Journal of Cardiology 65 (2015) 37–41

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Journal of Cardiology
journal homepage: www.elsevier.com/locate/jjcc

Original article

Pericardial fat volume is an independent risk factor for the severity of

coronary artery disease in patients with preserved ejection fraction
Kiyotaka Okura (MD)a,*, Koji Maeno (MD)a, Seiichiro Okura (MD)a,
Hitoshi Takemori (MD)a, Daishu Toya (MD)a, Nobuyoshi Tanaka (MD)a,
Shiro Miyayama (MD)b
a
Department of Medicine, Fukui-ken Saiseikai Hospital, Fukui, Japan
b
Department of Radiology, Fukui-ken Saiseikai Hospital, Fukui, Japan

A R T I C L E I N F O A B S T R A C T

Article history: Objectives: The aim of this study was to assess the relationship between the pericardial fat volume (PFV)
Received 22 January 2014 and the characteristics of coronary plaques in patients with ischemic heart disease (IHD).
Received in revised form 25 March 2014 Background: It has been suggested that pericardial adipose tissue promotes plaque development in
Accepted 30 March 2014
coronary artery disease (CAD).
Available online 17 May 2014
Methods: We analyzed the cardiac computed tomography scans in consecutive patients suspected of
CAD. PFV was quantified using validated software and indexed to body surface area, and the severity of
Keywords:
coronary stenosis was evaluated in the patients who underwent coronary angiography. A total of 105
Pericardial fat volume
Ischemic heart disease
subjects (mean age, 68  10 years) with IHD were categorized into tertiles of body surface area-indexed PFV
Severity of coronary lesions values (PFVi, cm3/m2): low-tertile, PFVi < 81.2 cm3/m2; mid-tertile, 81.2 cm3/m2  PFVi  114 cm3/m2;
Body mass index high-tertile, PFVi > 114 cm3/m2. Their body mass index (BMI), waist circumference, Gensini score (GS), and
Waist circumference coronary plaque component were evaluated.
Results: The GS was significantly different between the high-tertile and the low-tertile groups,
indicating a stepwise decrease in GS from high-tertile to mid-tertile and to low-tertile. PFVi had a
significant positive correlation with BMI (p = 0.0001) and GS (p < 0.0001). However, no significant
association was found between GS and BMI. On the multivariate analysis, high PFVi remained an
independent predictor for the coronary artery disease severity (p < 0.001), while BMI and waist
circumference were not independent predictors.
Conclusions: Obese patients were found to have more PFVi, and the characteristics of their coronary
lesions were more severe. Pericardial adipose tissue as unique ectopic fat might be more highly
associated with IHD progression.
ß 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

Introduction Kaya et al. [4] reported that an echocardiographic epicardial fat

Pericardial fat is a type of visceral adipose tissue (VAT) that is
defined as the adipose tissue between the surface of the myocardium
and the epicardium. Similar to other VAT, pericardial fat serves an
important endocrine and inflammatory function, given its direct
apposition to the myocardium and coronary arteries [1,2].
Pericardial fat may play a central role in the pathogenesis of
cardiovascular disease, mediated by its inflammatory properties [3].
DOI of commentary article: http://dx.doi.org/10.1016/j.jjcc.2014.07.004.
* Corresponding author at: Department of Medicine, Fukui-ken Saiseikai Hospital,
7-1 Funabashi, Wadanaka-cho, Fukui 918-8503, Japan. Tel.: +81 776 23 1111;
fax: +81 776 28 8518.
E-mail address: kokura-fki@umin.ac.jp (K. Okura).
thickness is independently associated with the presence of coronary
artery disease (CAD), and Dagvasumberel et al. [5] reported
epicardial adipose tissue/body surface area was the single predictor
for >50% coronary luminal narrowing in men. Recent studies
demonstrated that 64-multi detector computed tomography
(MDCT) is suitable for volumetric quantization. However, there
have been no reports on the association between the pericardial fat
volume (PFV) and the severity of coronary lesions. We, therefore,
hypothesized that the pericardial fat increased steeply in patients
with significant CAD. In this study, body surface area-indexed PFV
(PFVi, cm3/m2) was measured by MDCT, and the relationship
between the PFVi and the severity of CAD was evaluated in patients
referred for coronary angiography.

http://dx.doi.org/10.1016/j.jjcc.2014.03.015
0914-5087/ß 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
38 K. Okura et al. / Journal of Cardiology 65 (2015) 37–41
Methods
Study population
A total of 105 consecutive ischemic heart disease (IHD) patients
who underwent MDCT angiograms and coronary angiography
between May 2012 and September 2013 were evaluated. Patients
with a history of previous cardiac surgery, percutaneous coronary
intervention, symptomatic heart failure, acute coronary syndrome,
cardiomyopathy, and severe renal failure were excluded from the
study. Written, informed consent was obtained from all patients.
Cardiac computed tomography scan protocol
Cardiac CT scans were performed with MDCT scanner (Aquilion
64, Toshiba Medical Systems, Tokyo, Japan) used with parameters
as previously reported [6]. Reconstruction sets at 75% of the cardiac
cycle or at a particular optimal phase were prepared from the raw
data files. The contrast material (Omnipaque-300; Daiichi-Sankyo
Pharmaceutical, Tokyo, Japan) was administered using a mechani-
cal power injector through a 20-gauge cannula inserted into the
antecubital vein. To minimize differences in the arterial enhance-
ment across the patients, a body weight-tailored contrast material
dose (0.7 mL/kg) and fixed injection duration (9 s) were used [7].
An oral b-blocker (metoprolol, 20 mg) was administered immedi-
ately prior to CT imaging to maintain heart rates at <65 bpm and
thus improve image resolution. The reconstructed CT image data
were transferred to a workstation for post-processing (ZIO M900,
Admin/ZIO, Tokyo, Japan).
Quantification of epicardial fat volume with CT
PFV was measured three-dimensionally in all patients using
contrast-enhanced images, as reported previously [7–9]. Segmen-
tation of the overall volume was automatically interpolated using
manually defined tracings. Next, PFV was quantified by calculating
the total volume of the tissue whose CT density ranged from 190
to 30 Hounsfield units within the pericardial cavity using the
workstation (Fig. 1). We trimmed along the pericardial sac using
axial, coronal, and sagittal slices, volume-rendered images. PFV
was defined as any adipose tissue located within the pericardial
sac. A slice 1 cm above the most cranial slice including the left
anterior descending coronary artery (LAD) was defined to be the
superior border of the pericardial fat. Patients were categorized
according to tertiles of PFVi: low-tertile (PFVi < 81.2 cm3/m2,
n = 35); mid-tertile (81.2 cm3/m2  PFVi  114 cm3/m2, n = 35),
and high-tertile (PFVi > 114 cm3/m2, n = 35).
[(Fig._1)TD$IG]
Fig. 1. Representative case with high pericardial fat volume of a 49-year-old male with metabolic syndrome with a waist circumference of 106 cm. Invasive coronary
angiography shows a significant stenosis at the middle segment of the left anterior descending coronary artery (A, arrow). Angiography with 64-multi detector computed
tomography shows a large amount of pericardial fat (B). The parietal pericardium (open arrow), paracardial fat (P), epicardial fat (E), coronary sinus (CS), and esophagus (Eso)
are visible. Solid arrows (B), fatty deposits within the atrial septum. And pericardial adipose tissue has been reconstructed three-dimensionally (C). RV, right ventricle; LV, left
ventricle.
Coronary angiography and analysis
Based on the modified AHA classification, the coronary arteries
were divided into 17 segments, and the segments with a diameter
>2.0 mm were analyzed.
CAD was defined as 75% stenosis (according to the American
Heart Association classification) on conventional coronary angi-
ography. Conventional coronary angiograms were recorded in
multiple projections for the left and the right coronary arteries and
reviewed for significant coronary artery obstructions by cardiol-
ogists unaware of the amounts of pericardial fat.
The Gensini score (GS), an index of the severity of coronary
lesions, was calculated as the sum of all segment scores [10].
Severity scores assigned to the specific percentage luminal
diameter reduction of the coronary artery segment were 32 for
100%, 16 for 99%, 8 for 75%, 2 for 50%, and 1 for 25%. Each principal
vascular segment was assigned a multiplier in accordance with the
functional significance of the myocardial area supplied by that
segment: the left main coronary artery 5; the proximal segment
of the LAD 2.5; the proximal segment of the circumflex artery
2.5, and the mid-segment of the LAD 1.5.
Assessment of risk factors and covariates
Blood was drawn after an overnight fast. Hypertension was
defined as a systolic blood pressure 130 mmHg, a diastolic blood
pressure 85 mmHg, or the use of an antihypertensive treatment.
A fasting triglyceride level  150 mg/dL and a high-density
lipoprotein (HDL) cholesterol level < 40 mg/dL were considered
abnormal. Diabetes mellitus was diagnosed based on the criteria
set by the World Health Organization or by the use of hypoglyce-
mic agents or insulin. Abdominal obesity was defined as a waist
circumference 85 cm for Japanese males and 90 cm for
Japanese females [11]. Metabolic syndrome (MetS) was diagnosed
according to the modified Adult Treatment Panel III criteria, which
include the waist circumference with the presence of three or more
metabolic abnormalities [9].
Statistical analysis
Categorical variables are reported as numbers (%), and
continuous variables are reported as mean  SD. The chi-square
test was used for comparing categorical variables, and the unpaired t-
test was used for continuous variables. A p-value < 0.05 was
considered significant, and all tests were two-tailed. All analyses
were performed using SPSS 17.0 (SPSS Inc., Chicago, IL, USA).
 K. Okura et al. / Journal of Cardiology 65 (2015) 37–41 39

Results Table 1
Baseline characteristics of the study patients by tertiles of indexed pericardial fat
volume.
Study sample characteristics
Parameters Indexed pericardial fat volume (cm3/m2)
Table 1 lists the clinical characteristics of the study population Low-tertile Mid-tertile High-tertile
by tertiles of PFVi. Most patients were men (77%), and the mean age
Number 35 35 35
of all patients was 68  10 years. BMI and waist circumference were Age 65  10 70  8 68  11
significantly larger and hypertension was more common in the high- Male/female 27/8 23/12 26/9
tertile group than in the low-tertile group (p < 0.05). HDL-cholesterol Body mass index (kg/m2) 23.0  2.6 24.2  2.5 25.9  2.6*
was lower in the high-tertile group than in the low-tertile group Waist circumferences (cm) 85  9 87  8 93  8*
Hypertension (%) 22 (64) 25 (72) 26 (75)
(p < 0.05), and the prevalence of MetS was 41%. Fig. 1 shows a Dyslipidemia (%) 28 (82) 23 (66) 26 (75)
representative case of a patient with MetS with a large amount of LDL-cholesterol (mg/dL) 113  25 111  26 106  31
pericardial fat. HDL-cholesterol (mg/dL) 54  12 48  14 45  12*
Overall, the mean PFVi was 102  35 (range 35–210) cm3/m2. Triglycerides (mg/dL) 144  88 138  67 147  61
Diabetes mellitus (%) 14 (39) 10 (28) 13 (38)
Three-vessel disease was more frequent in the high-tertile group than
Fasting plasma glucose (mg/dL) 119  27 112  19 113  25
in the other groups (p < 0.05) (Table 2). GS was significantly different Hemoglobin A1c (%) 6.5  1.2 6.2  0.8 6.4  1.2
between the high-tertile group and the low-tertile group (p < 0.05), Metabolic syndrome 14 (39) 13 (38) 15 (44)
indicating a stepwise decrease in GS from high-tertile to mid-tertile (Adult Treatment Panel III) (%)
and to low-tertile. Current smoker (%) 19 (57) 20 (58) 18 (52)
Medications
Statins (%) 26 (75) 18 (52) 26 (75)
Correlations between PFVi, BMI, and the Gensini score ACE inhibitors or ARBs (%) 19 (54) 20 (58) 22 (65)
Ejection fraction 64  11 66  7 64  10
PFVi correlated positively with BMI (r = 0.376, p = 0.0001; on echocardiography, %
Fig. 2A). GS had a significant positive correlation with PFVi Data are presented as means  SD, number of patients (%). LDL, low-density
(r = 0.514, p < 0.0001; Fig. 2B). However, no significant association lipoprotein; HDL, high-density lipoprotein; ACE, angiotensin-converting enzyme;
was found between GS and BMI or waist circumference. ARB, angiotensin II receptor blocker.
*
p < 0.05 compared to the low-tertile group.

Factors associated with the Gensini score

Multiple risk factors have been associated with the severity of

CAD, including age, HDL-cholesterol, and PFVi. The results of
Table 2
univariate and multivariate linear regression analyses examining Comparison of MDCT and coronary angiography results for patients by tertiles of
the association between GS and these risk factors are shown in indexed pericardial fat volume.
Table 3. On univariate linear regression analysis, multiple risk
Parameters PFVi (cm3/m2)
factors, including age, HDL-cholesterol and PFVi, were significantly
related to GS (r = 0.248, r = 0.329, and r = 0.514, respectively, Low-tertile Mid-tertile High-tertile
p < 0.05). Multiple regression analysis was performed to identify PFV (cm3) 114  16 159  22 243  47*
the independent risk factors associated with the GS. HDL- PFVi (cm3/m2) 68  9 97  8 144  26*
cholesterol (B = 0.587; 95% CI: 1.049 to 0.126, p = 0.013), Coronary stenosis (375% diameter reduction)
1-Vessel disease, n (%) 20 (57) 23 (68) 14 (41)
and PFVi (B = 0.423; 95% CI: 0.235–0.611, p < 0.001) were the 2-Vessel disease, n (%) 9 (25) 6 (17) 10 (28)
strongest independent variables related to the Gensini score. 3-Vessel disease, n (%) 6 (17) 5 (14) 11 (31)*
Gensini score 28  23 32  28 54  34*

Discussion Data are presented as means  SD, number of patients (%). MDCT, 64-multi
detector computed tomography; PFV, pericardial fat volume; PFVi, indexed
pericardial fat volume.
Major findings *
p < 0.05 compared to the low-tertile group.

The present study demonstrated the relationship between

[(Fig._2)TD$IG]
coronary stenosis and PFVi as measured by MDCT. The major

A r = 0.376 B r = 0.514
y = 0.033x + 21.16 y = 0.442x - 8.79
(kg/m2) p = 0.0001 p < 0.0001
34 140
Body mass index

Gensini score

30 100

26
50

22
0
18
50 100 150 220 50 100 150 220

indexed pericardial fat volume values (cm3/m2)

Fig. 2. Regression plots showing the correlations between indexed pericardial fat volume values (PFVi) and (A) body mass index (BMI), (B) the Gensini score. PFVi had a
significant positive correlation with BMI (r = 0.376, p = 0.0001), Gensini score (r = 0.514, p < 0.0001).
40 K. Okura et al. / Journal of Cardiology 65 (2015) 37–41
Table 3
Correlations between the Gensini score and cardiovascular risk factors.
Univariate linear regression
r p
Age, years 0.248
Sex, male 0.003
Body mass index 0.135
Waist circumferences 0.198
Hypertension 0.191
LDL-cholesterol 0.122
HDL-cholesterol 0.329
Triglyceride 0.015
Fasting plasma glucose 0.095
Hemoglobin A1c 0.093
Metabolic syndrome 0.181
Active smoking 0.068
PFVi 0.514
Mutivariate linear regression (r = 0.554, p < 0.001)
B (95% CI) b p
HDL-cholesterol 0.587 ( 1.049 to 0.126) 0.26
PFVi 0.423 (0.235–0.611) 0.46
LDL, low-density lipoprotein; HDL, high-density lipoprotein; PFVi, indexed
pericardial fat volume; CI, confidence interval.
findings of the study were as follows. First, consistent with most
previous observations [4,6], it was demonstrated that accumula-
tion of PFVi was related to increased severity of CAD in patients
with preserved ejection fraction. Second, PFVi was positively
correlated with BMI and was increased in CAD subjects. Third, it
was found that the coronary severity score may not be correlated
with BMI and waist circumference. This result may be affected by
the fact that the number of obese patients was small, and the
degree of obesity of most patients in this study was not severe.
Finally, high PFVi was the independent predictor of the severity of
coronary disease, but markers of visceral adiposity (BMI and waist
circumference) were not. Of interest, PFVi remained a significant
predictor, suggesting that PFVi is not purely a reflection of VAT in
the predisposition to atherosclerosis. The present study is the first
to find that accumulation of PFVi was related to increased severity
of significant atherosclerotic disease in symptomatic CAD subjects.
Role of pericardial fat in the pathophysiology
Pericardial adipose tissue is recognized as ectopic fat depot in
close proximity to the myocardium and coronary arteries, and it is
suspected to be implicated in the pathogenesis of coronary
atherosclerosis. It has been hypothesized that, unlike large fat
deposits, such as visceral abdominal fat, which primarily act
systemically, pericardial fat probably acts locally through
mechano-structural or paracrine mechanisms. Several studies
have reported the potential role of epicardial fat in the
pathophysiology of coronary atherogenesis [1,2,7], and hypotheti-
cal mechanisms of epicardial fat in coronary atherogenesis have
been proposed [12], such as an endocrine effect through adventitial
vasa vasorum. Just like coronary arteries, coronary veins are also
surrounded by pericardial fat. Therefore, pericardial fat surround-
ing the thin-walled coronary veins may exert greater systemic
effects by diffusion of its small, metabolically active molecules into
the circulation. There may also be a direct paracrine effect.
Adipokines can diffuse in the interstitial fluid across the vascular
wall and stimulate atherogenesis. Pericardial fat is a metabolically
active fat depot that is in anatomic proximity to the myocardium,
sharing the same microcirculation, and may have important
paracrine effects.
In addition, Konishi et al. [7] have shown that pericardial fat had
significantly more leukocyte common antigen-positive cells in
CAD autopsy cases. Hirata et al. [1] reported that coronary
atherosclerosis is associated with macrophage polarization in
epicardial adipose tissue. Although the exact pathophysiologic
mechanism has not been characterized, it has been hypothesized
that pericardial fat releases pro-atherogenic inflammatory cyto-
0.014
0.980
kines in close proximity to the coronary arteries [3]. Hirata et al. [2]
0.186 suggested that chronic inflammation in epicardial fat may
0.070 influence the pathogenesis of coronary atherosclerosis by inflam-
0.060 matory cell infiltration in patients with CAD. Recent reports by
0.237
other investigators have suggested that epicardial fat may act as a
0.001
0.885 paracrine organ that affects the coronary arteries by promoting
0.342 chronic inflammation [13] and endothelial dysfunction.
0.381 Atherosclerotic plaque formation involves a cascade of events,
0.079 initiated by endothelial dysfunction, followed by inflammatory cell
0.520
infiltration into the intima, transcytosis of cholesterol-rich
<0.001
lipoproteins, oxidative modification, foam cell formation, and
smooth muscle cell proliferation.
0.013 Pericardial fat as a predictor of CAD
<0.001
Previous studies have demonstrated that pericardial fat could
mediate the development of CAD. It has been found that pericardial
fat could contribute to coronary atherosclerosis, myocardial
ischemia [14], coronary plaque characteristics [12], and future
cardiovascular events [15]. In the present study, PFVi was related
to the presence, extension, and stenosis severity of coronary
plaque. These findings are in good agreement with a recent report
by Mahabadi et al. [16], who found that epicardial fat is associated
with coronary events in the general population independent of
cardiovascular risk factors.
Furthermore, the PFVi was comparable among patients with
stenotic and non-stenotic plaques, suggesting that the accumula-
tion of pericardial fat is associated with early stages of coronary
atherogenesis. Pericardial adipose tissue plays a crucial role in the
development of CAD and atherosclerosis, beyond systemic obesity.
In this study, PFVi was found to be independently associated with
CAD severity, even though it is a small amount of body fat. These
findings suggest that pericardial fat is more highly associated with
the early development of CAD than simple anthropometric
measures of abdominal obesity.
Hence, PFVi measurement may provide novel, additional risk
stratification for patients suspected of having CAD, as well as
visceral adipose tissue [17]. Together, these results suggest that an
increased PFVi may serve as a marker for severe atherosclerosis
and might also be a risk factor for significant CAD in the general
population. Furthermore, PFVi assessment could contribute to the
prevention and management of CAD in patients with preserved
ejection fraction. The present finding that the association of PFVi
with coronary atherosclerosis was not completely explained by
standard risk factors is consistent with the evidence suggesting
that the link between PFVi and obesity-related complications may
involve novel biological pathways.
Study limitations
The present study has several limitations. First, we did not have
data on visceral fat measurements, which could have influenced
the incident CAD [17]. Instead, we used BMI and waist circumfer-
ence as surrogate markers of visceral adiposity, and the inclusion of
these markers in the multivariate model did not attenuate the
association of PFVi with the severity of CAD.
Second, data were obtained in routine medical care. Therefore,
we could not measure serum or tissue inflammatory cytokines and
adipokines, both of which can lead to accelerated atherosclerosis
or plaque vulnerability. However, our main aim was to investigate
the relationship between the PFVi and the severity of CAD.
 K. Okura et al. / Journal of Cardiology 65 (2015) 37–41
Third, our study was a single-center design and the inclusion of
self-referred patients may have harbored an inherent bias. Finally,
no follow-up data were available. Indeed, whether PFVi quantity
may have a prognostic value needs to be evaluated in prospective
follow-up studies.
Conclusions
This study demonstrated a significant association between the
severity of CAD and PFVi, but not with waist circumference or BMI.
Importantly, PFVi with preserved ejection fraction might be more
highly associated with the progression of IHD. Therefore, PFVi
measurement may be viewed as an indicator of global atherogenic risk.
Acknowledgment
The authors would like to express their deep appreciation to
Mr. Yasunobu Noji for his help in data analysis.
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