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Association between epicardial adipose tissue volume and myocardial salvage in patients with a first ST-segment elevation myocardial infarction: An epicardial adipose tissue paradox
Epicardial adipose tissue (EAT), defined as the adipose tissue between the visceral pericardium and the outer margin of the myocardium, is associated with coronary artery disease in the general population. However, the clinical implications of EAT in patients with ST-segment elevation myocardial infarction (STEMI) remain unclear.
Methods
A total of 142 patients with a first STEMI, who received reperfusion therapy within 12 h from symptom onset, were enrolled. All patients underwent cardiac magnetic resonance imaging to evaluate infarct core (Core), area at risk (AAR), and EAT volume. Myocardial salvage index (MSI) was defined as AAR minus Core divided by AAR. Patients in the lower tertile of EAT volume were classified as the low EAT group (group L) and the other two-thirds as the high EAT group (group H).
Results
The mean MSI was lower in group L than in group H (0.43 ± 0.13 vs 0.49 ± 0.13, p = 0.01), and the mean extent of Core was higher in group L than in group H (25 ± 10% vs 19 ± 10%, p < 0.01). Multivariate linear regression analysis including coronary risk factors and previously reported predictors of infarct size demonstrated that EAT volume was an independent predictor of MSI (β coefficient = 0.002 per 1 mL, p = 0.002).
Conclusions
A lower EAT volume is associated with less myocardial salvage and larger infarct size in patients with a first STEMI.
Epicardial adipose tissue (EAT), defined as the adipose tissue between the visceral pericardium and the outer margin of the myocardium, can be considered an endocrine organ that secretes pro-inflammatory and anti-inflammatory cytokines and chemokines including adiponectin [
]. EAT volume is associated with coronary calcification as advanced atherosclerosis, cardiovascular risk factors, the incidence of myocardial infarction, and the severity of coronary artery disease in the general population [
Increase in epicardial fat volume is associated with greater coronary artery calcification progression in subjects at intermediate risk by coronary calcium score: a serial study using non-contrast cardiac CT.
Association of epicardial fat with cardiovascular risk factors and incident myocardial infarction in the general population: the Heinz Nixdorf Recall Study.
]. Thus, EAT volume may reflect the stage of coronary atherosclerosis, resulting in cardiovascular events. However, in some patients, ST-segment elevation myocardial infarction (STEMI) is not caused by advanced atherosclerosis, but by early atherosclerosis, as represented by positive remodeling with plaque rupture [
Positive remodeling of the coronary arteries detected by magnetic resonance imaging in an asymptomatic population: MESA (Multi-Ethnic Study of Atherosclerosis).
Cardiac magnetic resonance imaging (CMR) is the gold standard for evaluating infarct size and myocardial salvage (MS) in patients with acute myocardial infarction (AMI) [
Retrospective determination of the area at risk for reperfused acute myocardial infarction with T2-weighted cardiac magnetic resonance imaging: histopathological and displacement encoding with stimulated echoes (DENSE) functional validations.
We prospectively investigated the associations of EAT volume with myocardial salvage index (MSI) and infarct size in patients with a first STEMI.
Materials and methods
Patients
From January 2012 through September 2014, we screened 267 consecutive patients with a first STEMI who received reperfusion therapy within 12 h of symptom onset in Yokohama City University Medical Center. STEMI was defined as chest pain lasting for at least 30 min, accompanied by ST-segment elevation [
] and an increase in the serum creatine phosphokinase (CPK) level to more than twice the upper limit of normal. We excluded patients with any of the following characteristics: informed consent was not obtained, history of previous myocardial infarction or coronary-artery bypass surgery, stent thrombosis, clinical instability precluding CMR, estimated glomerular filtration rate (eGFR) of less than 30 mL/min/1.73 m2, or contraindications to CMR. A total of 142 patients met the eligibility criteria and were enrolled (Fig. 1).
Fig. 1Study flow chart. Of 267 screened patients, 142 were enrolled in the present study. CMR, cardiac magnetic resonance imaging; eGFR, estimated glomerular filtration rate.
After admission, 5000 U of heparin was given. All patients received aspirin (a 200-mg loading dose, followed by 100 mg/d) and clopidogrel (a 300-mg loading dose, followed by 75 mg/d). Glycoprotein (GP) IIb/IIIa inhibitors were not used, because they have not been approved for use in Japan. All patients had a final Thrombolysis in Myocardial Infarction (TIMI) flow grade of 2 or 3. The study protocol was approved by the Yokohama City University Medical Center Institutional Review Board, and all patients gave written informed consent (UMIN-CTR ID: UMIN000012027).
Blood sampling
Biochemistry data including CPK, creatine kinase MB (CK-MB), and high-sensitivity C-reactive protein (hs-CRP) were evaluated on admission and at 3-h intervals during the first 24 h and then daily until discharge. Brain natriuretic peptide (BNP) was evaluated on admission, 6 h after admission, and daily until discharge. The high molecular weight adiponectin level was evaluated on admission by a commercial laboratory (SRL, Tokyo, Japan) in a randomly chosen group of 45 (32%) of the 142 subjects.
CMR protocol
All patients underwent CMR on day 10 ± 4 using a 1.5-T CMR system with an 8-element phased-array cardiac coil (MAGNETOM Avanto, Siemens Medical Solutions, Inc., Erlangen, Germany). Black-blood T2-weighted CMR images were acquired in 3 short-axis views, and typical parameters were as follows: repetition time (TR) 2 R–R intervals, echo time (TE) 78 ms, flip angle (FA) 180°, and 10-mm slice thickness. After scout imaging, cine true fast images with steady precession (True-FISP) sequences were obtained. Cine images were acquired in 6–8 short-axis views and 1 long-axis view at rest (TR 39.2 ms, TE 1.94 ms, FA 80°, 10-mm slice thickness). An infusion of 0.1 mmol/kg gadolinium–diethylenetriamine pentaacetic acid (Gd-DTPA) (Magnevist, Bayer Schering Pharma, Berlin, Germany) was given, and late gadolinium enhancement (LGE) images were acquired 10–15 min later using a phase-sensitive inversion recovery method; the images included 6–8 short-axis views at rest (TR 943.2 ms, TE 1.33 ms, FA 40°, 10-mm slice thickness). All images were acquired during breath-holding at end expiration.
CMR analysis
All CMR images were independently interpreted by 2 experienced observers blinded to the angiographic and clinical data using Q-MASS MR 7.5 imaging system (Medis, Leiden, The Netherlands). After review of the cine images, left ventricular (LV) volumes (end-diastolic volume index, EDVI; end-systolic volume index, ESVI) and ejection fraction (EF) were calculated by manually tracing the LV endocardial and epicardial borders on the short-axis images at end-diastole and end-systole. EAT was defined as the adipose tissue between the visceral pericardium and the outer margin of the myocardium. EAT area was calculated from consecutive short-axis images at end-diastole (Fig. 2), and EAT volume was calculated by the disk method, as described previously [
Fig. 2CMR Analysis of Core and EAT. LGE CMR. (B) Analysis of LGE CMR. Red area shows infarct core. (C) Cine CMR. White arrow shows EAT. CMR, cardiac magnetic resonance imaging; EAT, epicardial adipose tissue; LGE, late gadolinium enhancement.
This manual tracing was also performed on LGE and T2-weighted images. The myocardial segment containing the region of high signal intensity (SI) myocardium was then outlined, and the maximum SI within this region was determined. A region of interest (ROI) was placed at the remote non-infarcted myocardium with uniform myocardial suppression. We used the full-width at half-maximum method (FWHM) to define the infarct core (Core) on LGE images, as described previously [
]. Core was defined as the myocardium with SI equivalent to >50% of the maximal SI. Microvascular obstruction (MVO) was defined as a dark area within the hyperenhanced area on LGE images. MVO was manually traced and considered as part of Core. The infarct size was defined as the extent of Core. On T2-weighted images, myocardial tissue with an SI of at least 2 SD above the mean SI obtained in the remote non-infarcted myocardium was considered the area at risk (AAR) [
Intramyocardial hemorrhage was defined as a dark area within the hyperenhanced area on T2-weighted images that was considered to belong to the AAR. All measurements were calculated by the planimetric method and expressed as grams of myocardium. The values were normalized to LV mass and represented as % of LV mass.
We divided the 142 patients into 2 groups according to their EAT volume. Patients belonging to the lower tertile of EAT volume were categorized into the low EAT group (group L) and the other two-thirds into the high EAT group (group H).
Coronary artery findings on coronary angiography
The extent index
The extent index was evaluated as described previously [
Coronary artery findings on pre-intervention intravascular ultrasound
Protocol
Intravenous heparin was given during percutaneous coronary intervention to maintain an activated clotting time of ≥250 s. Thrombus aspiration was performed in patients with obvious thrombus formation on angiography, intravascular ultrasound (IVUS), or both. IVUS was performed with a 40-MHz IVUS catheter, prior to any balloon inflation or stent implantation, using a Boston Scientific system (Boston Scientific Co., Boston, MA, USA) or a Terumo system (Terumo Co., Tokyo, Japan). The catheter was pulled back with an automatic pullback speed of 0.5 mm/s.
IVUS analysis
All IVUS images were analyzed by an investigator who was blinded to the angiographic and clinical data. Conventional IVUS image analysis was performed using the commercially available software package Echo Plaque (Indec Systems, Mountain View, CA, USA) for the Boston Scientific system and VISIWAVE (Terumo Co.) for the Terumo system. Quantitative analyses were performed (Supplemental method 2) according to the American College of Cardiology clinical expert consensus document on IVUS [
American College of Cardiology Clinical Expert Consensus Document on Standards for Acquisition, Measurement and Reporting of Intravascular Ultrasound Studies (IVUS). A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents.
]. We defined lesions with ruptured plaque (RP) on IVUS as follows: (1) lesions with fissure/dissection; or (2) lesions without fissure/dissection, but where the injection of saline or contrast medium confirmed communication between the plaque and the coronary artery lumen.
Statistical analysis
Continuous variables are expressed as means ± SD for normally distributed variables, and as medians (25th to 75th percentiles) for variables with skewed distributions. Differences between the groups were tested using Student's t-test for normally distributed variables, the Mann–Whitney test for variables with skewed distributions, and the chi-square test or Fisher's exact test as appropriate for categorical variables. Correlations between continuous variables were determined using Pearson correlation coefficients. We built a multivariate linear regression analysis using a forced inclusion model for the prediction of MSI. Coronary risk factors [age, male sex, body mass index (BMI), hypertension, diabetes mellitus, dyslipidemia, and current smoker], previously reported predictors of infarct size [culprit left descending coronary artery (LAD), initial TIMI flow grade >1, final TIMI flow grade 3, pre-infarct angina within 24 h, and symptom onset to reperfusion time] [
Influence of pre-infarction angina, collateral flow, and pre-procedural TIMI flow on myocardial salvage index by cardiac magnetic resonance in patients with ST-segment elevation myocardial infarction.
], and EAT volume were included. All statistical tests were 2-tailed, and p < 0.05 was considered to indicate statistical significance. SPSS version 18.0 (SPSS Japan Inc., Tokyo, Japan) was used for all statistical analyses.
Results
Baseline characteristics
The baseline characteristics of the 142 patients are shown in Table 1. The mean BMI was lower in group L than in group H (p < 0.01).
Table 1Baseline characteristics.
Variables
All patients (n = 142)
Group L (n = 47)
Group H (n = 95)
p-Value
Age, y
64 ± 12
63 ± 11
64 ± 13
0.77
Men, n (%)
121 (85)
44 (94)
77 (81)
0.047
Body mass index, kg/m2
24.9 ± 3.7
23.5 ± 2.6
25.6 ± 3.9
<0.01
Infarct-related artery, n (%)
0.10
Left anterior descending coronary artery
73 (51)
30 (64)
43 (45)
Right coronary artery
56 (40)
13 (28)
43 (45)
Left circumflex coronary artery
13 (9)
4 (8)
9 (10)
Number of diseased vessels, n (%)
0.83
1
92 (65)
29 (62)
63 (66)
2
35 (25)
13 (28)
22 (23)
3
15 (10)
5 (10)
10 (11)
Killip class >1, n (%)
22 (15)
10 (21)
12 (13)
0.16
Initial TIMI flow grade >1, n (%)
31 (22)
13 (28)
18 (19)
0.24
Final TIMI flow grade 3, n (%)
132 (93)
45 (96)
87 (92)
0.20
Pre-infarct angina within 24 h, n (%)
54 (38)
18 (38)
36 (38)
0.96
Symptom onset to reperfusion time, h
3.4 ± 2.6
3.8 ± 3.1
3.3 ± 2.3
0.26
Hypertension, n (%)
76 (54)
23 (49)
53 (56)
0.44
Diabetes mellitus, n (%)
50 (35)
17 (36)
33 (35)
0.87
Dyslipidemia, n (%)
121 (85)
38 (81)
83 (87)
0.30
Current smoker, n (%)
76 (54)
24 (51)
52 (55)
0.68
Medication use on admission, n (%)
Aspirin
7 (5)
3 (6)
4 (4)
0.43
Beta blocker
5 (4)
2 (4)
3 (3)
0.54
ACE-I or ARB
25 (18)
8 (17)
17 (18)
0.88
Statin
18 (13)
8 (17)
10 (11)
0.27
Laboratory data
Peak CPK, IU/L
2990 ± 2290
3433 ± 2164
2770 ± 2330
0.11
Peak CK-MB, IU/L
267 ± 207
313 ± 213
244 ± 200
0.06
Peak BNP, pg/mL
266 ± 280
284 ± 248
258 ± 295
0.60
Peak hs-CRP, mg/dL
6.6 (3.8–10.2)
7.0 (3.7–10.6)
6.6 (3.8–10.1)
0.87
eGFR, mL/min/1.73 m2
73 ± 21
77 ± 26
70 ± 19
0.08
Glucose on admission, mg/dL
174 ± 61
176 ± 64
173 ± 59
0.76
Fasting glucose, mg/dL
109 ± 24
107 ± 17
110 ± 26
0.57
HbA1c, %
6.2 ± 1.2
6.2 ± 0.9
6.3 ± 1.4
0.74
LDL cholesterol, mg/dL
132 ± 34
125 ± 33
135 ± 35
0.11
HDL cholesterol, mg/dL
43 ± 10
42 ± 9
43 ± 11
0.48
Triglycerides, mg/dL
103 (64–166)
86 (58–130)
109 (65–169)
0.06
CMR parameters
LVEF, %
44 ± 11
41 ± 11
46 ± 11
0.03
LVEDVI, mL/m2
80 ± 19
89 ± 23
75 ± 15
<0.01
MSI
0.47 ± 0.13
0.43 ± 0.13
0.49 ± 0.13
0.01
Core, % of LV mass
21 ± 10
25 ± 10
19 ± 10
<0.01
MVO, % of LV mass
1.0 ± 2.0
1.1 ± 2.0
0.9 ± 2.1
0.53
EAT volume, mL
37 ± 21
16 ± 6
48 ± 18
<0.01
The extent index
1.08 ± 0.46
0.89 ± 0.44
1.18 ± 0.45
<0.01
TIMI, thrombolysis in myocardial infarction; ACE-I, angiotensin-converting enzyme inhibitors; ARB, angiotensin II receptor blockers; CPK, creatine phosphokinase; CK-MB, creatine phosphokinase MB; Peak BNP, peak brain natriuretic peptide during hospitalization; Peak hs-CRP, peak high-sensitivity C-reactive protein during hospitalization; eGFR, estimated glomerular filtration rate; HbA1c, glycosylated hemoglobin A1C; LDL, low-density lipoprotein; HDL, high-density lipoprotein; LV, left ventricular; EF, ejection fraction; EDVI, end-diastolic volume index; MSI, myocardial salvage index; Core, infarct core; MVO, microvascular obstruction; EAT, epicardial adipose tissue; Group L, low EAT group; Group H, high EAT group.
Associations of EAT volume with MSI and infarct size
The mean MSI was lower in group L than in group H (0.43 ± 0.13 vs 0.49 ± 0.13, p = 0.01), and the mean extent of Core was higher in group L than in group H (25 ± 10% vs 19 ± 10%, p < 0.01) (Table 1).
Univariate analyses revealed that culprit LAD and EAT volume were predictors of MSI (Table 2). Multivariate analysis including coronary risk factors and previously reported predictors of infarct size demonstrated that culprit LAD (β coefficient = −0.089, p < 0.001) and EAT volume (β coefficient = 0.002 per 1 mL, p = 0.002) were independent predictors of MSI (Table 2).
Table 2Univariate linear regression analyses and multivariate linear regression analysis by forced inclusion models for the prediction of MSI.
Variables
Univariate
Multivariate
B
95% CI for β
p-Value
B
95% CI for β
p-Value
Age, per 1 year
0.000
−0.002 to 0.002
0.868
0.677
Men
−0.027
−0.090 to 0.035
0.390
0.451
BMI, per 1 kg/m2
−0.002
−0.008 to 0.004
0.464
0.065
Culprit LAD
−0.098
−0.140 to −0.057
<0.001
−0.089
−0.132 to −0.047
<0.001
Initial TIMI flow grade >1
0.013
−0.041 to 0.067
0.633
0.157
Final TIMI flow grade 3
0.008
−0.079 to 0.095
0.852
0.331
Pre-infarct angina within 24 h
−0.019
−0.065 to 0.027
0.416
0.573
Symptom onset to reperfusion time, per 1 h
0.006
−0.002 to 0.015
0.152
0.357
Hypertension
0.014
−0.031 to 0.058
0.543
0.856
Diabetes mellitus
−0.027
−0.074 to 0.019
0.245
0.083
Dyslipidemia
0.050
−0.012 to 0.112
0.115
0.112
Current smoker
0.012
−0.033 to 0.056
0.600
0.247
EAT volume, per 1 mL
0.002
0.001 to 0.003
0.002
0.002
0.001 to 0.003
0.002
All forced inclusion variables are shown in univariate analyses. BMI, body mass index; LAD, left anterior descending coronary artery; TIMI, thrombolysis in myocardial infarction; EAT, epicardial adipose tissue.
Association between EAT volume and coronary artery findings
On the basis of angiographic findings, the extent index was lower in group L than in group H, as shown in Table 1 (0.89 ± 0.44 vs 1.18 ± 0.45, p < 0.01).
Although pre-intervention IVUS was performed routinely in our center, the IVUS catheter could not be advanced distal to the culprit lesion before intervention in 12 patients, and the images were of poor quality for analysis in 6 patients. Therefore, we evaluated pre-intervention IVUS images in 124 patients (84%): 42 in group L and 82 in group H. Of these 124 patients, RP was noted in 69 patients (56%). RP was found in significantly higher proportions of patients in group L than in group H (79% vs 44%, p < 0.001) (Table 3).
Table 3Pre-intervention IVUS findings (n = 124).
Variables
All patients (n = 124)
Group L (n = 42)
Group H (n = 82)
p-Value
Soft plaque morphology, n (%)
79 (64)
32 (76)
47 (57)
0.039
EEM volume, mm3
176 ± 56
169 ± 50
178 ± 60
0.414
Lumen volume, mm3
53 ± 20
51 ± 17
54 ± 22
0.533
P+M volume, mm3
123 ± 45
118 ± 40
124 ± 48
0.467
Positive remodeling, n (%)
68 (55)
29 (69)
39 (48)
0.023
Ruptured plaque, n (%)
69 (56)
33 (79)
36 (44)
<0.001
IVUS, intravascular ultrasound; EEM, external elastic membrane; P+M, plaque plus media; EAT, epicardial adipose tissue; Group L, low EAT group; Group H, high EAT group.
Plasma adiponectin levels predict cardiovascular events in the observational Arita Cohort Study in Japan: the importance of the plasma adiponectin levels.
]; therefore, we assessed adiponectin levels only in men (n = 39). The adiponectin level negatively correlated with the EAT volume (R = −0.352, p = 0.028) (Fig. 3).
Fig. 3Correlation between EAT volume and adiponectin levels in men (n = 39). Solid line shows the line of best fit. EAT, epicardial adipose tissue.
The principal finding of the present study was that a lower EAT volume was associated with less myocardial salvage and a larger infarct size in patients with a first STEMI who received reperfusion therapy within 12 h from symptom onset. To the best of our knowledge, this is the first study to demonstrate a relation between EAT and MSI.
Effect of EAT in patients with STEMI
EAT is associated with inflammatory mediators and coronary atherosclerosis [
Increase in epicardial fat volume is associated with greater coronary artery calcification progression in subjects at intermediate risk by coronary calcium score: a serial study using non-contrast cardiac CT.
Association of epicardial fat with cardiovascular risk factors and incident myocardial infarction in the general population: the Heinz Nixdorf Recall Study.
]. Available evidence suggests that EAT has adverse effects on the myocardium. On the other hand, EAT secretes anti-inflammatory cytokines and chemokines, including adiponectin, and supplies energy to the myocardium. It also protects the coronary arteries under physiological and metabolically high-demand conditions [
]. Their results also suggested a cardioprotective effect of EAT in patients with CAD. However, they did not limit their study population to patients with AMI, and the backgrounds and disease stages of their subjects were heterogeneous, precluding any clear conclusions. In the present study, we demonstrated that a lower EAT volume was associated with less myocardial salvage and a larger infarct size in patients with a first STEMI, suggesting that EAT had a cardioprotective effect in a specific condition.
Associations of EAT with MSI and infarct size
During the progression of coronary atherosclerosis, fibroatheroma leading to positive remodeling develops as early atherosclerosis. On the other hand, calcification of the atherosclerotic plaque begins in middle age and is ubiquitously observed in older individuals [
]. This stage can thus be considered advanced atherosclerosis. The results of our study showed that a lower EAT volume was associated with early atherosclerosis (low extent index, and high incidence of positive remodeling or RP). The low EAT volume might be a marker of early atherosclerosis which was associated with RP in cases of STEMI. We previously reported that RP is related to a large infarct size in patients with AMI [
]. This finding supports the results of the present study, showing that a smaller EAT volume was associated with less myocardial salvage and a larger infarct size.
Although the present study used CMR for evaluating EAT volume, we think the result of the present study can apply to the echocardiography or multi-detector computer tomography (MDCT) for evaluating EAT volume. If the EAT volume evaluated by echocardiography is low on admission in patients with STEMI, they may be high risk with low MSI and large infarct size. Facilitated percutaneous coronary intervention may be an option in such high-risk patients. If the EAT volume evaluated by MDCT is low and there are vulnerable plaques evaluated by MDCT in stable patients, they may be high risk with low MSI and large infarct size when STEMI occur in them. Aggressive medical therapy may be needed in such patients to avoid large acute myocardial infarction.
In addition, we found an inverse correlation between culprit LAD and MSI even though there was no significant difference in terms of symptom onset to reperfusion time between patients with culprit LAD and patients with culprit non-LAD. In the present study, patients with culprit LAD had higher blood pressure on admission (152 ± 34 mmHg vs 134 ± 41 mmHg, p = 0.004), and higher heart rate on admission (81 ± 16 bpm vs 67 ± 21 bpm, p < 0.001) than patients with culprit non-LAD had. These might result in low MSI in patients with culprit LAD because of high myocardial oxygen demand in an acute phase of STEMI.
Association between EAT and adiponectin
Pischon et al. demonstrated that an increased adiponectin level is associated with a lower risk of myocardial infarction in the general population [
]. In contrast, however, several studies showed that an increased adiponectin level is an independent predictor of cardiovascular events in patients with AMI [
Impact of adiponectin and leptin on long-term adverse events in Japanese patients with acute myocardial infarction. Results from the Nagoya Acute Myocardial Infarction Study (NAMIS).
Usefulness of adiponectin as a predictor of all cause mortality in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention.
]. In accordance with this hypothesis, Kojima et al. demonstrated that the adiponectin level decreased immediately after the onset of AMI and speculated that this decrease resulted from the consumption of adiponectin in response to inflammation or RP [
]. These findings suggest that we have to differentially interpret adiponectin levels between patients with AMI and the general population. In the present study, EAT volume negatively correlated with adiponectin levels in patients with STEMI. Increased adiponectin levels might be needed to heal inflammation or RP in patients with low EAT volume.
Limitations
Our study had several limitations. First, the study group comprised a relatively small number of patients enrolled at a single center. Second, although we used CMR for the calculation of EAT, CMR may not be the standard method for the calculation of EAT. MDCT has been most frequently used for the calculation of EAT in previous studies. However, some studies with MDCT did not distinguish EAT from pericardial fat which was located in outer surface of the pericardium [
]. On the other hand, CMR can discriminate EAT and pericardial fat clearly. Moreover, there were surely some previous studies using CMR for the calculation of EAT. Therefore, we used CMR for the calculation of EAT. Third, although there were significant differences of IVUS findings between group L and group H, there was no significant difference of proportion of patients who had final TIMI flow grade 3 between group L and group H. In our institution, we used an aggressive thrombus aspiration device, distal protection device, or nicorandil in accordance with IVUS findings to prevent no-reflow phenomenon. As a result, there were no significant differences in incidence of no-reflow phenomenon and microvascular obstruction between group L and group H in the present study. These procedures might affect the result of the present study. Fourth, we did not measure adiponectin levels in all patients. However, in our opinion, the use of 45 patients (32%) in the present study was probably sufficient to demonstrate an association between EAT volume and adiponectin levels. Fifth, because we excluded high-risk patients such as those who had severe chronic kidney disease or clinical instability, our findings may not apply to these subgroups of patients.
Conclusions
A lower EAT volume is associated with early atherosclerosis, less myocardial salvage, and a larger infarct size in patients with a first STEMI who receive reperfusion therapy within 12 h from symptom onset.
Funding sources
None.
Disclosures
None.
Appendix A. Supplementary data
The following are the supplementary data to this article:
Increase in epicardial fat volume is associated with greater coronary artery calcification progression in subjects at intermediate risk by coronary calcium score: a serial study using non-contrast cardiac CT.
Association of epicardial fat with cardiovascular risk factors and incident myocardial infarction in the general population: the Heinz Nixdorf Recall Study.
Positive remodeling of the coronary arteries detected by magnetic resonance imaging in an asymptomatic population: MESA (Multi-Ethnic Study of Atherosclerosis).
Retrospective determination of the area at risk for reperfused acute myocardial infarction with T2-weighted cardiac magnetic resonance imaging: histopathological and displacement encoding with stimulated echoes (DENSE) functional validations.
American College of Cardiology Clinical Expert Consensus Document on Standards for Acquisition, Measurement and Reporting of Intravascular Ultrasound Studies (IVUS). A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents.
Influence of pre-infarction angina, collateral flow, and pre-procedural TIMI flow on myocardial salvage index by cardiac magnetic resonance in patients with ST-segment elevation myocardial infarction.
Plasma adiponectin levels predict cardiovascular events in the observational Arita Cohort Study in Japan: the importance of the plasma adiponectin levels.
Impact of adiponectin and leptin on long-term adverse events in Japanese patients with acute myocardial infarction. Results from the Nagoya Acute Myocardial Infarction Study (NAMIS).
Usefulness of adiponectin as a predictor of all cause mortality in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention.
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