Skip to main content
Erschienen in: BMC Cardiovascular Disorders 1/2020

Open Access 01.12.2020 | Research article

Epicardial adipose tissue is a predictor of ascending aortic dilatation in hypertensive patients, but not paracardial adipose tissue

verfasst von: Onur Argan, Eyup Avci, Tarik Yildirim, Ozgen Safak

Erschienen in: BMC Cardiovascular Disorders | Ausgabe 1/2020

Abstract

Background

Ascending aortic aneurysms are one of the major causes of mortality. In recent years, there is a growing interest of epicardial adipose tissue (EAT) and related diseases. The aim of this study was to investigate the relationship of EAT, and PAT with ascending aortic dilatation (AAD).

Methods

We included 934 patients with hypertension in this study. The patients were evaluated by a complete transthoracic echocardiographic examination, including measurements of EAT, PAT, and aortic dimensions. Aortic size index (ASI) was used for diagnosing AAD. The patients were divided into two groups: dilated ascending aorta diameter (ASI ≥ 21 mm / m2, n = 102) or normal aortic diameter (ASI < 21 mm / m2, n = 832) according to the ASI. Characteristics of these patients were compared before and after propensity score matching analysis.

Results

Patients with AAD were older (72.3 ± 11.6 vs. 61.7 ± 12.7 years, p <  0.001), had more female gender (66% vs. 54%,p = 0.021) than patients with normal ascending aorta (AA). After propensity score matching analysis (77 vs. 77), EAT [OR:1.461, %95CI (1.082–1.974), p = 0.013] was independently associated with AAD in multivariate logistic regression analysis. In ROC curve analysis, EAT > 0.45 cm had 51.9% sensitivity and 62.3% specificity [AUC = 0.617, P = 0.012, 95% CI (0.529–0.707)].

Conclusion

Based on our findings, increased EAT may be suggested as an independent risk factor for AAD due to local or systemic effects in hypertensive patients.
Hinweise

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Abkürzungen
EAT
Epicardial adipose tissue
AAD
Ascending aortic dilatation
BMI
Body mass index
PAT
Paracardial adipose tissue
BSA
Body surface area
CAD
Coronary artery disease
DM
Diabetes mellitus
AA
Ascending aorta
EF
Ejection fraction
LVEDD
Left ventricle end diastolic diameter
LA
Left atrium
Hb
Haemoglobin
Htc
Haematocrit
AST
Aspartate transaminase
ALT
Alanine transaminase
eGFR
Estimated glomerular filtration rate

Background

Ascending aortic aneurysms and dissections are one of the major causes of mortality [1]. Despite important recent development in understanding of its pathogenesis, the role of haemodynamics and other reasons are partially known yet. The pathogenesis of ascending aortic dilatation (AAD) includes several factors with systemic and local effects. The aetiology is multifactorial, including environmental and genetic factors that play important roles in progression of aortic disease [2]. Given that the pathogenesis of AAD maintains unclear, the main reason seems to be related to the deficiencies or defects in structural proteins, such as collagen and elastin in the aortic wall [3]. Changes of the extracellular matrix are suggested as a key factor in the pathogenesis of AAD [24]. Cystic medial degeneration responsible for weakened aortic wall is related to the degeneration of smooth muscle cell and elastic fibre apoptosis [5]. Also, the inflammatory process associated with atherosclerosis causes aortic dilatation [6].
Hypertension is one of the considerable risk factors for AAD. AAD is often observed in hypertensive patients compared with normotensive individuals and is correlated with cardiac and noncardiac organ injury in hypertensive patients [24]. Hypertension is one of the most common diseases and a worldwide health problem. It is related to stroke, renal disease, cardiac disease, aortic disease, mortality and morbidity. It generally progresses silently until it causes end organ damage. However, it is a treatable and preventable disease.
In recent years, there is a growing interest towards the effects of epicardial adipose tissue (EAT) on hypertension and cardiovascular risk factors. EAT is a visceral adipose tissue found between the pericardium and the myocardium [7]. It is generally placed in the atrioventricular and interventricular groove throughout the coronary arteries. There is no any fascia between the myocardium and EAT; therefore, they have same microcirculation. EAT secretes antiinflammatory and antiatherogenic mediators and supplies energy to the myocardium [810]. However, under pathological conditions, EAT appears to play a critical role in atherosclerosis, hypertension and progression of metabolic diseases as it acts as a proinflammatory and prothrombotic organ [11]. Tumour necrosis factor alpha, interleukin-6 and monocyte chemoattractant protein-1, secreted from the EAT [12], immediately affect atherosclerosis [13, 14]. As a result, increased EAT is related to atherosclerosis [15]. EAT may play a provocative role for AAD with paracrine and systemic endocrine effects on vessels [16].
Paracardial adipose tissue (PAT) is an ectopic fat depot surrounding the heart [17, 18]. It is placed anterior to the EAT and outside the parietal layer of the pericardium [19]. The pericardium restricts the communication between the PAT and EAT. Studies about the different roles between EAT and PAT are limited. A few studies showed that PAT was more closely related with abdominal visceral adipose tissue and metabolic risk than EAT. It is also recommended that PAT might be a marker for increased metabolic risk and visceral adipose tissue on thoracic imaging [1721].
The focus of the studies has been commonly on EAT, neglecting the potentially additive effects by the PAT on cardiovascular diseases. The aim of this study was to investigate the associations of EAT, and PAT with AAD in hypertensive patients.

Methods

The present study included 934 hypertensive patients who underwent complete transthoracic echocardiographic examination involving measurements of aortic dimensions, EAT and PAT. When diagnosing AAD, we used the body surface area (BSA)-adjusted classifications. For this purpose, we used Roman’s classification (aortic size index, ASI) [22]. ASI was calculated by the following formula: ASI = AA diameter (mm)/ BSA (m2) [23]. AAD was defined as a ASI ≥ 21 mm/m2 according to the Roman’s classification [23]. A total of 102 hypertensive patients with AAD were compared with 832 hypertensive patients with normal aortic diameter. Exclusion criteria were bicuspid and rheumatic aortic valve disease, Marfan syndrome, Ehlers-Danlos syndrome, Familial Thoracic Aortic Aneurysm Syndrome, Turner Syndrome and other connective tissue disorders, infectious conditions, restrictive and hypertrophic cardiomyopathy, renal failure requiring dialysis, malignancy and pregnancy. Hypertension was defined as the documentation of a blood pressure of more than 140/90 mmHg or the use of antihypertensive drugs.
The study was approved by the Institutional Ethics Committee and conducted in accordance with the principles set out in the Declaration of Helsinki.
The demographic data included gender, age, body mass index (BMI), a history of coronary artery disease (CAD) and diabetes mellitus (DM). BMI was calculated by the following formula: BMI = weight (kg) / height2 (m). BSA was calculated using formule; BSA (m2) = ([Height (cm) x Weight (kg)]/ 3600)½ . The echocardiographic data involved EAT, PAT, ejection fraction (EF), left ventricle end diastolic diameter (LVEDD), left atrium (LA) diameter, right ventricle diameter and mitral, aortic and tricuspid valve diseases.
For biochemical data, we collected haemoglobin (Hb), haematocrit (Htc), white blood cell count, platelet, creatinine, urea, HbA1c, aspartate transaminase (AST), alanine transaminase (ALT), total cholesterol, HDL cholesterol, LDL cholesterol and triglyceride levels. The estimated glomerular filtration rate (eGFR) was calculated using the Modification of Diet in Renal Disease formula.
Transthoracic echocardiography was carried out using a Vivid S5 GE Healthcare system. Each patient underwent two-dimensional transthoracic echocardiography according to the recommendations of the European Association of Echocardiography [24]. Parasternal long axis view was used to view the proximal AA. The ascending aortic diameters were calculated between the inner edges of the aortic lumen perpendicular to the long axis 2 cm above the sinotubular junction at the end of the diastole in views showing the largest aortic diameter [16]. The parasternal long axis view was performed to measure maximal EAT thickness. EAT was defined as echo-free space between the outer wall of the myocardium and the visceral layer of the pericardium [14]. PAT was defined as the hypoechoic space in front of EAT and on the external pericardium [1425]. The values were measured in three cardiac cycles and were averaged.

Statistical analysis

The SPSS 13.0 (SPSS Inc., an IBM Company, Chicago, USA) was used for statistical analyses. Data were tested for distribution using the Kolmogorov–Smirnov test. Categorical variables were introduced as percentages. Continuous variables were introduced as mean ± SD, and abnormally distributed variables are introduced as median (25–75 percentages). Normally distributed continuous variables were analysed with the 2-tailed Student’s t test, and not normally distributed variables were analysed with the Mann–Whitney U test. Categorical data were analysed using the Fisher’s exact test or chi square. Pearson and Spearman tests were used for correlation analysis. Since the study was nonrandomized, a logistic regression model with propensity scores was created in order to balance patient characteristics and perform propensity-matched analysis of the patients with and without AAD. Clinical determinants of the hypertensive patients with AAD were established using univariate and multivariable logistic regression analyses. Logistic regression analyses were performed for the multivariate analysis of independent variables, which were included if they were statistically significant in the univariate analyses. Receiver-operating characteristic (ROC) curve graphics were used to determine the cutoff value of EAT. A p value < 0.05 was accepted as statistically significant.

Results

A total of 934 hypertensive patients were divided into the following two groups: patients with ascending aortic dilatation (AAD) (102 patients) and patients with normal ascending aorta (AA) (832 patients). Baseline characteristics and echocardiographic and biochemical parameters are summarised in Table 1.
Table 1
Baseline characteristics of patients with and without aortic dilatation
Characteristic
Aortic Dilatation
(n = 102)
Normal Aorta
(n = 832)
P-value
Age (years)
72.3 ± 11.6
61.7 ± 12.7
<  0.001
Female n (%)
67 (66)
446 (54)
0.021
Body mass index (kg/m2)
26.8 ± 4.5
30.7 ± 4.9
<  0.001
BSA (m2)
1.70 ± 0.19
1.90 ± 0.19
<  0.001
Height (m)
156 ± 8
164 ± 9
<  0.001
Weight (kg)
66 ± 13
83 ± 14
<  0.001
Coronary Artery disease n (%)
29 (29)
195 (23)
0.265
Diabetes mellitus n (%)
18 (18)
245 (29)
0.012
Dyslipidemia n (%)
33 (32)
272 (33)
0.945
Echocardiographic parameters
 Ejection fraction (%)
57.6 ± 7.4
59.4 ± 5.7
0.005
 Epicardial adipose tissue (cm)
0.48 ± 0.15
0.44 ± 0.11
<  0.001
 Paracardial adipose tissue (cm)
0.49 ± 0.18
0.49 ± 0.17
0.738
 Ascending aortic diameter (mm)
38.5 ± 4.2
34.0 ± 3.6
<  0.001
 LVEDD (mm)
48.6 ± 4.6
47.8 ± 4.0
0.092
 Left atrium diameter (mm)
38.2 ± 5.9
36.4 ± 5.7
0.004
 Right ventricular diameter (mm)
23.1 ± 2.5
23.2 ± 2.9
0.628
 Left ventricular hypertrophy n (%)
44 (44)
280 (34)
0.042
 E
80 ± 25
78 ± 24
0.461
 A
89 ± 18
83 ± 18
0.003
 E/A
0.9 ± 0.3
1.0 ± 0.3
0.057
 e’
6.9 ± 1.7
7.3 ± 1.9
0.046
 E/ e’
11.9 ± 3.3
11.3 ± 4.4
0.158
Mitral regurgitation
  
<  0.001
Grade-1n(%)
25 (25)
155 (19)
 
Grade-2 n (%)
14 (14)
50 (6)
 
Grade-3n(%)
4 (4)
9 (1)
 
Aortic regurgitation
  
<  0.001
Grade-1 n (%)
30 (29)
129 (16)
 
Grade-2 n (%)
20 (20)
47 (6)
 
Grade-3 n (%)
4 (4)
3 (0)
 
Tricuspid regurgitation
  
0.007
Grade-1 n (%)
42 (41)
342 (41)
 
Grade-2 n (%)
15 (15)
68 (8)
 
Grade-3 n (%)
10 (10)
38 (5)
 
Aortic stenosis
  
<  0.001
Grade-1 n (%)
9 (9)
12 (1)
 
Grade-2 n (%)
1 (1)
5 (1)
 
Grade-3 n (%)
1 (1)
0 (0)
 
Medications
 Calcium canal bloker n (%)
46 (45)
401 (48)
0.554
 ACE -I/ARB n (%)
65 (64)
553 (67)
0.581
 Beta-bloker n (%)
48 (47)
275 (33)
0.005
 Doxazosine n (%)
2 (2)
31 (4)
0.362
 Thiazide diuretic n (%)
46 (46)
415 (50)
0.450
 Statin n (%)
24 (24)
151 (18)
0.189
 Acetylsalicylic acid n (%)
23 (23)
192 (23)
0.905
Biochemical parameters
 Hemoglobin (g/dl)
12.7 ± 2.0
13.4 ± 1.7
<  0.001
 WBC (/mm3)
6.9 ± 2.0
7.3 ± 2.1
0.085
 Platelet (× 103/μL)
232 ± 79
249 ± 74
0.032
 eGFR (ml/min)
68.9 ± 22.0
78.1 ± 19.1
<  0.001
 Glucose (mg/dl)
10.9.6 ± 24.7
125.7 ± 53.0
0.003
 HbA1c (%)
6.2 ± 0.7
6.5 ± 1.3
0.033
 Total Cholesterol (mg/dl)
201 ± 27
200 ± 29
0.876
 LDL Cholesterol (mg/dl)
123 ± 32
118 ± 30
0.108
 HDL Cholesterol (mg/dl)
48 ± 11
47 ± 10
0.324
 Triglyceride (mg/dl)
132 (92–180)
167 (109–209)
0.004
 AST (U/L)
19 (17–23)
22 (18–26)
0.002
 ALT (U/L)
14 (12–19)
18 (14–25)
<  0.001
BSA body surface area, AST Aspartate transaminase, ALT Alanine transaminase, WBC White blood cell count, LVEDD Left ventricular end diastolic diameter, eGFR Estimated glomerular filtration rate. ACE Angiotensin-converting enzyme inhibitors, Angiotensin II receptor blockers, BMI body mass index
Patients with AAD were older than the patients with normal AA (72.3 ± 11.6 vs. 61.7 ± 12.7 years, p <  0.001), had more female gender (66% vs. 54%,p = 0.021) compared with patients with normal ascending aorta (AA). BMI and BSA were lower in patients with AAD than patients with normal AA (Table 1). EAT thickness (0.48 ± 0.15, p <  0.001) was significantly higher in the patients with AAD compared with the patients with normal AA. There was no difference between groups regarding PAT thickness (0.49 ± 0.18 vs 0.49 ± 0.17, p = 0.738). β-Blocker usage is higher in patients with AAD than patients with normal AA.
In biochemical analyses, eGFR was lower in patients with AAD than patients with normal AA (68.9 ± 22.0 vs 78.1 ± 19.1, p <  0.001).
After propensity score matching analysis (77 vs. 77), EAT and age were significantly higher in patients with AAD than those without AAD (0.49 ± 0.16 vs 0.42 ± 0.10, P = 0.002; 69.8 ± 11.4 vs 64.4 ± 11.3, p <  0.001, respectively). Characteristics of the population after matching are presented in Table 2. In the matched population, EAT was associated with AAD in multivariate logistic regression analysis [OR:1.461, %95CI (1.082–1.974), p = 0.013] (Table 3).
Table 2
Baseline characteristics of patients with and without aortic dilatation after matching.
Characteristic
Aortic Dilatation (n = 77)
Normal Aorta (n = 77)
P-value
Age (years)
69.8 ± 11.4
64.4 ± 11.3
<  0.001
Female n (%)
50 (65)
48 (62)
0.014
Body mass index (kg/m2)
27.8 ± 4.5
29.6 ± 5.1
0.018
BSA (m2)
1.74 ± 0.16
1.87 ± 0.25
<  0.001
Height (m)
158 ± 8
162 ± 11
0.021
Weight (kg)
70 ± 11
78 ± 18
0.001
Coronary Artery disease n (%)
25 (33)
13 (17)
0.025
Diabetes mellitus n (%)
15 (15)
15 (15)
1.000
Dyslipidemia n (%)
28 (36)
23 (30)
0.392
Echocardiographic parameters
 Ejection fraction (%)
58.0 ± 7.3
58.5 ± 6.2
0.679
 Epicardial adipose tissue (cm)
0.49 ± 0.16
0.42 ± 0.10
0.002
 Paracardial adipose tissue (cm)
0.49 ± 0.18
0.49 ± 0.17
0.941
 Ascending aortic diameter (mm)
39.0 ± 3.8
29.3 ± 3.1
<  0.001
 LVEDD (mm)
48.8 ± 4.5
46.8 ± 4.3
0.005
 Left atrium diameter (mm)
38.3 ± 6.1
35.0 ± 6.9
0.002
 Right ventricular diameter (mm)
23.1 ± 2.5
22.7 ± 3.4
0.416
 Left ventricular hypertrophy n (%)
32 (42)
23 (30)
0.130
 E
80 ± 25
78 ± 21
0.610
 A
87 ± 18
86 ± 16
0.639
 E/A
0.9 ± 0.3
0.9 ± 0.2
0.478
 e’
7.1 ± 1.6
7.5 ± 2.0
0.234
 E/ e’
11.7 ± 3.3
11.1 ± 3.6
0.344
Mitral regurgitation
  
0.189
Grade-1n(%)
18 (23)
19 (25)
 
Grade-2 n (%)
11 (14)
5 (7)
 
Grade-3n(%)
2 (0)
0 (0)
 
Aortic regurgitation
  
0.710
Grade-1 n (%)
21 (27)
17 (22)
 
Grade-2 n (%)
11 (14)
15 (20)
 
Grade-3 n (%)
2 (3)
1 (1)
 
Tricuspid regurgitation
  
0.595
Grade-1 n (%)
32 (42)
35 (46)
 
Grade-2 n (%)
10 (13)
5 (7)
 
Grade-3 n (%)
6 (8)
7 (9)
 
Aortic stenosis
  
0.565
Grade-1 n (%)
4 (5)
3 (4)
 
Grade-2 n (%)
0 (0)
(1)
 
Grade-3 n (%)
0 (0)
0 (0)
 
Medications
   
Calcium canal bloker n (%)
35 (46)
35 (46)
1.000
ACE -I/ARB n (%)
50 (65)
47 (61)
0.617
Beta-bloker n (%)
31 (40)
24 (31)
0.239
Doxazosine n (%)
2 (3)
1 (1)
0.560
Thiazide diuretic n (%)
37 (48)
34 (44)
0.628
Statin n (%)
22 (29)
10 (13)
0.017
Acetylsalicylic acid n (%)
21 (27)
11 (14)
0.047
Biochemical parameters
 Hemoglobin (g/dl)
12.9 ± 1.8
13.0 ± 1.8
0.671
 WBC (/mm3)
7.2 ± 2.0
7.1 ± 2.1
0.639
 Platelet (×103/μL)
243 ± 74
250 ± 83
0.570
 eGFR (ml/min)
72.2 ± 21.2
77.4 ± 16.5
0.093
 Glucose (mg/dl)
112.3 ± 26.8
108.1 ± 25.1
0.320
 HbA1c (%)
6.3 ± 0.7
6.2 ± 0.9
0.474
 Total Cholesterol (mg/dl)
201 ± 31
201 ± 25
0.965
 LDL Cholesterol (mg/dl)
120 ± 33
120 ± 32
0.836
 HDL Cholesterol (mg/dl)
48 ± 12
47 ± 10
0.774
 Triglyceride (mg/dl)
134 (91–180)
140 (107–181)
0.994
 AST (U/L)
19 (17–22)
22 (19–26)
0.231
 ALT (U/L)
15 (12–18)
17 (13–24)
0.459
BSA body surface area, AST Aspartate transaminase, ALT Alanine transaminase, WBC White blood cell count, LVEDD Left ventricular end diastolic diameter, eGFR Estimated glomerular filtration rate. ACE Angiotensin-converting enzyme inhibitors, Angiotensin II receptor blockers, BMI body mass index
Table 3
Univariate and multivariate analysis of ascending aort dilatation
Variables
Univariate
OR (95% CI)
P-value
Multivariate
OR(95% CI)
P-value
Age (years)
1.030 (1.006–1.056)
0.016
  
Coronary artery disease
1.548 (1.155–2.074)
0.027
  
Female
1.119 (0.580–2.158)
0.738
  
Statin
2.680 (1.171–6.135)
0.020
  
ASA
2.250 (0.999–5.067)
0.050
  
eGFR (mL/min)
0.985 (0.969–1.003)
0.014
  
EAT thickness (mm)
1.548 (1.155–2.074)
0.003
1461 (1.082–1.974)
0.013
eGFR Estimated glomerular filtration rate, ASA acetylsalicylic asid, EAT Epicardial adipose tissue
ROC curve analysis was performed to predict AAD in the matched population (Fig. 1). EAT > 0.45 cm had 51.9% sensitivity and 62.3% specificity [AUC = 0.617, P = 0.012, 95% CI (0.529–0.707)].

Discussion

In this study, we found that EAT are independent predictor for AAD in hypertensive patients.
The normal diameter of the AA depends on the patient’s age, sex and body size [26]. Similarly to our study, Bon et al. showed that higher age was associated with larger descending aortic diameters. The causes of aortic aneurysms differ according to the location of the aorta. In younger patients, thoracic aortic aneurysms with genetic reasons generally include the AA and aortic root. These reasons include connective tissue disorders, such as Ehlers-Danlos Syndrome, Marfan Syndrome, Loeys–Dietz Syndrome, Familial Thoracic Aortic Aneurysm Syndrome, Turner Syndrome and bicuspid aortic valve. Also, cystic medial degeneration can be seen in thoracic aortic aneurysms that are not due to a connective tissue disorder but have a genetic connection. Other reasons of thoracic aortic aneurysms are aortitis (syphilis is the most common cause) or inflammation of the aorta. A total of 39% of the variance in descending aortic diameter and 21% of the variance in ascending aortic diameter were explained by sex, age, traditional cardiovascular risk factors and anthropometrics [27]. Consequently, only a small part of the causes of ascending aortic aneurysm could be explained by conventional risk factors. The influence of these cardiovascular risk factors seems of limited importance in elucidating the overall reasons for aortic dilatation.
EAT may help fill this gap. There are two possible mechanisms for the association between EAT and AAD. First, EAT has a paracrine and systemic endocrine role. It can secrete several active molecules, such as tumour necrosis factor, resistin, adiponectin and IL-6 [28, 29]. Second, EAT is one of the parts of the visceral adipose tissue, and, therefore, it is associated with CAD, cardiovascular risk factors, hypertension and metabolic syndrome [3032]. These specifications of EAT may be a possible causative role of AAD.
In the literature, PAT and EAT have been used interchangeably, because they were thought to be identical adipose depots. However, paracardial and epicardial adipose tissues are clearly different embriologically, physiologically, anatomically and clinically. Despite this, the literature frequently contradictorily discriminates between the two adipose tissues [33]. EAT is the fat depot placed between the myocardium and visceral pericardium, whereas PAT is the fat depot outside the pericardium and on the external surface of the parietal pericardium as defined by imaging studies and autopsies [1434]. So, EAT is the adipose tissue depot immediately adjacent to the myocardium, whereas PAT is the outer adipose tissue of the heart.
EAT originates from the splanchnopleuric mesoderm, whereas PAT originates from the thoracic primitive mesenchyme. EAT is supplied by the coronary arteries, whereas PAT is supplied by the noncoronary system. Also, no any fascia separates the EAT and coronary arteries; therefore, EAT and myocardium share the same circulation. Because of this link, EFT is metabolically an active tissue and the source of cytokines and interacts directly through vasocrine and paracrine mechanisms to the myocardium, coronary and systemic circulation [34]. This is not true for PAT. PAT does not directly interact with the myocardium and may only contact indirectly through acts like ectopic visceral adipose tissue. As a result, pericardial and EATs are clinically different [35].
CAD is correlated with AAD in univariate regression analysis, but this correlation was not determined in multivariate regression analysis after matching. Atherosclerosis can lead to aortic dilatation, especially in aortic arch and descending aorta. Unlike dilatation of the descending aorta, the role of atherosclerosis in the aetiology of AAD is controversial, and AAD is not generally due to atherosclerosis. Most aetiology of the AADs are classified as idiopathic [36, 37].
Interestingly, the presence of DM was related to a smaller ascending and descending aortic diameter in the literature [38]. This phenomenon might be caused by high glucose levels associated with DM which inhibits intermediate-phase secretion of the matrix metalloproteinases. Similarly, protective effect of DM has already been shown in the abdominal aorta [39, 40]. However, this phenomenon may be more remarkable in abdominal aorta than AA. We did not find any relationship between DM and AAD.
It has been shown that there was a relationship between EAT density and arterial inflammation and cardiovascular risk prediction. This adipose tissue-arterial wall association may play a role in the formation of AAD [41].
The findings of this study may support the hypothesis that increased EAT, but not PAT, may have a critical role in AAD.

Conclusion

Only a little part of the aetiology of AAD was explained by age, sex, traditional cardiovascular risk factors and anthropometrics. EAT may have a key role in AAD. Based on our findings, increased EAT, and BMI were independent predictors for AAD in hypertensive patients. Increased EAT may be effective in progressing aortic dilatation due to local or systemic effects. However, this relationship was not observed in PAT. We believe that further studies are needed to explain the role of different types of adipose tissue in the pathogenesis of AAD. Adipose tissue-focused diagnosis and treatments can provide new insight to the patients with AAD.

Study limitations

This was primarily a cross-sectional study retrospective in nature. MRI and computed tomography are frequently used in the evaluation of adipose tissue. Although MRI is the modality of choice for water/fat separation, CT is considered to gold standard for volumetric adipose tissue analyses. However, we used echocardiography to measure EAT. Also, there are some limitations to the measurement of EAT and PAT by echocardiography. Echocardiographic imaging only allows for a rough estimation of the adipose tissue [42, 43]. The restricted acoustic window limits the imaging of total adipose tissue volume and determining regional differences in adipose tissue distribution. Nevertheless, there is a close correlation between MRI and echocardiography imaging of EAT [44, 45]. In our study, predictive value of EAT for AAD was modest. The cutt-off values of epicardial fat for AAD prediction are not well defined in literature. Whether or not echocardiographic epicardial fat thickness may really have the diagnostic properties to serve as an indicator of AAD should be analyzed in large, randomized studies.

Acknowledgements

Not applicable.
The study was designed retrospectively. Kocaeli University Ethics Committee waivered the need for informed consent regarding the retrospective data and approved this study.
Not applicable.

Competing interests

The authors declare that they have no competing interests.
Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://​creativecommons.​org/​licenses/​by/​4.​0/​. The Creative Commons Public Domain Dedication waiver (http://​creativecommons.​org/​publicdomain/​zero/​1.​0/​) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Literatur
1.
Zurück zum Zitat Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey DE, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease. J Am Coll Cardiol. 2010;55:e27–e129.CrossRef Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey DE, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease. J Am Coll Cardiol. 2010;55:e27–e129.CrossRef
2.
Zurück zum Zitat Ramanath VS, Oh JK, Sundt TM, Eagle KA. Acute aortic syndromes and thoracic aortic aneurysm. Mayo Clin Proc. 2009;84:465–81.CrossRef Ramanath VS, Oh JK, Sundt TM, Eagle KA. Acute aortic syndromes and thoracic aortic aneurysm. Mayo Clin Proc. 2009;84:465–81.CrossRef
3.
Zurück zum Zitat Baxter BT, Davis VA, Minion DJ, Wang YP, Lynch TG, McManus BM. Abdominal aortic aneurysms are associated with altered matrix proteins of the nonaneurysmal aortic segments. J Vasc Surg. 1994;19:797–803.CrossRef Baxter BT, Davis VA, Minion DJ, Wang YP, Lynch TG, McManus BM. Abdominal aortic aneurysms are associated with altered matrix proteins of the nonaneurysmal aortic segments. J Vasc Surg. 1994;19:797–803.CrossRef
4.
Zurück zum Zitat El-Hamamsy I, Yacoub MH. Cellular and molecular mechanisms of thoracic aortic aneurysms. Nature Rev Cardiol. 2009;6:771–86.CrossRef El-Hamamsy I, Yacoub MH. Cellular and molecular mechanisms of thoracic aortic aneurysms. Nature Rev Cardiol. 2009;6:771–86.CrossRef
5.
Zurück zum Zitat Albornoz G, Coady MA, Roberts M, Davies RR, Tranquilli M, Rizzo JA, et al. Familial thoracic aortic aneurysms and dissections – incidence, modes of inheritance, and phenotypic patterns. Ann Thorac Surg. 2006;82:1400–5.CrossRef Albornoz G, Coady MA, Roberts M, Davies RR, Tranquilli M, Rizzo JA, et al. Familial thoracic aortic aneurysms and dissections – incidence, modes of inheritance, and phenotypic patterns. Ann Thorac Surg. 2006;82:1400–5.CrossRef
6.
Zurück zum Zitat Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation. 2002;105:1135–43.CrossRef Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation. 2002;105:1135–43.CrossRef
9.
Zurück zum Zitat Ferdinand KC, Nasser SA. Management of essential hypertension. Cardiol Clin. 2017;35:231–46.CrossRef Ferdinand KC, Nasser SA. Management of essential hypertension. Cardiol Clin. 2017;35:231–46.CrossRef
10.
Zurück zum Zitat Acet H, Ertas F, Akil MA, et al. New inflammatory predictors for non-valvular atrial fibrillation: echocardiographic epicardial fat thickness and neutrophil to lymphocyte ratio. Int J Cardiovasc Imaging. 2014;30:81–9.CrossRef Acet H, Ertas F, Akil MA, et al. New inflammatory predictors for non-valvular atrial fibrillation: echocardiographic epicardial fat thickness and neutrophil to lymphocyte ratio. Int J Cardiovasc Imaging. 2014;30:81–9.CrossRef
14.
Zurück zum Zitat Iacobellis G, Willens HJ. Echocardiographic epicardial fat: a review of research and clinical applications. J Am Soc Echocardiogr. 2009;22:1311–9.CrossRef Iacobellis G, Willens HJ. Echocardiographic epicardial fat: a review of research and clinical applications. J Am Soc Echocardiogr. 2009;22:1311–9.CrossRef
17.
Zurück zum Zitat Wheeler GL, Shi R, Beck SR, Langefeld CD, Lenchik L, Wagenknecht LE, Freedman BI, Rich SS, Bowden DW, Chen MY, Carr JJ. Pericardial and visceral adipose tissues measured volumetrically with computed tomography are highly associated in type 2 diabetic families. Investig Radiol. 2005;40(2):97–101.CrossRef Wheeler GL, Shi R, Beck SR, Langefeld CD, Lenchik L, Wagenknecht LE, Freedman BI, Rich SS, Bowden DW, Chen MY, Carr JJ. Pericardial and visceral adipose tissues measured volumetrically with computed tomography are highly associated in type 2 diabetic families. Investig Radiol. 2005;40(2):97–101.CrossRef
19.
Zurück zum Zitat El Khoudary SR, Shields KJ, Janssen I, Budoff MJ, Everson-Rose SA, Powell LH, Matthews KA. Postmenopausal Women With Greater Paracardial Fat Have More Coronary Artery Calcification Than Premenopausal Women: The Study of Women's Health Across the Nation (SWAN) Cardiovascular Fat Ancillary Study. J Am Heart Assoc. 2017;6(2). https://doi.org/10.1161/JAHA.116.004545. El Khoudary SR, Shields KJ, Janssen I, Budoff MJ, Everson-Rose SA, Powell LH, Matthews KA. Postmenopausal Women With Greater Paracardial Fat Have More Coronary Artery Calcification Than Premenopausal Women: The Study of Women's Health Across the Nation (SWAN) Cardiovascular Fat Ancillary Study. J Am Heart Assoc. 2017;6(2). https://​doi.​org/​10.​1161/​JAHA.​116.​004545.
20.
Zurück zum Zitat Thanassoulis G, Massaro JM, Hoffmann U, Mahabadi AA, Vasan RS, O’Donnell CJ, et al. Prevalence, distribution, and risk factor correlates of high pericardial and intrathoracic fat depots in the Framingham heart study. Circ Cardiovasc Imaging. 2010;3:559–66.CrossRef Thanassoulis G, Massaro JM, Hoffmann U, Mahabadi AA, Vasan RS, O’Donnell CJ, et al. Prevalence, distribution, and risk factor correlates of high pericardial and intrathoracic fat depots in the Framingham heart study. Circ Cardiovasc Imaging. 2010;3:559–66.CrossRef
21.
Zurück zum Zitat Chen O, Sharma A, Ahmad I, Bourji N, Nestoiter K, Hua P, et al. Correlation between pericardial, mediastinal, and intrathoracic fat volumes with the presence and severity of coronary artery disease, metabolic syndrome, and cardiac risk factors. Eur Heart J Cardiovasc Imaging. 2015;16:37–46.CrossRef Chen O, Sharma A, Ahmad I, Bourji N, Nestoiter K, Hua P, et al. Correlation between pericardial, mediastinal, and intrathoracic fat volumes with the presence and severity of coronary artery disease, metabolic syndrome, and cardiac risk factors. Eur Heart J Cardiovasc Imaging. 2015;16:37–46.CrossRef
22.
Zurück zum Zitat Roman MJ, Devereux RB, Kramer-Fox R, O’Loughlin J. Two-dimensional echocardiographic aortic root dimensions in normal children and adults. Am J Cardiol. 1989;64(8):507–12.CrossRef Roman MJ, Devereux RB, Kramer-Fox R, O’Loughlin J. Two-dimensional echocardiographic aortic root dimensions in normal children and adults. Am J Cardiol. 1989;64(8):507–12.CrossRef
23.
Zurück zum Zitat Davies RR, Gallo A. CoadyMAet al.; novel measurement of relative aortic size predicts rupture of thoracic aortic aneurysms. Ann Thorac Surg. 2006;81(1):169–77.CrossRef Davies RR, Gallo A. CoadyMAet al.; novel measurement of relative aortic size predicts rupture of thoracic aortic aneurysms. Ann Thorac Surg. 2006;81(1):169–77.CrossRef
24.
Zurück zum Zitat Sicari R, Galderisi M, Voigt JU, Habib G, et al. The use of pocket-size imaging devices: a position statement of the European Association of Echocardiography. Eur J Echocardiogr. 2011;12:85–7.CrossRef Sicari R, Galderisi M, Voigt JU, Habib G, et al. The use of pocket-size imaging devices: a position statement of the European Association of Echocardiography. Eur J Echocardiogr. 2011;12:85–7.CrossRef
25.
Zurück zum Zitat Davidovich D, Gastaldelli A, Sicari R. Imaging cardiac fat. Eur Heart J Cardiovasc Imaging. 2013;14:625–30.CrossRef Davidovich D, Gastaldelli A, Sicari R. Imaging cardiac fat. Eur Heart J Cardiovasc Imaging. 2013;14:625–30.CrossRef
27.
Zurück zum Zitat Farasat SM, Morrell CH, Scuteri A, et al. Do hypertensive individuals have enlarged aortic root diameters? Insights from studying the various subtypes of hypertension. Am J Hypertens. 2008;21:558–63.CrossRef Farasat SM, Morrell CH, Scuteri A, et al. Do hypertensive individuals have enlarged aortic root diameters? Insights from studying the various subtypes of hypertension. Am J Hypertens. 2008;21:558–63.CrossRef
32.
Zurück zum Zitat Bruun JM, Lihn AS, Verdich C, Pedersen SB, Toubro S, Astrup A, et al. Regulation of adiponectin by adipose tissue-derived cytokines: in vivo and in vitro investigations in humans. Am J Physiol Endocrinol Metab. 2003;285:E527–33.CrossRef Bruun JM, Lihn AS, Verdich C, Pedersen SB, Toubro S, Astrup A, et al. Regulation of adiponectin by adipose tissue-derived cytokines: in vivo and in vitro investigations in humans. Am J Physiol Endocrinol Metab. 2003;285:E527–33.CrossRef
33.
Zurück zum Zitat Iacobellis G. Epicardial and pericardial fat: close, but very different. Obesity. 2009;17:625.CrossRef Iacobellis G. Epicardial and pericardial fat: close, but very different. Obesity. 2009;17:625.CrossRef
34.
Zurück zum Zitat Iacobellis G, Corradi D, Sharma AM. Epicardial adipose tissue: anatomic, biomolecular and clinical relationships with the heart. Nat Clin Pract Cardiovasc Med. 2005;2:536–43.CrossRef Iacobellis G, Corradi D, Sharma AM. Epicardial adipose tissue: anatomic, biomolecular and clinical relationships with the heart. Nat Clin Pract Cardiovasc Med. 2005;2:536–43.CrossRef
36.
Zurück zum Zitat Cuspidi C, Meani S, Fusi V, Valerio C, Sala C, Zanchetti A. Prevalence and correlates of aortic root dilatation in patients with essential hypertension: relationship with cardiac and extracardiac target organ damage. J Hypertens. 2006;24:573–80.CrossRef Cuspidi C, Meani S, Fusi V, Valerio C, Sala C, Zanchetti A. Prevalence and correlates of aortic root dilatation in patients with essential hypertension: relationship with cardiac and extracardiac target organ damage. J Hypertens. 2006;24:573–80.CrossRef
38.
Zurück zum Zitat Bons LR, Rueda-Ochoa OL, El Ghoul K, Rohde S, Budde RP, Leening MJ, Vernooij MW, Franco OH, van der Lugt A, Roos-Hesselink JW, Kavousi M, Bos D. Sex-specific distributions and determinants of thoracic aortic diameters in the elderly. Heart. 2019;24. pii: heartjnl-2019-315320. https://doi.org/10.1136/heartjnl-2019-315320. Bons LR, Rueda-Ochoa OL, El Ghoul K, Rohde S, Budde RP, Leening MJ, Vernooij MW, Franco OH, van der Lugt A, Roos-Hesselink JW, Kavousi M, Bos D. Sex-specific distributions and determinants of thoracic aortic diameters in the elderly. Heart. 2019;24. pii: heartjnl-2019-315320. https://​doi.​org/​10.​1136/​heartjnl-2019-315320.
39.
Zurück zum Zitat Golledge J, Karan M, Moran CS, et al. Reduced expansion rate of abdominal aortic aneurysms in patients with diabetes may be related to aberrant monocyte–matrix interactions. Eur Heart J. 2008;29:665–72.CrossRef Golledge J, Karan M, Moran CS, et al. Reduced expansion rate of abdominal aortic aneurysms in patients with diabetes may be related to aberrant monocyte–matrix interactions. Eur Heart J. 2008;29:665–72.CrossRef
40.
Zurück zum Zitat Lederle FA. The strange relationship between diabetes and abdominal aortic aneurysm. Eur J Vasc Endovasc Surg. 2012;43:254–6.CrossRef Lederle FA. The strange relationship between diabetes and abdominal aortic aneurysm. Eur J Vasc Endovasc Surg. 2012;43:254–6.CrossRef
42.
Zurück zum Zitat Sicari R, Sironi AM, Petz R, et al. Pericardial rather than epicardial fat is a cardiometabolic risk marker: an MRI vs echo study. J Am Soc Echocardiogr. 2011;24:1156–62.CrossRef Sicari R, Sironi AM, Petz R, et al. Pericardial rather than epicardial fat is a cardiometabolic risk marker: an MRI vs echo study. J Am Soc Echocardiogr. 2011;24:1156–62.CrossRef
43.
Zurück zum Zitat Eroglu S. How do we measure epicardial adipose tissue thickness by transthoracic echocardiography? Anatol J Cardiol. 2015;15:416–9.CrossRef Eroglu S. How do we measure epicardial adipose tissue thickness by transthoracic echocardiography? Anatol J Cardiol. 2015;15:416–9.CrossRef
44.
Zurück zum Zitat Iacobellis G, Assael F, Ribaudo MC, et al. Epicardial fat from echocardiography: a new method for visceral adipose tissue prediction. Obes Res. 2003;11:304–10.CrossRef Iacobellis G, Assael F, Ribaudo MC, et al. Epicardial fat from echocardiography: a new method for visceral adipose tissue prediction. Obes Res. 2003;11:304–10.CrossRef
45.
Zurück zum Zitat Christensen RH, Hansen CS, von Scholten BJ, Jensen MT, Pedersen BK, Schnohr P, Vilsbøll T, Rossing P, Jørgensen PG. Epicardial and pericardial adipose tissues are associated with reduced diastolic and systolic function in type 2 diabetes. Diabetes Obes Metab. 2019;21(8):2006–11. https://doi.org/10.1111/dom.13758.CrossRefPubMed Christensen RH, Hansen CS, von Scholten BJ, Jensen MT, Pedersen BK, Schnohr P, Vilsbøll T, Rossing P, Jørgensen PG. Epicardial and pericardial adipose tissues are associated with reduced diastolic and systolic function in type 2 diabetes. Diabetes Obes Metab. 2019;21(8):2006–11. https://​doi.​org/​10.​1111/​dom.​13758.CrossRefPubMed
Metadaten
Titel
Epicardial adipose tissue is a predictor of ascending aortic dilatation in hypertensive patients, but not paracardial adipose tissue
verfasst von
Onur Argan
Eyup Avci
Tarik Yildirim
Ozgen Safak
Publikationsdatum
01.12.2020
Verlag
BioMed Central
Erschienen in
BMC Cardiovascular Disorders / Ausgabe 1/2020
Elektronische ISSN: 1471-2261
DOI
https://doi.org/10.1186/s12872-020-01431-2

Weitere Artikel der Ausgabe 1/2020

BMC Cardiovascular Disorders 1/2020 Zur Ausgabe

Update Kardiologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.