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Coronary artery disease

Relationship of epicardial adipose tissue by echocardiography to coronary artery disease

S-G Ahn, H-S Lim, D-Y Joe, S-J Kang, B-J Choi, S-Y Choi, M-H Yoon, G-S Hwang, S-J Tahk, J-H Shin

Department of Cardiology, Ajou University Medical Centre, Suwon, Republic of Korea

Correspondence to:

Dr J-H Shin, Department of Cardiology, Ajou University Medical Centre, San 5, Wonchon-Dong, Youngtong-Gu, Suwon, Republic of Korea 443– 721; shinjh@ajou.ac.kr

Accepted 18 September 2007 Published Online First 8 October 2007

ABSTRACT Objective: To study the relationship of echocardiographic epicardial adipose tissue (EAT) with coronary artery disease (CAD) risk factors and the extent of coronary atherosclerosis. Methods: EAT thickness was measured in 527 patients undergoing their first coronary angiography. EAT was defined as an echo-lucent area on the free wall of the right ventricle on the still image of the two-dimensional echocardiogram at end diastole in the parasternal long- axis and parasternal short-axis views. A CT scan at the umbilicus was acquired to measure abdominal visceral adipose tissue (VAT) from a random sample of 30 patients. The extent of coronary atherosclerosis was assessed using a coronary atherosclerosis score based on the quantitative coronary angiography results. Results: EAT thickness was correlated with abdominal VAT (r s = 0.626, p,0.001), age (r s = 0.480, p ,0.001), waist circumference (r s = 0.309, p,0.001), body mass index (r s = 0.233, p ,0.001), C reactive protein (r s = 0.224, p ,0.001), and the homoeostasis model assessment score (r s = 0.249, p ,0.001). EAT was thicker in subjects with CAD than in those without CAD (4.0 vs 1.5 mm, p ,0.001). Patients with unstable angina had thicker EAT than those with stable angina or atypical chest pain (4.0, 3.0, and 1.5 mm, respectively, p ,0.001). EAT ( >3.0 mm) was an independent factor of CAD on multiple logistic analysis (odds ratio = 3.357; 95% CI 2.177 to 5.175, p ,0.001). Conclusions: These results suggest that EAT may reflect the amount of visceral fat, which is associated with insulin resistance and inflammation. The echocardio- graphic measurement of EAT may provide additional information for assessing CAD risk and predicting the extent and activity of CAD.

It is increasingly evident that visceral adipose tissue (VAT) plays a leading part in the development of the metabolic syndrome (MS) and that it is an important coronary artery disease (CAD) risk factor. 13 Waist circumference and imaging mod- alities, such as abdominal computed tomography (CT) and magnetic resonance imaging (MRI), have been used to estimate VAT. 4 5 Recently, it was reported that epicardial adipose tissue (EAT) measured by transthoracic echocardiography in obese subjects was well correlated with abdominal VAT assessed by MRI and that echocardiographic EAT could be used as a reliable imaging indicator of VAT. 6 However, to date, the clinical significance of EAT, which is observed during transthoracic echocardiographic examination done as part of a CAD investigation, has not been studied in patients with angina. Therefore, we determined

whether echocardiographic EAT reflects VAT in subjects presenting with angina. We also investi- gated the relationship of EAT to CAD risk factors, MS, the extent of angiographic CAD, and disease activity.

PATIENTS AND METHODS Patient population

EAT thickness was measured consecutively and prospectively in 527 patients (mean (SD) age 58 (11) years, 267 male) undergoing their first cor- onary angiography owing to chest pain between January 2005 and October 2005 in our hospital. Patients were excluded from the study if they had any of the following: active inflammation or inflammatory disease, chronic kidney disease, a history of prior revascularisation, heart failure, cardiomyopathy and acute myocardial infarction. Ambiguous cases with possible pericardial effusion were also excluded. Anthropometric measures, such as body mass index and waist and hip circumferences were collected. Plasma lipid pro- files, C reactive protein, fibrinogen, uric acid and cardiac enzymes were measured. The homoeostasis model assessment (HOMA) score, which reflects insulin resistance, was calculated in non-diabetic patients using fasting plasma insulin and glucose concentrations as previously described. 7 Patients with more than three of five criteria based on the updated ATP guideline were considered to have the MS. Central obesity was considered to be present if the waist circumference was > 90 cm in men and > 80 cm in women, which are the threshold values for the Asian population. 3 The MS score was defined as the number of MS components present. The study protocol was approved by our institu- tional review board, and all patients gave their written informed consent.

Measurement of echocardiographic epicardial adipose tissue

Two-dimensional transthoracic echocardiography (Sequoia C256 with 2.5 MHz transducer; Siemens, Mountain View, California, USA) was performed. Recordings of six cycles of the two-dimensional parasternal long-axis view and the parasternal short-axis view at the basal left ventricular level were obtained. We increased the depth of each view until the aortic and mitral valves were positioned lowest on the screen to allow for better visualisation and accurate estimation of EAT. EAT was measured on the free wall of the right ventricle in the still images of the two-dimensional echo- cardiogram obtained at end diastole on both

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Coronary artery disease

2014 - Published by group.bmj.com Coronary artery disease Echocardiographic measurement of epicardial adipose tissue

Echocardiographic measurement of epicardial adipose tissue (EAT). (A) Parasternal long-axis view; (B) parasternal short-axis view at the

mitral valve level. AO, aorta; LV, left ventricle; RV, right ventricle. Anterior echo-lucent space between the linear echo-dense parietal pericardium and the epicardium was considered to be EAT (arrows). Mediastinal fat, seen as en echo-lucent area located above the parietal pericardium, was not included in the EAT measurement.

Figure 1

parasternal long-axis and short-axis views (fig 1). The anterior echo-lucent space between the linear echo-dense parietal pericardium and the right ventricular epicardium was consid- ered to be EAT. Mediastinal fat presenting as an echo-lucent area above the parietal pericardium was not included in the measurement of EAT. The average value of two images obtained in the parasternal long-axis and short-axis views was calculated.

Measurement of abdominal visceral adipose tissue

A random sample of 30 patients had CT scans using a GE Highspeed Advantage (GE Medical System, Milwaukee, USA) according to our hospital’s protocol. All scans were performed in the supine position using a slice diameter of 40 cm with a thickness of 3 mm. The images were generated with a 200 mA,

120–140 kV beam for a duration of a second. Scans were displayed in a matrix of 5126512 picture elements. We selected a sequence of five images obtained at 3 mm intervals. The central image of the sequence was located at the umbilicus; two images were above and two images were below this level. On each CT image, the intra-abdominal cavity was outlined by tracing the transverse fascia excluding the vertebral body. The CT attenuation score for fat ranged from 2 50 to 2250. After three-dimensional reconstruction of the images, abdominal VAT volumes were calculated using histogram-based volume analysis.

Coronary angiography

Quantitative coronary angiographic analysis (Quantcor QCA, version 4.0; Pie Medical Imaging, Maastricht, The Netherlands)

Table 1

Baseline characteristics according to the thickness of epicardial adipose tissue (EAT) (n = 527)

Characteristics

EAT , 3.0 mm (n = 263)

EAT > 3.0 mm (n = 264)

p Value

Age (years), mean (SD) Men, No (%) Body mass index (kg/m 2 ), mean (SD) Waist circumference (cm), mean (SD) Hypertension, No (%) Diabetes, No (%) Smoking, No (%) Metabolic syndrome, No (%) Angiographic CAD, No (%) Unstable angina, No (%) Total cholesterol (mmol/l), mean (SD) Triglyceride (mmol/l), mean (SD) HDL cholesterol (mmol/l), mean (SD) LDL cholesterol (mmol/l), mean (SD) C reactive protein (mg/l), mean (SD) HOMA score, mean (SD)* Uric acid (mmol/l), mean (SD) Fibrinogen (g/l), mean (SD)

54 (11)

63 (9)

,

0.001

138 (52)

129 (49)

0.407

24.7 (3.2)

25.7 (2.9

,

0.001

87.6 (9.8)

92.0 (8.0)

,

0.001

119 (45)

173 (66)

,

0.001

50 (19)

75 (28)

0.011

94 (36)

82 (31)

0.255

131 (50)

196 (74)

,

0.001

79 (30)

181 (69)

,

0.001

60 (23)

152 (58)

, 0.001

4.42 (0.88)

4.55 (1.01)

0.072

1.66 (1.02)

1.76 (1.06)

0.248

1.22 (0.34)

1.14 (0.26)

0.028

2.46 (0.75)

2.66 (0.85)

0.006

2.0 (4.0)

2.9 (5.2)

0.040

2.2 (1.9)

2.8 (2.3)

0.006

303 (95)

321 (178)

0.135

3.4 (0.9)

3.7 (1.0)

0.001

*The homoeostasis model assessment (HOMA) score was calculated only in non-diabetic patients (n = 402). CAD, coronary artery disease; HDL, high-density lipoprotein; LDL, low-density lipoprotein.

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Coronary artery disease

2014 - Published by group.bmj.com Coronary artery disease Figure 2 Frequency histogram of epicardial adipose tissue

Figure 2

Frequency histogram of epicardial adipose tissue thickness.

was performed by one single experienced technician who was unaware of the patients’ clinical information. On quantitative analysis of the coronary angiograms, the presence of one or more stenoses >50% in diameter of a major epicardial vessel was considered to be significant CAD. The extent of CAD was quantified using the number of vessels with > 50% stenosis and

a coronary atherosclerosis score as follows. 8 The coronary artery tree was divided into nine segments: the left main coronary artery, the proximal, mid-, and distal left anterior descending

artery, the proximal circumflex artery including the first obtuse marginal branch, the circumflex artery distal to the first marginal branch, the proximal and mid-right coronary artery, and the posterior descending artery. Each of these segments was scored from 0 to 3 depending on the most severe stenosis using the following system: 0 = normal, 1 = stenosis between 1% and 49%, 2 = stenosis between 50% and 99%, and 3 = total occlusion. A coronary atherosclerosis score was generated as the sum of the scores in all segments.

Statistics

SPSS version 12.0 (SPSS Inc., Chicago, Illinois, USA) was used for statistical analysis. All continuous variables are expressed as mean (SD); categorical variables are expressed as number and percentage. We compared the characteristics of patients who had , 3.0 mm of EAT with those who had > 3.0 mm of EAT. Comparisons of continuous variables were performed using the unpaired Student t test. Analyses of discrete variables were performed using x 2 tests. Owing to its skewed distribution, the significance of any differences between groups in the median values of EAT thickness were evaluated using the Wilcoxon rank-sum test. Comparison of EAT thickness according to the MS score, the number of vessels with > 50% narrowing, and the

the number of vessels with > 50% narrowing, and the Figure 3 abdominal visceral adipose tissue

Figure 3

abdominal visceral adipose tissue volume (n = 30).

Correlation between epicardial adipose tissue thickness and

clinical presentation was done using the Kruskal–Wallis test. Correlations of EAT with various clinical and biochemical variables, including abdominal VAT, were examined by Spearman correlation analysis. A set of well-recognised CAD risk factors were included in a logistic regression model of

angiographic CAD. 1 9 EAT thickness was then added to this model to determine whether there was any additional prognostic value. A receiver operating characteristic curve analysis was used to assess the discrimination of CAD based on well-known CAD risk factors and EAT thickness. One- sample paired t test was performed to evaluate inter- and intraobserver variability in the measurement of EAT from 30 randomly selected subjects. Variability was expressed as mean (SD) of the absolute difference between the two sets of measurements.

RESULTS Clinical characteristics

Table 1 lists patients’ detailed clinical characteristics according to the thickness of EAT. Our study group consisted of 527 patients (267 men) with a mean (SD) age of 58 (11) years. The MS criteria were fulfilled in 327 patients. There were 125 diabetic patients and 212 patients who presented with unstable angina. On coronary angiography, significant CAD was detected in 260 patients. The patients who had > 3.0 mm of EAT were older and had higher body mass index and greater waist circumference than those who had , 3.0 mm of EAT. Additionally, there were more prevalent hypertension, diabetes, MS, angiographic CAD, and unstable angina, and the level of low-density lipoprotein cholesterol, C reactive protein, HOMA score, uric acid, and fibrinogen was higher. Additionally, the level of high-density lipoprotein cholesterol was lower in patients who had > 3.0 mm of EAT compared with those who had , 3.0 mm of EAT.

Epicardial adipose tissue thickness

The frequency histogram of EAT thickness was skewed to the left (fig 2). EAT thickness ranged from 0 through 12 mm. The mean (SD) and median values of EAT thickness were 3.2 (2.5) and 3.0 mm, respectively. There was no difference in EAT thickness between men and women (median 2.5 vs 3 mm,

Table 2

biochemical and angiographic variables (n = 527)

Correlations of epicardial adipose tissue with clinical,

Variable

r s Coefficient

p Value

Age Body mass index (kg/m 2 ) Waist circumference (cm) Total cholesterol (mmol/l) LDL cholesterol (mmol/l) Triglyceride (mmol/l) HDL cholesterol (mmol/l) Fasting glucose (mmol/l)* Fasting insulin (pmol/l)* HOMA score* C reactive protein (mg/l) Fibrinogen (g/l) Metabolic syndrome score Coronary atherosclerosis score Number of vessels > 50% stenosis

0.480

,

0.001

0.233

,

0.001

0.309

,

0.001

0.087

0.047

0.122

0.005

0.108

0.014

2 0.105

0.017

0.168

,

0.001

0.230

,

0.001

0.249

,

0.001

0.224

,

0.001

0.237

,

0.001

0.321

,

0.001

0.323

,

0.001

0.444

, 0.001

*Correlations of epicardial adipose tissue with fasting insulin, glucose concentrations, and homoeostasis model assessment (HOMA) score were performed only in non- diabetic patients (n = 402). HDL, high-density lipoprotein; LDL, low-density lipoprotein.

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Coronary artery disease

2014 - Published by group.bmj.com Coronary artery disease Figure 4 Comparison of epicardial adipose tissue thickness
2014 - Published by group.bmj.com Coronary artery disease Figure 4 Comparison of epicardial adipose tissue thickness
2014 - Published by group.bmj.com Coronary artery disease Figure 4 Comparison of epicardial adipose tissue thickness
2014 - Published by group.bmj.com Coronary artery disease Figure 4 Comparison of epicardial adipose tissue thickness
2014 - Published by group.bmj.com Coronary artery disease Figure 4 Comparison of epicardial adipose tissue thickness
2014 - Published by group.bmj.com Coronary artery disease Figure 4 Comparison of epicardial adipose tissue thickness

Figure 4 Comparison of epicardial adipose tissue thickness according to the number of components of the metabolic syndrome (A), the angiographic severity of coronary artery disease (CAD) (B), and the clinical presentation (C). Box plots show median, 25th and 75th centile values for EAT. *p , 0.001 vs one vessel and > 2 vessels; {p = 0.049 vs > 2 vessels.

p = 0.123). The absolute values of the mean paired differences and the standard deviations of the differences were 0.0200 (0.37637), p = 0.773 and 0.0033 (0.46866), p = 0.969 for inter- and intraobserver variability for EAT measurement respectively, indicating good reproducibility.

Relationship of epicardial adipose tissue to abdominal visceral adipose tissue and various clinical, biochemical and angiographic variables

EAT thickness had a good correlation with abdominal VAT as measured by CT scan (fig 3). Table 2 presents the correlations of EAT with clinical, biochemical and angiographic variables. EAT thickness was correlated with age, body mass index, waist circumference, total cholesterol, low-density lipoprotein choles- terol, triglyceride, C reactive protein, and fibrinogen levels; EAT thickness was inversely correlated with the high-density lipoprotein cholesterol level. However, the degree of correlation was not strong. EAT thickness was correlated with fasting glucose, insulin concentrations, and the HOMA score in non- diabetic patients. EAT thickness was also correlated with the MS score, the coronary atherosclerosis score, and the number of vessels with > 50% narrowing.

Comparison of the thickness of epicardial adipose tissue according to the presence of the metabolic syndrome

The median EAT thickness was higher in patients with MS than in those without MS (3.5 vs 1.6 mm, p, 0.001). EAT thickness increased linearly as the MS score increased; median EAT thickness values for those with 0, 1, 2, 3, 4, or 5 MS components were 1.0, 1.5, 2.0, 3.0, 3.5, and 4.5 mm, respectively (fig 4A).

Table 3

factors (n = 527)

Multiple logistic analysis of coronary artery disease risk

Risk factors

Odds ratio (95% CI)

p Value

Age Male >45 years Female > 55 years Smoking Hypertension Diabetes mellitus C reactive protein > 1 mg/l Epicardial adipose tissue > 3 mm

3.775 (1.931 to 6.254)

,

0.001

 

0.011

1.801 (1.142 to 2.842) 1.842 (1.200 to 2.826) 2.555 (1.544 to 4.227) 1.696 (1.117 to 2.576) 3.357 (2.177 to 5.175)

 

0.005

,

0.001

0.013

, 0.001

Comparison of the thickness of epicardial adipose tissue according to the presence of coronary artery disease, the extent of coronary artery disease, and the clinical presentation

EAT was thicker in patients with significant CAD than in those without CAD (4.0 vs 1.5 mm, p, 0.001). Patients with multi- vessel CAD had significantly thicker EAT than those with single-vessel disease and normal coronary arteries or minimal CAD (multivessel CAD, 4 vs single-vessel disease, 3.5 vs normal or minimal CAD, 1.5 mm, respectively, p, 0.001, fig 4B). The median EAT thickness was greater in patients with unstable angina than in those with stable angina or atypical chest pain (unstable angina, 4 vs stable angina, 3 vs atypical chest pain, 1.5 mm, respectively, p, 0.001, fig 4C).

Epicardial adipose tissue as a predictor of coronary artery disease

Table 3 shows the multiple logistic analysis of the CAD risk factors. In addition to the well-known CAD risk factors, such as age, smoking, hypertension, C reactive protein, and diabetes, epicardial adipose tissue was an independent factor associated with angiographic CAD in this study population. The receiver operating characteristic curve using the predicted probability from the logistic regression model in table 3 excluding EAT yielded an area under the curve of 0.739 (95% CI 0.695 to 0.783, p, 0.001). When EAT thickness was added to the CAD risk factors, the area under the curve improved to 0.783 (95% CI 0.742 to 0.824, p ,0.001, fig 5).

DISCUSSION

The present study demonstrated that echocardiographic EAT could be used as another imaging indicator of VAT and that EAT was related to various CAD risk factors, MS, and the severity of angiographic CAD. Although the presence of epicardial fat has been discussed in previous autopsy studies, 10 11 its clinical significance and function have not been extensively studied. It has been suggested that EAT may act as a local energy supply for the adjacent myocardium or act as a buffer against toxic levels of free fatty acids, or both. 12 EAT was also proposed as a source of several inflammatory mediators, given that EAT had higher levels of inflammatory markers than subcutaneous adipose tissue in patients undergoing coronary artery bypass surgery. 13 As far as we know, our paper is the first study to have evaluated the clinical significance of EAT measured by echocardiography in patients presenting with angina.

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Coronary artery disease

2014 - Published by group.bmj.com Coronary artery disease Figure 5 Combined receiver-operating characteristic curves

Figure 5 Combined receiver-operating characteristic curves of the coronary artery disease (CAD) risk factors and the combined predicted probability adding epicardial adipose tissue (EAT) thickness in predicting angiographic CAD.

Relationship to the metabolic syndrome

MS is not a unique disease entity, but is an agglomeration of

inter-related metabolic risk factors. 3 Several surrogate markers are used to estimate visceral fat. Waist circumference has been used as a component of MS since it reflects intra-abdominal fat mass. However, it often cannot discriminate between subcuta- neous and visceral fat. Imaging techniques such as abdominal CT scan and MRI are certainly more precise and reliable, but they are expensive. 4 5 Recently, echocardiographic EAT assess- ment has been proposed as a new imaging indicator of VAT, since it has a good correlation with abdominal VAT measured by MRI. 6 The present study confirms that echocardiographic EAT thickness has a good correlation with abdominal VAT as measured by CT scan. Insulin resistance has been known to be an important factor in the pathogenesis of MS. 2 In the present study, the HOMA score, which represents insulin resistance, was weakly correlated with EAT thickness. These results are consistent with an earlier study that reported that EAT was significantly related to obesity-related insulin resistance. 14 Patients with MS had thicker EAT than those without MS, and EAT thickness increased linearly with an increase in the number of MS components. These results suggest that echocardiographic EAT thickness might be used as another imaging indicator of VAT, which is known to be related to insulin resistance and has a key role in the development of MS.

Relationship to the extent of coronary artery disease

Several studies have shown that increased abdominal VAT is

associated with CAD. 15 16 We investigated the relationship between EAT thickness and the extent of coronary athero- sclerosis. The subjects with angiographically significant CAD had thicker EAT than those without CAD. There was a moderate correlation between the thickness of EAT and the coronary atherosclerosis score. EAT thickness increased as the number of vessels with > 50% stenosis increased. On multiple logistic analysis of various CAD risk factors, EAT was an independent factor associated with CAD. These results are consistent with an earlier study that demonstrated that pericardial fat volume measured on CT scan was an indepen-

dent variable for the presence of angiographic CAD in Japanese men. 17 Thus, EAT may be considered to be an independent factor associated with CAD that can be used to predict the

extent of coronary atherosclerosis.

Relationship to coronary artery disease activity

It has been reported that human EAT has a high concentration of inflammatory mediators, such as tumour necrosis factor, monocyte chemotactic protein-1, interleukin 1b, interleukin 6, and interleukin 6 soluble receptors, and that it expresses a pathogenic profile of adipocytokines in patients undergoing coronary artery bypass graft surgery; this suggests that EAT is a

site of active inflammation. 13 18 We demonstrated a statistically significant correlation between EAT thickness and the C reactive protein level, though the degree of correlation was weak. The median EAT thickness was higher in subjects with unstable angina than in those with atypical chest pain or stable angina. These findings suggest that EAT may serve as a source

of inflammation that can influence CAD activity.

Echocardiographic method for the measurement of epicardial adipose tissue

We selected an area above the right ventricular free wall on the parasternal view to measure EAT thickness, as described

previously. 6 Autopsy studies have reported that this area has a somewhat higher EAT layer thickness. 1012 The parasternal views, which are the routinely obtained standard images during transthoracic echocardiography, allow the simple measurement of EAT thickness on the right ventricle with good reproduci- bility. The median EAT thickness was lower in our study cohort than in the previous study population. 6 This disagreement may be due to different study cohorts. Our study population was Asian and had a lower body mass index, whereas the previous study population was performed in obese Caucasian subjects. The echo-lucent area between the parietal pericardium and the right ventricular epicardium was considered to be EAT. Although massive pericardial fat could be misdiagnosed as

pericardial effusion, 19 in most patients we could differentiate pericardial effusion from epicardial fat using M-mode echocar- diography. Pericardial effusion was delineated as a more homogeneous echo-free space with clear visualisation of both pericardial layers on M-mode echocardiography. In contrast, compared with pericardial effusion, EAT presented as a some- what inhomogeneous, whitish-speckled, echo-lucent area. Patients in whom it was difficult to differentiate epicardial fat from a pericardial effusion were excluded from the study.

Limitations

The present study has several limitations. First, the study group was highly selected, since it involved only Asian patients undergoing their first coronary angiography due to chest pain. As well, the design of our study was cross-sectional. A prospective cohort study might be necessary to elucidate the clinical significance of EAT in the general population. Second, EAT thickness on the right ventricular free wall does not exactly represent the amount of total epicardial fat. In some subjects, there is also abundant epicardial fat on the left ventricular apex. 10 However, previous studies have shown that there is a good correlation between EAT thickness on echocardiography and on MRI; thus, echocardiography appears to be an accurate method to estimate EAT thickness. 6 One can assume that EAT thickness on the right ventricular free wall assesses the total amount of epicardial fat, since this area is known to have the highest epicardial fat layer, 1012 and EAT thickness on the right ventricular free wall was well correlated with abdominal VAT both in the present study and in a previous study. 6 Third, the coronary atherosclerosis score does not represent the actual atheroma volume or plaque burden; it is a crude method for

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Coronary artery disease

estimating CAD severity. However, coronary angiography is the most widely used technique for assessing coronary anatomy, and this score was validated in a previous study that compared C reactive protein with the extent of CAD. 8

CONCLUSION

In conclusion, measuring EAT thickness using transthoracic echocardiography is both simple and feasible. The present study results indicate that EAT may reflect the amount of visceral fat, which is related to insulin resistance and inflammation. The echocardiographic measurement of EAT may provide additional information for estimating CAD risk, diagnosing the MS, and predicting the presence of coronary atherosclerosis.

Acknowledgements: We are indebted to Dr Seung-Soo Sheen for his statistical assistance.

Funding: Supported by a grant from the Korean Society of Echocardiography.

Competing interests: None declared.

Ethics approval: Obtained.

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on July 10, 2014 - Published by group.bmj.com Relationship of epicardial adipose tissue by

Relationship of epicardial adipose tissue by echocardiography to coronary artery disease

S-G Ahn, H-S Lim, D-Y Joe, et al.

Heart 2008 94: e7 originally published online October 8, 2007

doi: 10.1136/hrt.2007.118471

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