 61 in EAT-3 (EAT >5.4 mm). Parameters of systolic and diastolic function were comparable between tertiles. Patients in EAT-3 had the lowest global longitudinal strain (GLS) and left atrial contractile strain (LASct). Linear regression showed that a one-unit increase in EAT thickness (mm) was independently associated with a decrease in GLS (%) (β-coefficient - 0.404, p = 0.002), and a decrease in LASct (%) (β-coefficient - 0.544, p = 0.027). Furthermore, EAT-3 independently predicted cardiac dysfunction as defined by a GLS < 18% (OR 2.8, p = 0.013) and LASct<14% (OR 2.5, p = 0.045). Increased EAT thickness in subjects with obesity without known cardiac disease was independently associated with subclinical cardiac dysfunction. Our findings suggest that EAT might play a role in the early stages of cardiac dysfunction in obesity before this may progress to overt clinical disease. This article is protected by copyright. All rights reserved.

Epicardial Adipose Tissue Assessed by Computed Tomography and Echocardiography Are Associated With Adverse Cardiovascular Outcomes: A Systematic Review and Meta-Analysis

Epicardial adipose tissue (EAT) has garnered attention as a prognostic and risk stratification factor for cardiovascular disease. This study, via meta-analyses, evaluates the associations between EAT and cardiovascular outcomes stratified across imaging modalities, ethnic groups, and study protocols. Medline and Embase databases were searched without date restriction on May 2022 for articles that examined EAT and cardiovascular outcomes. The inclusion criteria were (1) studies measuring EAT of adult patients at baseline and (2) reporting follow-up data on study outcomes of interest. The primary study outcome was major adverse cardiovascular events. Secondary study outcomes included cardiac death, myocardial infarction, coronary revascularization, and atrial fibrillation. Twenty-nine articles published between 2012 and 2022, comprising 19 709 patients, were included in our analysis. Increased EAT thickness and volume were associated with higher risks of cardiac death (odds ratio, 2.53 [95% CI, 1.17-5.44]; P=0.020; n=4), myocardial infarction (odds ratio, 2.63 [95% CI, 1.39-4.96]; P=0.003; n=5), coronary revascularization (odds ratio, 2.99 [95% CI, 1.64-5.44]; P<0.001; n=5), and atrial fibrillation (adjusted odds ratio, 4.04 [95% CI, 3.06-5.32]; P<0.001; n=3). For 1 unit increment in the continuous measure of EAT, computed tomography volumetric quantification (adjusted hazard ratio, 1.74 [95% CI, 1.42-2.13]; P<0.001) and echocardiographic thickness quantification (adjusted hazard ratio, 1.20 [95% CI, 1.09-1.32]; P<0.001) conferred an increased risk of major adverse cardiovascular events. The utility of EAT as an imaging biomarker for predicting and prognosticating cardiovascular disease is promising, with increased EAT thickness and volume being identified as independent predictors of major adverse cardiovascular events. URL: https://www.crd.york.ac.uk/prospero; Unique identifier: CRD42022338075.

The relationship between epicardial adipose tissue thickness and arrhythmias in patients with hypertension: a 3.0T cardiac magnetic resonance study.

To investigate the relationship between epicardial adipose tissue (EAT) thickness using cardiac magnetic resonance imaging (CMR) and arrhythmias in hypertensive patients. Fifty-four hypertensive patients with arrhythmias (HTN [arrhythmias+]), 79 hypertensive patients without arrhythmias (HTN [arrhythmias-]), and 39 normal controls were retrospectively enrolled. EAT thickness was measured on cine images. Analysis of covariance with Bonferroni's post hoc correction, Pearson or Spearman analysis, receiver operating characteristic curve, and intraclass correlation coefficient analysis were performed. All hypertensive patients had impaired left ventricular (LV) and left atrial (LA) myocardial deformation, and HTN (arrhythmias+) patients displayed higher LV myocardial native T1, LA volume index, and increased EAT thickness than HTN (arrhythmias-) patients and normotensive controls. The presence of LV late gadolinium enhancement (LGE) was higher in hypertensive patients with arrhythmias than in those without arrhythmias. EAT thickness metrics significantly correlated with age, systolic blood pressure, body mass index, triglycerides and high-density lipoprotein levels, LV mass index and native T1 (all p < 0.05). EAT thickness parameters were able to differentiate hypertensive patients with arrhythmias from those without arrhythmias and normal controls, and the right ventricular free wall had the highest diagnostic performance. An accumulation of EAT thickness could further induce cardiac remodeling, promote myocardial fibrosis, and exaggerate function in hypertensive patients with arrhythmias. CMR-derived EAT thickness metrics could be a useful imaging marker for differentiating hypertensive patients with arrhythmias, which might be a potential target for the prevention of cardiac remodeling and arrhythmias.

Epicardial fat accumulation and left heart remodelling in patients with chronic coronary syndrome.

Patients with chronic coronary syndrome (CCS) suffer from subsequent cardiovascular events, even after complete revascularization; thus, elucidation of the underlying pathophysiological mechanisms is required. Epicardial adipose tissue (EAT) is increasingly recognized as a metabolically active organ with a key role in the pathogenesis of metabolic-related cardiac diseases. The present study investigated the association between EAT burden and left heart remodelling in patients with CCS. We studied 267 CCS patients (210 men; 71 ± 9 years) with complete revascularization and normal left ventricular (LV) ejection fraction who underwent follow-up echocardiography. All patients underwent the measurement of EAT thickness and speckle-tracking analysis to evaluate LV global longitudinal strain (LVGLS) and left atrial (LA) phasic strain. The mean EAT thickness was 5.0 ± 1.8 mm. Age, sex, body mass index, and diabetes mellitus were independently associated with EAT thickness (all P < 0.05). Multivariable linear regression analysis demonstrated that EAT thickness was significantly associated with LV mass index, early diastolic mitral annular velocity, and LA conduit strain independent of age, sex, and cardiovascular risk factors (all P < 0.05). On the other hand, there was no relationship between EAT thickness and LV systolic parameters including LV ejection fraction and LVGLS. CCS patients with increased EAT thickness had unfavourable left heart remodelling. The assessment of EAT thickness by echocardiography may have clinical utility as a simple surrogate to aid in risk stratification for impaired left heart function in CCS patients.

Epicardial Adipose Tissue Was Highly Associated with Reduction in Left Ventricular Diastolic Function as Early as in Adolescence.

Epicardial adipose tissue (EAT) is increased in adolescents with obesity and may play a role in early cardiovascular pathophysiological changes. There is a lack of evidence focusing on the association between EAT and cardiac function in adolescents. This study explored associations between EAT, left ventricle (LV) geometric, and LV functional changes in adolescents. Adolescent volunteers between 10 and 20 years of age were included. Body mass index (BMI) was presented as age- and sex-specific BMI z-scores. Blood samples for glucose metabolism, lipid profiles, and high-sensitivity C-reactive protein (hs-CRP) were obtained. EAT thickness, LV hypertrophy, and LV diastolic function were measured by echocardiography. The mean age of the 276 adolescents was 13.51 ± 2.44 years. BMI z-score was strongly associated with EAT thickness (r = 0.77; p < 0.001). Multivariable analysis revealed that age, insulin resistance, total cholesterol to high-density lipoprotein cholesterol ratio, and hs-CRP were independent predictors of increased EAT thickness. After adjusting for sex, age, and BMI z-score by multivariable analysis, EAT thickness was a strong predictor of higher LV mass indexed to height2.7, higher relative wall thickness, lower mitral annulus e'/a', and higher E/e' of the mitral annulus. There was no association between EAT and LV ejection fraction. EAT was highly associated with LV hypertrophy and reduction in LV diastolic function, independent of BMI z-score in the enrolled adolescents. Of note, the negative impacts of EAT on LV geometry and diastolic function occurred as early as in adolescence. This highlights the importance of preventing obesity and EAT deposition early in life.

Epicardial adipose tissue related to left atrial and ventricular function in heart failure with preserved versus reduced and mildly reduced ejection fraction.

Different associations between epicardial adipose tissue (EAT) and cardiac function have been suggested in patients with heart failure with preserved (HFpEF) versus reduced and mildly reduced ejection fraction (HFrEF/HFmrEF). However, few studies have directly compared the association between EAT and left atrial (LA) and left ventricular (LV) function in patients with HFpEF and HFrEF/HFmrEF. We studied EAT thickness using transthoracic echocardiography in a multicentre cohort of 149 community-dwelling controls without heart failure, 99 patients with HFpEF, and 366 patients with HFrEF/HFmrEF. EAT thickness was averaged from parasternal long-axis and short-axis views, respectively, and off-line speckle tracking analysis was performed to quantify LA and LV function. Data were validated in an independent cohort of 626 controls, 243 patients with HFpEF, and 180 patients with HFrEF/HFmrEF. For LV function, LV global longitudinal strain (GLS) was measured in both derivation and validation cohorts. For LA function, LAGLS at reservoir, contractile and conduit phase were measured in the derivation cohort, and only LAGLS at reservoir phase was measured in the validation cohort. In the derivation cohort, EAT thickness was lower in HFrEF/HFmrEF (7.3 ± 2.5 mm) compared to HFpEF (8.3 ± 2.6 mm, p < 0.05) and controls (7.9 ± 1.8 mm, p < 0.05). Greater EAT thickness was associated with better LV and contractile LA function in HFrEF/HFmrEF, but not in HFpEF (p for interaction <0.05). These findings were confirmed in the validation cohort, where EAT thickness was lower in HFrEF/HFmrEF (6.7 ± 1.4 mm) compared to HFpEF (9.6 ± 2.8 mm; p < 0.05) and controls (7.7 ± 2.3 mm; p < 0.05). Greater EAT thickness was associated with better LV and reservoir LA function in patients with HFrEF/HFmrEF but worse LV and reservoir LA function in patients with HFpEF (p for interaction <0.05). Thickened EAT (EAT thickness >10 mm) was associated with LA dysfunction (LAGLS at reservoir phase <23%) in HFpEF, but not in HFrEF/HFmrEF. Epicardial adipose tissue thickness is greater in patients with HFpEF than HFrEF/HFmrEF. Increased EAT thickness is associated with worse LA and LV function in HFpEF but the opposite in HFrEF/HFmrEF.

The association between epicardial adipose tissue and prognosis in heart failure with preserved and reduced ejection fraction

Abstract Funding Acknowledgements Type of funding sources: None. Background. Recent evidence shows that increased epicardial adipose tissue (EAT) thickness is associated with metabolic syndrome, microvascular dysfunction and enhanced pericardial restraint. Purpose. We measured echocardiography-derived EAT thickness in a population of heart failure (HF) patients with reduced (HFrEF) and preserved (HFpEF) ejection fraction to examine the relationship between EAT and prognosis at clinical follow-up. Methods. We prospectively enrolled 393 consecutive HF outpatients (205 HFrEF, 188 HFpEF) who had been referred to our hospital due to dyspnoea and/or effort intolerance. We performed a resting clinical and biohumoral evaluation, followed by combined cardiopulmonary-echocardiography exercise stress. We considered a composite endpoint of cardiovascular death and HF-related hospitalization during follow-up. Results. Patients with HFpEF displayed greater EAT thickness (median 8 mm, interquartile range [IQR] 4–12 mm) than HFrEF (median 3 mm, IQR 2–6 mm; p &amp;lt; 0.0001). During a median follow-up of 20.9 months (IQR 15-25 months), 34 cardiovascular deaths and 146 HF hospitalizations were reported, with no significant differences between the two HF phenotypes. EAT was shown to predict adverse events independently from body mass index, waist circumference and other well-established prognostic markers in HF (such as NT-proBNP and peak oxygen consumption). The risk of adverse events increased with increasing EAT thickness in HFpEF and with EAT thinning in HFrEF. Kaplan-Meier analyses for the composite endpoint showed that in HFpEF, the survival probability was significantly lower in patients with thicker EAT than those with thinner EAT. In HFrEF, conversely, patients with increased EAT thickness had a higher survival probability than those with reduced EAT thickness (Figure 1). Conclusion. EAT accumulation is increased in HFpEF compared to HFrEF and carries different prognostic meanings in the two subsets. In HFpEF, EAT thickening portends adverse outcomes, which may be due to the secretion of pro-inflammatory and pro-atherogenic adipokines and increased mechanical restraint. In HFrEF, EAT thinning is associated with a worse prognosis, probably reflecting a more advanced catabolic state (e.g., cardiac cachexia). Larger studies are needed to determine whether or not EAT has a causal role in influencing progression and survival in the different HF phenotypes. Abstract Figure 1

Epicardial Adipocyte-derived TNF-α Modulates Local Inflammation in Patients with Advanced Coronary Artery Disease.

Epicardial Adipose Tissue (EAT) surrounds the epicardium and can mediate harmful effects related to Coronary Artery Disease (CAD). We explored the regional differences between adipose stores surrounding diseased and non-diseased segments of coronary arteries in patients with advanced CAD. We enrolled 32 patients with known CAD who underwent coronary artery bypass graft (CABG) surgery. Inflammatory mediators were measured in EAT biopsies collected from a region of the Left Anterior Descending Artery (LAD) with severe stenosis (diseased segment) and without stenosis (non-diseased segment). Mean age was 64.3±11.1 years, and mean EAT thickness was 7.4±1.9 mm. Dyslipidemia was the most prevalent comorbidity (81% of the patients). Out of a total of 11 cytokines, resistin (p=0.039), matrix metallopeptidase 9 (MMP-9) (p=0.020), C-C motif chemokine ligand 5 (CCL-5) (p=0.021), and follistatin (p=0.038) were significantly increased in the diseased compared with the non-diseased EAT segments. Indexed tumor necrosis factor-alpha (TNF-α), defined as the diseased to non-diseased cytokine levels ratio, was significantly correlated with increased EAT thickness both in the whole cohort (p=0.043) and in a subpopulation of patients with dyslipidemia (p=0.009). Treatment with lipid-lowering agents significantly decreased indexed TNF-α levels (p=0.015). No significant alterations were observed in the circulating levels of these cytokines with respect to CAD-associated comorbidities. Perivascular EAT is a source of cytokine secretion in distinct areas surrounding the coronary arteries in patients with advanced CAD. Adipocyte-derived TNF-α is a prominent mediator of local inflammation.

Epicardial Adipose Tissue Thickness is Higher in Right Ventricular Outflow Tract Tachycardia

ABSTRACT Introduction: Idiopathic ventricular arrhythmias, which occur in the absence of structural heart disease, are commonly originating from the outflow tract, and 80% of the them arise from the right ventricle. Epicardial adipose tissue (EAT), which originates from the splanchnopleuric mesoderm, has been shown to be an important source of inflammatory mediators and plays an important role in cardiac autonomic function by epicardial ganglionated plexuses. EAT may potentially contribute to the pathophysiology of idiopathic right ventricular outflow tract (RVOT) tachycardia by different mechanisms. In this study, we aimed to investigate the relationship between EAT thickness and RVOT tachycardia. Methods: This study included 55 patients (32 male, 23 female) with RVOT tachycardia and 60 control subjects (38 male, 22 female). Patients who had more than three consecutive ventricular beats over 100 bpm with specific morphological features on the electrocardiogram (ECG) were diagnosed with RVOT tachycardia. EAT thickness was measured by transthoracic echocardiography. Results: EAT thickness was significantly higher in the RVOT tachycardia group (p &lt;0.05). Ejection fraction (EF), and the thickness of the posterior wall of the left ventricle and of the interventricular septum were significantly lower, and left ventricular end-diastolic diameter, left ventricular end-systolic diameter, and left atrial diameter were significantly higher in patients who had RVOT tachycardia compared to normal subjects (p &lt;0.05). Conclusion: Patients who were diagnosed with RVOT tachycardia had increased EAT thickness compared to normal subjects. The underlying mechanism of the condition could be mechanical, metabolic, infiltrative, or autonomic effects of the EAT.

Myocardial injury in COVID-19 patients is associated with the thickness of epicardial adipose tissue.

Aim High sensitive troponin (hs-TnI) levels may increase secondary to Coronavirus disease-2019 (COVID-19), and this increase is associated with cardiovascular mortality in COVID-19 patients. Epicardial adipose tissue (EAT) is associated with myocardial injury directly as a reservoir tissue for coronavirus, and indirectly through mediators it secretes as an apocrine gland. We aimed to evaluate the relationship between myocardial injury secondary to COVID-19 infection and EAT thickness.Material and methods Thoracic computed tomography (CT) was performed in 73 consecutive patients diagnosed with COVID-19. EAT thickness and volume were calculated by two radiologists blind to the study data. We formed two groups according to hs-TnI concentrations, patients with myocardial damage (hs-TnI ≥11.6 ng / l) and without myocardial damage (hs-TnI&lt;11.6 ng / dl).Results A total of 46 patients were women (63.0 %). The mean age was 66.4±12.3 yrs in the myocardial injury group and 55.9±9.7 yrs in the group without myocardial injury (p&lt;0.001). There were 20 hypertensive patients (68.9 %) in the injury group, while there were 12 hypertensive patients (27.3 %) in the group without injury (p=0.001). Glucose, C-reactive protein, D-dimer, white blood cell count, neutrophil, and neutrophil / lymphocyte ratio were higher in the injury group (p&lt;0.05, for all variables). The mean EAT thickness was 5.6±1.6 mm in the injury group, whereas it was 4.8±1.8 mm in the group without injury (p=0.031). EAT thickness of 4.85 mm and above was associated with the myocardial injury with 65 % sensitivity and 39 % specificity (AUC=0.65, 95 % CI: 0.52-078, p=0.031).Conclusion In patients with COVID-19 infection, higher rates of myocardial injury were observed as the EAT thickness increased. Epicardial adipose tissue, contributes to cytokine-mediated myocardial injury either directly or indirectly by acting as a reservoir for coronavirus. Increased EAT thickness is associated with myocardial injury in COVID-19 patients.

Echocardoographic measurements of epicardial adipose tissu: A new marker of cardiovascular risk level?

Epicardial adipose tissue (EAT) is a small but biologically active ectopic fat depot that surrounds the heart. Given its rapid metabolism, secretory profile, and simple measurability, epicardial fat has drawn attention among researchers. It has been suggested that an increased thickness and volume of EAT is associated with increase risk of cardiovascular disease. To quantify the relation between cardiovascular risk factors and epicardial adipose tissue measured by echocardiography in patients undergoing invasive coronary angiography for suspected coronaropaphy. Sixty patients (64.5 ± 10.9 years, 58% men) undergoing invasive coronary angiography for suspected coronaropathy were enrolled prospectively, in the period between January 2020 and October 2020. Transthoracic echocardiography was performed. EAT thickness was measured perpendicular to the right ventricular free wall at end-diastole. Cradiovascular risk was estimated based on the levels of cardiovascular risk suggested in the guidelines of dyslipidemia published in 2019 by the European Society Of Cardiology. Association of EAT with cardiovascular risk factors and cardiovascular risk levels were studied. Overall average thickness was 9.2 ± 2.2 mm (range 4.4–15.1). The bivariate analysis showed positive associations of the EAT with age, blood pressure, smoking, glycemia, insulin dose, and triglyceride ( P < 0.05). The cardiovascular risk factors most strongly associated with EAT thickness were hypertension and diabetes. We found that EAT was thicker in patients with obstructive coronary artery disease compared with individuals with normal angiography or non-obstructive coronary disease ( P = 0.01). Patients with EAT > 5 mm, had higher cardiovascular risk ( P = 0.02), and higher prevalence of obstructive coronary artery disease ( P = 0.004). Increased EAT thickness is associated with cardiovascular risks factors and coronary artery disease.

ASSOCIATION BETWEEN EPICARDIAL ADIPOSE TISSUE THICKNESS AND PARAMETERS OF THE LEFT VENTRICULAR DIASTOLIC FUNCTION AND LEFT VENTRICULAR REMODELING IN PATIENTS WITH ABDOMINAL OBESITY

Objective: The aim of study to assess the correlation between epicardial adipose tissue (EAT) with the parameters of the left ventricular remodeling and diastolic function in patients with abdominal obesity. Design and method: The study included 104 patients (37,5% men, 62.5% women), mean age 38.59 ± 6.09 years with abdominal obesity (waist circumference (WT) &gt; 80 cm in women, &gt; 94 cm in men), without cardiovascular diseases and diabetes mellitus. All patients underwent transthoracic echocardiographic examination (Vivid 7, Vivid 9 (GE Healthcare, USA)): left ventricular (LV) mass, LV mass index, LV mass/height index, LV diastolic function (assessed by the E/e’ ratio, Emlat, Emsept, Em/Am ratio) were estimated; EAT thickness measured on the free wall of the right ventricle from both parasternal long- and short-axis views at end-systole and end-diastole during three cardiac cycles. Results: The average of EAT thickness was at end-systole 6,7 ± 2,0 mm, end-diastole- 4,2 ± 1,7 mm. EAT correlated with WT (EAT at end-systole r = 0,43; p &lt; 0,05; EAT at end-diastole r = 0,43; p &lt; 0,05). EAT thickness was significantly correlated with LV diastolic function: positive correlation with E/Em ratio (EAT at end-systole r = 0,62; p &lt; 0,05; EAT at end-diastole r = 0,56; p &lt; 0,05); negative correlation was found with Em/Am ratio (EAT at end-systole r = -0,66; p &lt; 0,05; EAT at end-diastole r = -0,59; p &lt; 0,05); Emlat (EAT at end-systole r = -0,62; p &lt; 0,05; EAT at end-diastole r = -0,51; p &lt; 0,05); Emsept (EAT at end-systole r = -0,65; p &lt; 0,05; EAT at end-diastole r = -0,60; p &lt; 0,05). EAT thickness correlated with with LV mass (EAT at end-systole r = 0,52; p &lt; 0,05; EAT at end-diastole r = 0,51; p &lt; 0,05); LV mass index (EAT at end-systole r = 0,31; p &lt; 0,05; EAT at end-diastole r = 0,32; p &lt; 0,05); (EAT at end-systole r = 0,52; p &lt; 0,05; EAT at end-diastole r = 0,51; p &lt; 0,05); LV mass/height index (EAT at end-systole r = 0,44; p &lt; 0,05; EAT at end-diastole r = 0,43; p &lt; 0,05). Conclusions: The data suggest that EAT as ectopic visceral fat depot may affect on diastolic function and LV remodeling. Increased EAT thickness is strongly associated with LV diastolic disfunction.

Impact of epicardial adipose tissue increase after ST elevation Myocardial Infarction (STEMI) on IL-13 and left ventricular remodelling

Abstract Background The role of epicardial adipose tissue (EAT) in myocardial diseases is well established, and several evidence suggest that EAT may negatively affect left ventricular (LV) remodelling through an imbalanced production and secretion of pro and anti-inflammatory cytokines. Of these, the IL-13 it is known to play a positive activity on cardiac remodelling. Nowadays, the crosstalk between EAT and the myocardium is still poorly understood and the effects of myocardial ischemia on morphological and functional properties of EAT are almost unknown. Purpose In the present study we explored whether an increase of EAT thickness after STEMI might be associated with unfavourable LV remodelling at 3 months (T1). We also evaluated the relationship between changes (Δ) of EAT thickness and systemic levels of Interleukin (IL)-13 which is known to play a favourable activity on LV remodelling after STEMI. Methods We enrolled 66 patients with first STEMI, undergoing primary percutaneous angioplasty. At baseline and at 3 months we performed a complete echocardiogram, including EAT maximal thickness assessment, and determined circulating levels of IL-13. Results At 3 months after STEMI, the population was stratified into two groups according to different EAT remodelling after cardiac event: Group 1, patients with an increased EAT thickness (Δ EAT&amp;gt;1; 30 patients) and Group 2, patients with unchanged or decreased EAT thickness (Δ EAT&amp;lt;1). The two groups did not differ for age, gender and atherosclerotic risk factors. Group 1 had a worse LV remodelling at 3 months with higher LV diastolic and systolic volumes, lower LV ejection fraction (p=0.003; p=0.013; p=0.013 respectively) and worse diastolic function (E/e'; p=0.011). Of interest, EAT thickness increase was paralleled by circulating IL-13 reduction (p=0.022). Conclusion Myocardial injury can result in EAT increase which is associated to worse LV remodelling probably through the loss of the protective role of IL-13. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): This research has been funded by the University of Naples “Federico II” and “Compagnia di San Paolo e l'Istituto Banco di Napoli” within the competitive grant STAR 2018; Valentina Parisi is the principal investigator

Epicardial Adipose Tissue and IL-13 Response to Myocardial Injury Drives Left Ventricular Remodeling After ST Elevation Myocardial Infarction.

IntroductionLeft ventricular (LV) remodeling after ST-segment elevation myocardial infarction (STEMI) is explained only in part by the infarct size, and the inter-patient variability may be ascribed to different inflammatory response to myocardial injury. Epicardial adipose tissue (EAT) is a source of inflammatory mediators which directly modulates the myocardium. EAT increase is associated to several cardiovascular diseases; however, its response to myocardial injury is currently unknown. Among inflammatory mediators, IL-13 seems to play protective role in LV regeneration, but its variations after STEMI have not been described yet. Purpose: In the present study we analyzed the association between infarct-related changes of EAT and IL-13 in post-STEMI LV remodeling.MethodsWe enrolled 100 patients with STEMI undergoing primary angioplasty. At the enrolment (T0) and after 3 months (T1), we measured EAT thickness by echocardiography and circulating levels of IL-13 by ELISA.ResultsAt T1, the 60% of patients displayed increased EAT thickness (ΔEAT > 0). ΔEAT was directly associated to LV end-diastolic volume (r = 0.42; p = 0.014), LV end-systolic volume (r = 0.42; p = 0.013) and worse LV ejection fraction (LVEF) at T1 (r = −0.44; p = 0.0094), independently of the infarct size. In the overall population IL-13 levels significantly decreased at T1 (p = 0.0002). The ΔIL-13 was directly associated to ΔLVEF (r = 0.42; p = 0.017) and inversely related to ΔEAT (r = −0.51; p = 0.022), thus suggesting a protective role for IL-13.ConclusionThe variability of STEMI-induced “inflammatory response” may be associated to the post-infarct LV remodeling. ΔEAT thickness and ΔIL-13 levels could be novel prognostic markers in STEMI patients.

Epicardial adipose tissue thickness is not associated with adverse cardiovascular events in patients undergoing haemodialysis

In non-haemodialysis (HD) patients, increased epicardial adipose tissue (EAT) thickness was significantly associated with adverse cardiovascular (CV) events. This study was designed to investigate whether EAT thickness was a useful parameter in the prediction of adverse CV events in HD patients. In addition, we also evaluated the major correlates of EAT thickness in these patients. In 189 routine HD patients, we performed a comprehensive transthoracic echocardiographic examination with assessment of EAT thickness. The definition of CV events included CV death, non-fatal stroke, non-fatal myocardial infarction, peripheral artery disease, and hospitalization for heart failure. The follow-up period for CV events was 2.5 ± 0.7 years. Thirty-one CV events were documented. The multivariable analysis demonstrated that older age, smoking status, the presence of diabetes mellitus and coronary artery disease, and low albumin levels were independently correlated with adverse CV events. However, increased EAT thickness was not associated with adverse CV events (P = 0.631). Additionally, older age, female sex, low haemoglobin, and low early diastolic mitral annular velocity were correlated with high EAT thickness in the univariable analysis. In the multivariable analysis, older age and female sex were still correlated with high EAT thickness. In conclusion, high EAT thickness was associated with older age and female sex in the multivariable analysis in our HD patients. However, EAT thickness was not helpful in predicting adverse CV events in such patients. Further large-scale studies are necessary to verify this finding.