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• W2078588918 abstract "Patients with coronary artery disease and/or type 2 diabetes mellitus (DM) generally exhibit more epicardial adipose tissue (EAT) than healthy controls. Recently, it has been proposed that EAT affects vascular function and structure by secreting proinflammatory and vasoactive substances, thereby potentially contributing to the development of cardiovascular disease. In the present study, the interrelation of EAT, coronary vasomotor function, and coronary artery calcium was investigated in patients with and without DM, who were evaluated for coronary artery disease. Myocardial blood flow (MBF) was assessed at rest and during adenosine-induced hyperemia using [15O]-water positron emission tomography combined with computed tomography to quantify coronary artery calcium and EAT in 199 patients (46 with DM). In this cohort (mean age 58 ± 10 years), the patients with DM had a greater body mass index, heart rate, and systolic blood pressure at rest (all p <0.05). Coronary artery calcium and the EAT volumes were comparable between those with and without DM. Both patient groups showed comparable MBF at rest and coronary vascular resistance. A lower hyperemic MBF and coronary flow reserve (CFR) and greater hyperemic coronary vascular resistance (all p <0.05) was observed in the patients with DM. A pooled analysis showed a positive association of EAT volume with hyperemic coronary vascular resistance but not with the MBF at rest, hyperemic MBF, or coronary vascular resistance at rest. In the group analysis, the EAT volume was inversely associated with hyperemic MBF (r = −0.16, p = 0.05) and CFR (r = −0.17, p = 0.04) and positively with hyperemic coronary vascular resistance (r = 0.26, p = 0.002) only in patients without DM. Multivariate regression analysis, adjusted for age, gender, and body mass index, showed an independent association between the EAT volume and hyperemic MBF (β = −0.16, p = 0.02), CFR (β = −0.16, p = 0.04), and hyperemic coronary vascular resistance (β = 0.25, p <0.001) in the non-DM group. In conclusion, these results suggest a role for EAT in myocardial microvascular dysfunction; however, once DM has developed, other factors might be more dominant in contributing to impaired myocardial microvascular dysfunction. Patients with coronary artery disease and/or type 2 diabetes mellitus (DM) generally exhibit more epicardial adipose tissue (EAT) than healthy controls. Recently, it has been proposed that EAT affects vascular function and structure by secreting proinflammatory and vasoactive substances, thereby potentially contributing to the development of cardiovascular disease. In the present study, the interrelation of EAT, coronary vasomotor function, and coronary artery calcium was investigated in patients with and without DM, who were evaluated for coronary artery disease. Myocardial blood flow (MBF) was assessed at rest and during adenosine-induced hyperemia using [15O]-water positron emission tomography combined with computed tomography to quantify coronary artery calcium and EAT in 199 patients (46 with DM). In this cohort (mean age 58 ± 10 years), the patients with DM had a greater body mass index, heart rate, and systolic blood pressure at rest (all p <0.05). Coronary artery calcium and the EAT volumes were comparable between those with and without DM. Both patient groups showed comparable MBF at rest and coronary vascular resistance. A lower hyperemic MBF and coronary flow reserve (CFR) and greater hyperemic coronary vascular resistance (all p <0.05) was observed in the patients with DM. A pooled analysis showed a positive association of EAT volume with hyperemic coronary vascular resistance but not with the MBF at rest, hyperemic MBF, or coronary vascular resistance at rest. In the group analysis, the EAT volume was inversely associated with hyperemic MBF (r = −0.16, p = 0.05) and CFR (r = −0.17, p = 0.04) and positively with hyperemic coronary vascular resistance (r = 0.26, p = 0.002) only in patients without DM. Multivariate regression analysis, adjusted for age, gender, and body mass index, showed an independent association between the EAT volume and hyperemic MBF (β = −0.16, p = 0.02), CFR (β = −0.16, p = 0.04), and hyperemic coronary vascular resistance (β = 0.25, p <0.001) in the non-DM group. In conclusion, these results suggest a role for EAT in myocardial microvascular dysfunction; however, once DM has developed, other factors might be more dominant in contributing to impaired myocardial microvascular dysfunction. The present study investigated the effect of type 2 diabetes mellitus (DM) on the interaction of epicardial adipose tissue (EAT) and coronary artery calcium (CAC) as measured using computed tomography and vasomotor function determined by [15O]-water positron emission tomography. The present cohort study used data obtained from 199 patients, 46 with and 153 without DM, who were evaluated for coronary artery disease and therefore referred for CAC scoring and positron emission tomography myocardial blood flow (MBF) measurements using a hybrid positron emission tomography/computed tomography scanner (Gemini TF 64, Philips Healthcare, Best, The Netherlands). The patients were included retrospectively when the positron emission tomography findings (see positron emission tomography methods) did not indicate regional perfusion defects or otherwise signs of myocardial ischemia, defined by a coronary flow reserve (CFR)1Fleming R.M. The pathogenesis of vascular disease.in: Chang J.C. Textbook of Angiology. Springer-Verlag, New York1999: 787-798Google Scholar, 2Fleming R.M. Harrington G.M. Fleming Harrington redistribution wash-in washout (FHRWW): the platinum standard for nuclear cardiology.in: Fleming R.M. Establishing Better Standards of Care in Doppler Echocardiography, Computed Tomography and Nuclear Cardiology. Intech Publishing, Rijeka, Croatia2011Crossref Google Scholar <2 in any vascular territory.3Danad I. Raijmakers P.G. Appelman Y.E. Harms H.J. de H.S. van den Oever M.L. Heymans M.W. Tulevski I.I. van K.C. Hoekstra O.S. Lammertsma A.A. Lubberink M. van Rossum A.C. Knaapen P. Hybrid imaging using quantitative H215O PET and CT-based coronary angiography for the detection of coronary artery disease.J Nucl Med. 2013; 54: 55-63Crossref PubMed Scopus (92) Google Scholar In addition, patients were only included if electrocardiography did not show signs of a previous myocardial infarction, and echocardiography showed normal left ventricular function without wall motion abnormalities. The patients were classified as having DM when they had a positive history of DM currently treated with oral glucose-lowering agents and/or insulin. The exclusion criteria were atrial fibrillation, second- or third-degree atrioventricular block, symptomatic asthma, and pregnancy. In addition to DM, the coronary risk factors were assessed in all patients. Hypertension was defined as blood pressure ≥140/90 mm Hg or the use of antihypertensive medication. Hypercholesterolemia was defined as a total cholesterol level of ≥5 mmol/L or treatment with cholesterol-lowering medication. A positive family history of coronary artery disease was defined by the presence of coronary artery disease in first-degree relatives <55 years old for men or <65 years old for women. The need for written informed consent was waived by the institutional review board (local ethics committee) because of the nature of the study, which consisted solely of clinical data collection. The patients were instructed to refrain from the consumption of products containing caffeine or xanthine for 24 hours before the scan. After a scout computed tomographic scan for patient positioning and 2 minutes after the start of intravenous adenosine infusion (140 μg/kg/min), 370 MBq of [15O]-water was injected as a 5-ml (0.8 ml/s) bolus, followed immediately by a 35-ml saline flush (2 ml/s). A 6-minute emission scan was started simultaneously with the administration of [15O]-water. Next, a respiration-averaged, low-dose computed tomographic scan (30 mA, rotation time 0.5 second, pitch 0.829, collimation 64 × 0.625) was acquired to correct for attenuation during normal breathing.4Lubberink M. Harms H.J. Halbmeijer R. de H.S. Knaapen P. Lammertsma A.A. Low-dose quantitative myocardial blood flow imaging using 15O-water and PET without attenuation correction.J Nucl Med. 2010; 51: 575-580Crossref PubMed Scopus (44) Google Scholar Adenosine infusion was terminated after the low-dose computed tomographic scan. After an interval of 10 minutes to allow for decay of [15O]-water and washout of the adenosine, an identical positron emission tomographic sequence was performed during at rest conditions. Using the 3-dimensional row action maximum likelihood algorithm, images were reconstructed into 22 frames (1 × 10, 8 × 5, 4 × 10, 2 × 15, 3 × 20, 2 × 30, and 2 × 60), applying all appropriate corrections. Parametric MBF images were generated, and quantitative analysis was performed using in-house developed software (Cardiac VUer).5Harms H.J. Knaapen P. de H.S. Halbmeijer R. Lammertsma A.A. Lubberink M. Automatic generation of absolute myocardial blood flow images using [15O]H2O and a clinical PET/CT scanner.Eur J Nucl Med Mol Imaging. 2011; 38: 930-939Crossref PubMed Scopus (100) Google Scholar MBF is expressed as ml/min/g of perfusable tissue.6Cerqueira M.D. Weissman N.J. Dilsizian V. Jacobs A.K. Kaul S. Laskey W.K. Pennell D.J. Rumberger J.A. Ryan T. Verani M.S. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart: a statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association.Circulation. 2002; 105: 539-542Crossref PubMed Scopus (5228) Google Scholar Patients underwent computed tomographic scanning for CAC and EAT. The CAC scores and EAT volumes were obtained during a single breath hold using noncontrast-enhanced computed tomography. Images were acquired using 64 × 0.625-mm section collimation, a 420-ms gantry rotation time, 120-kV tube voltage, and a tube current of 100 to 120 mA, depending on the patients' body size. Coronary calcification was defined as plaque with an area of 1.03 mm2 and a density of ≥130 Hounsfield units. The CAC scores were calculated according to the method described by Agatston et al.7Agatston A.S. Janowitz W.R. Kaplan G. Gasso J. Hildner F. Viamonte Jr., M. Ultrafast computed tomography-detected coronary calcium reflects the angiographic extent of coronary arterial atherosclerosis.Am J Cardiol. 1994; 74: 1272-1274Abstract Full Text PDF PubMed Scopus (92) Google Scholar The EAT volume was measured using dedicated volumetric software (Extended Brilliance Workspace, Philips Healthcare, Best, The Netherlands). The most cranial slice taken into account was at the level of the pulmonary trunk, and the most caudal slice was identified as the last slice containing any portion of the myocardium. Within this area of interest, the pericardium was manually traced to distinguish epicardial from pericardial adipose tissue. EAT was defined automatically based on the Hounsfield units (Figure 1).8Taguchi R. Takasu J. Itani Y. Yamamoto R. Yokoyama K. Watanabe S. Masuda Y. Pericardial fat accumulation in men as a risk factor for coronary artery disease.Atherosclerosis. 2001; 157: 203-209Abstract Full Text Full Text PDF PubMed Scopus (220) Google Scholar, 9Yong H.S. Kim E.J. Seo H.S. Kang E.Y. Kim Y.K. Woo O.H. Han H. Pericardial fat is more abundant in patients with coronary atherosclerosis and even in the non-obese patients: evaluation with cardiac CT angiography.Int J Cardiovasc Imaging. 2010; 26: 53-62Crossref PubMed Scopus (30) Google Scholar Contiguous 3-dimensional voxels between −190 and −30 Hounsfield units were identified as EAT voxels. The region within the pericardium was reconstructed into a 3-dimensional image, resulting in a quantitative measurement of the EAT volume. All computed tomographic scans were analyzed by experienced radiologists and cardiologists who were unaware of the positron emission tomographic results. The rate pressure product (systolic blood pressure × heart rate) was calculated as an index of cardiac work both at rest and during hyperemia. The MBF at rest corrected for the rate pressure product was calculated by dividing the MBF by the rate pressure product and multiplying by 104. CFR was defined as the ratio between the hyperemic and at rest MBF,1Fleming R.M. The pathogenesis of vascular disease.in: Chang J.C. Textbook of Angiology. Springer-Verlag, New York1999: 787-798Google Scholar, 2Fleming R.M. Harrington G.M. Fleming Harrington redistribution wash-in washout (FHRWW): the platinum standard for nuclear cardiology.in: Fleming R.M. Establishing Better Standards of Care in Doppler Echocardiography, Computed Tomography and Nuclear Cardiology. Intech Publishing, Rijeka, Croatia2011Crossref Google Scholar and CFR was corrected for the rate pressure product as the ratio of the hyperemic and corrected at rest MBF. Coronary vascular resistance at rest and during hyperemia was calculated by dividing the mean arterial pressure by the MBF.10Knaapen P. Camici P.G. Marques K.M. Nijveldt R. Bax J.J. Westerhof N. Gotte M.J. Jerosch-Herold M. Schelbert H.R. Lammertsma A.A. van Rossum A.C. Coronary microvascular resistance: methods for its quantification in humans.Basic Res Cardiol. 2009; 104: 485-498Crossref PubMed Scopus (81) Google Scholar The normally distributed continuous variables are expressed as the mean ± SD; otherwise, the median with the interquartile range was used. Categorical variables are expressed as actual numbers or percentages. t Tests or Mann-Whitney U tests were used to determine the group differences for continuous variables and the chi-square test or Fisher exact test for categorical variables. Correlation coefficients were calculated using Pearson's product moment correlation. Multivariate analysis was performed to determine whether the association between EAT and MBF was independent of traditional coronary risk factors. Statistical analyses were performed using SPSS Statistics software, version 20 (IBM, Armonk, New York). p Values <0.05 were considered statistically significant. The baseline patient characteristics are listed in Table 1. The patients with DM had a greater body mass index and a greater frequency of hypertension and hypercholesterolemia. Consequently, the patients with DM used statins and angiotensin-II antagonists more often. Only the patients with DM used glucose-lowering therapy. No other medications differed between the patients with and without DM.Table 1Patient characteristicsVariableAll Patients (n = 199)DMp Value Between GroupsNo (n = 153)Yes (n = 46)Age (yrs)58 ± 1057 ± 1059 ± 120.35Men111 (56)86 (56)25 (54)0.87BMI (kg/m2)26.9 ± 4.126.3 ± 3.828.9 ± 4.5<0.001Hypertension95 (49)66 (44)29 (63)0.03Hypercholesterolemia73 (37)46 (31)27 (59)<0.001Current smoker81 (41)61 (41)20 (44)0.87Family history of CAD109 (56)86 (57)23 (50)0.40Statins121 (62)85 (57)36 (78)0.01β Blockers122 (62)93 (62)29 (63)0.90Aspirin136 (31)103 (69)33 (72)0.72ACE inhibitors34 (17)24 (16)10 (22)0.38At-II antagonists41 (20)25 (17)15 (32)0.02Calcium antagonist44 (22)32 (21)12 (26)0.35Insulin therapy14 (7)NA14 (30)NAData are presented as mean ± SD or n (%).ACE = angiotensin-converting enzyme; AT-II = angiotensin-II; BMI = body mass index; CAD = coronary artery disease; NA = not applicable. Open table in a new tab Data are presented as mean ± SD or n (%). ACE = angiotensin-converting enzyme; AT-II = angiotensin-II; BMI = body mass index; CAD = coronary artery disease; NA = not applicable. The hemodynamic parameters are listed in Table 2. At rest, the heart rate, systolic blood pressure, and rate pressure product were greater in the patients with DM. Hyperemic conditions elicited a significant increase in the heart rate and rate pressure product in both groups. Only in those without DM did hyperemia cause an increase in systolic blood pressure. No differences in heart rate, systolic and diastolic blood pressure, or rate pressure product during hyperemia were observed between the 2 groups.Table 2Hemodynamic data during positron emission tomographyVariableAll Patients (n = 199)DMp Value Between GroupsNo (n = 153)Yes (n = 46)Heart rate (beats/min) At rest64 ± 1163 ± 1167 ± 100.02 Hyperemia83 ± 1383 ± 1385 ± 150.44 p Value<0.001<0.001<0.001Systolic blood pressure (mm Hg) At rest113 ± 19112 ± 18119 ± 210.04 Hyperemia116 ± 20115 ± 19120 ± 220.12 p Value0.050.010.60Diastolic blood pressure (mm Hg) At rest60 ± 860 ± 861 ± 100.41 Hyperemia60 ± 960 ± 861 ± 110.41 p Value0.890.850.89RPP (mm Hg/min) At rest7,275 ± 1,8737,064 ± 1,8247,977 ± 1,907<0.01 Hyperemia9,729 ± 2,5089,575 ± 2,32610,299 ± 3,0010.14 p Value<0.001<0.001<0.001Data are presented as mean ± SD.RPP = rate product pressure. Open table in a new tab Data are presented as mean ± SD. RPP = rate product pressure. The MBF at rest was comparable between the 2 groups (p = 0.58; Figure 2). After correction for hemodynamic discrepancies (i.e., rate pressure product), however, the MBF at rest was diminished in those with DM (1.52 ± 0.57 vs 1.32 ± 0.38 ml/min/g, respectively; p = 0.03). Hyperemic MBF was impaired in those with DM (p = 0.03; Figure 2), just as was CFR (p = 0.02; Figure 2). Correction for the rate pressure product, however, abolished these differences in the CFR (2.21 ± 0.91 vs 2.15 ± 0.81, respectively; p = 0.71). The coronary vascular resistance at rest was comparable between the 2 groups (p = 0.42, Figure 3), but the minimal coronary vascular resistance was augmented in those with DM (p = 0.02; Figure 3).Figure 3Coronary vascular resistance (CVR) at rest and during hyperemia in patients without DM (non-DM; black bars) and those with DM (white bars). Data are presented as mean ± SD. *p <0.05, **p <0.001.View Large Image Figure ViewerDownload Hi-res image Download (PPT) As shown in Figures 4 and 5, the patients without and with DM had comparable EAT volumes (p = 0.31) and CAC scores (p = 0.13).Figure 5Whisker boxes and scatter plots of CAC scores (when added with 1) of those without DM (non-DM; hatched box and black dots) and those with DM (white box and white dots). Data are presented as median (range).View Large Image Figure ViewerDownload Hi-res image Download (PPT) In a pooled analysis, the EAT volume was only significantly associated with hyperemic coronary vascular resistance (p = 0.02; Figure 6) but not with other vasomotor function parameters, such as hyperemic MBF (Figure 6), CFR (Figure 6), or CAC (Table 3). In a separate analysis, in the non-DM group, EAT displayed significant univariate correlations with hyperemic MBF (p = 0.05, Figure 6) and CFR (p = 0.04, Figure 6), although the association with the minimal coronary vascular resistance became more apparent (p = 0.002, Figure 6). Multivariate regression analysis (adjusting for age, gender, and body mass index) revealed an independent association between the EAT volume and hyperemic MBF (β = −0.19, p = 0.01), CFR (β = −0.16, p = 0.04), and hyperemic coronary vascular resistance (β = 0.25, p <0.001). In patients with DM, the EAT volume was not related to any perfusion parameter (Figure 6).Figure 6Scatter plots of logarithmic transformed EAT volume and hyperemic MBF in (A) all patients (black triangles), (B) those without DM (non-DM; black dots), and (C) those with DM (white dots). Scatter plots of logarithmic transformed epicardial adipose tissue volume and coronary flow reserve in (D) all patients (black triangles), (E) those without DM (black dots), and (F) patients with DM (white dots). Scatter plots of logarithmic transformed epicardial adipose tissue volume and hyperemic coronary vascular resistance (CVR) in (G) all patients (black triangles), (H) those without DM (black dots), and (I) those with DM (white dots).View Large Image Figure ViewerDownload Hi-res image Download (PPT)Table 3Univariate analysis of epicardial adipose tissue (EAT) volume with coronary vasomotor function and coronary artery calcium (CAC)VariableAll Patients (n = 199)p ValuePatients Without DM (n = 153)p ValuePatients With DM (n = 46)p ValueMBF at rest (ml/min/g)0.020.750.050.57−0.010.95MBF at rest, corrected for RPP (m/mm Hg/g)−0.010.91−0.010.93−0.090.59Hyperemic MBF (ml/min/g)−0.110.14−0.160.05−0.010.94CFR−0.100.19−0.170.040.040.79CFR, corrected for RPP (mm Hg/min)−0.030.66−0.090.300.110.49CVR at rest (mm Hg/ml/min/g)0.040.550.020.820.120.43Hyperemic CVR (mm Hg/ml/min/g)0.170.020.260.0020.050.75Coronary artery calcium−0.010.950.070.52−0.150.45Data are presented as Pearson's r; EAT and CAC were logarithmic transformed because of non-normal distributions.CVR = coronary vascular resistance; RPP = rate pressure product. Open table in a new tab Data are presented as Pearson's r; EAT and CAC were logarithmic transformed because of non-normal distributions. CVR = coronary vascular resistance; RPP = rate pressure product. The purpose of the present analysis was to evaluate the effect of DM on the interrelations among EAT deposition, CAC, and coronary vasomotor function. Only in patients without DM, was an association between the EAT volume and coronary vasomotor dysfunction evident. The patients with DM showed no signs of an increased EAT volume compared with those without DM. Moreover, no association was found between the highly variable EAT volume and coronary vasomotor function in those with DM. The MBF at rest was comparable between both groups; however, after correction for differences in hemodynamics, the corrected MBF was lower in those with DM. Because of the more prevalent central obesity and insulin resistance, DM is associated with high blood pressure.11Ferrannini E. Cushman W.C. Diabetes and hypertension: the bad companions.Lancet. 2012; 380: 601-610Abstract Full Text Full Text PDF PubMed Scopus (385) Google Scholar Next to hypertension, a relatively elevated heart rate at rest is common in patients with DM and results from cardiovascular autonomic dysfunction with vagal impairment.12Vinik A.I. Ziegler D. Diabetic cardiovascular autonomic neuropathy.Circulation. 2007; 115: 387-397Crossref PubMed Scopus (799) Google Scholar Thus, in general, the myocardial metabolic demand will be augmented in patients with DM, thereby affecting the MBF at rest. In addition, the effect of DM on the metabolic milieu and insulin levels also affects the MBF at rest.13Sundell J. Knuuti J. Insulin and myocardial blood flow.Cardiovasc Res. 2003; 57: 312-319Crossref PubMed Scopus (53) Google Scholar However, studies on myocardial perfusion at rest in those with DM have been conflicting. The MBF at rest in those with DM, without correction for hemodynamics, has been reported to be comparable to that in control subjects,14Rijzewijk L.J. van der Meer R.W. Lamb H.J. de Jong H.W. Lubberink M. Romijn J.A. Bax J.J. de R.A. Twisk J.W. Heine R.J. Lammertsma A.A. Smit J.W. Diamant M. Altered myocardial substrate metabolism and decreased diastolic function in nonischemic human diabetic cardiomyopathy: studies with cardiac positron emission tomography and magnetic resonance imaging.J Am Coll Cardiol. 2009; 54: 1524-1532Abstract Full Text Full Text PDF PubMed Google Scholar, 15Danad I. Raijmakers P.G. Appelman Y.E. Harms H.J. de H.S. van den Oever M.L. van K.C. Allaart C.P. Hoekstra O.S. Lammertsma A.A. Lubberink M. van Rossum A.C. Knaapen P. Coronary risk factors and myocardial blood flow in patients evaluated for coronary artery disease: a quantitative [15O]H2O PET/CT study.Eur J Nucl Med Mol Imaging. 2012; 39: 102-112Crossref PubMed Scopus (52) Google Scholar decreased in a large population of patients referred for myocardial perfusion imaging,16Murthy V.L. Naya M. Foster C.R. Gaber M. Hainer J. Klein J. Dorbala S. Blankstein R. Di Carli M.F. Association between coronary vascular dysfunction and cardiac mortality in patients with and without diabetes mellitus.Circulation. 2012; 126: 1858-1868Crossref PubMed Scopus (339) Google Scholar and increased compared with patients without DM.17Picchi A. Limbruno U. Focardi M. Cortese B. Micheli A. Boschi L. Severi S. De Caterina R. Increased basal coronary blood flow as a cause of reduced coronary flow reserve in diabetic patients.Am J Physiol Heart Circ Physiol. 2011; 301: H2279-H2284Crossref PubMed Scopus (44) Google Scholar Hyperemic MBF was reduced and minimal coronary vascular resistance was increased in patients with DM. Because the perfusion at rest was comparable between both groups, this led to a lower CFR in the patients with DM. The latter is a consistent observation, documented by several studies, and represents coronary microvascular dysfunction.15Danad I. Raijmakers P.G. Appelman Y.E. Harms H.J. de H.S. van den Oever M.L. van K.C. Allaart C.P. Hoekstra O.S. Lammertsma A.A. Lubberink M. van Rossum A.C. Knaapen P. Coronary risk factors and myocardial blood flow in patients evaluated for coronary artery disease: a quantitative [15O]H2O PET/CT study.Eur J Nucl Med Mol Imaging. 2012; 39: 102-112Crossref PubMed Scopus (52) Google Scholar, 16Murthy V.L. Naya M. Foster C.R. Gaber M. Hainer J. Klein J. Dorbala S. Blankstein R. Di Carli M.F. Association between coronary vascular dysfunction and cardiac mortality in patients with and without diabetes mellitus.Circulation. 2012; 126: 1858-1868Crossref PubMed Scopus (339) Google Scholar, 18Yokoyama I. Momomura S. Ohtake T. Yonekura K. Nishikawa J. Sasaki Y. Omata M. Reduced myocardial flow reserve in non–insulin-dependent diabetes mellitus.J Am Coll Cardiol. 1997; 30: 1472-1477Abstract Full Text Full Text PDF PubMed Scopus (221) Google Scholar Nonetheless, the causal role of DM for impaired hyperemic perfusion is controversial, because obesity, a general feature of this metabolic disease, appears to be more tightly linked to vasomotor dysfunction than DM itself.15Danad I. Raijmakers P.G. Appelman Y.E. Harms H.J. de H.S. van den Oever M.L. van K.C. Allaart C.P. Hoekstra O.S. Lammertsma A.A. Lubberink M. van Rossum A.C. Knaapen P. Coronary risk factors and myocardial blood flow in patients evaluated for coronary artery disease: a quantitative [15O]H2O PET/CT study.Eur J Nucl Med Mol Imaging. 2012; 39: 102-112Crossref PubMed Scopus (52) Google Scholar In contrast to some previous reports,19Peix A. Cabrera L.O. Heres F. Rodriguez L. Valdes A. Valiente J. Garcia R. Licea M. Mendoza V. Garciga F. Rodriguez Y. Carrillo R. Mena E. Fernandez Y. Montero M. Dondi M. Interrelationship between myocardial perfusion imaging, coronary calcium score, and endothelial function in asymptomatic diabetics and controls.J Nucl Cardiol. 2011; 18: 398-406Crossref PubMed Scopus (12) Google Scholar, 20Versteylen M.O. Takx R.A. Joosen I.A. Nelemans P.J. Das M. Crijns H.J. Hofstra L. Leiner T. Epicardial adipose tissue volume as a predictor for coronary artery disease in diabetic, impaired fasting glucose, and non-diabetic patients presenting with chest pain.Eur Heart J Cardiovasc Imaging. 2012; 13: 517-523Crossref PubMed Scopus (33) Google Scholar, 21Wang C.P. Hsu H.L. Hung W.C. Yu T.H. Chen Y.H. Chiu C.A. Lu L.F. Chung F.M. Shin S.J. Lee Y.J. Increased epicardial adipose tissue (EAT) volume in type 2 diabetes mellitus and association with metabolic syndrome and severity of coronary atherosclerosis.Clin Endocrinol (Oxf). 2009; 70: 876-882Crossref PubMed Scopus (176) Google Scholar neither the EAT volume nor CAC were increased in the DM population. A potential explanation for this apparently conflicting observation was that the patient population in the present study did not show signs of obstructive coronary artery disease on cardiac perfusion positron emission tomographic scans. Hence, this cohort included patients with less advanced cardiac disease; thus, differences, related to DM status, in EAT and CAC were not detected. In the present study, no association was found between the EAT volume and CAC, irrespective of the presence of DM. Most previous studies have observed a positive association between EAT and CAC, both in patients evaluated for the presence of coronary artery disease22Djaberi R. Schuijf J.D. van Werkhoven J.M. Nucifora G. Jukema J.W. Bax J.J. Relation of epicardial adipose tissue to coronary atherosclerosis.Am J Cardiol. 2008; 102: 1602-1607Abstract Full Text Full Text PDF PubMed Scopus (152) Google Scholar, 23Bachar G.N. Dicker D. Kornowski R. Atar E. Epicardial adipose tissue as a predictor of coronary artery disease in asymptomatic subjects.Am J Cardiol. 2012; 110: 534-538Abstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar, 24Sarin S. Wenger C. Marwaha A. Qureshi A. Go B.D. Woomert C.A. Clark K. Nassef L.A. Shirani J. Clinical significance of epicardial fat measured using cardiac multislice computed tomography.Am J Cardiol. 2008; 102: 767-771Abstract Full Text Full Text PDF PubMed Scopus (175) Google Scholar, 25Bucci M. Joutsiniemi E. Saraste A. Kajander S. Ukkonen H. Saraste M. Pietila M. Sipila H.T. Teras M. Maki M. Airaksinen K.E. Hartiala J. Knuuti J. Iozzo P. Intrapericardial, but not extrapericardial, fat is an independent predictor of impaired hyperemic coronary perfusion in coronary artery disease.Arterioscler Thromb Vasc Biol. 2011; 31: 211-218Crossref PubMed Scopus (27) Google Scholar and in patients with asymptomatic DM.21Wang C.P. Hsu H.L. Hung W.C. Yu T.H. Chen Y.H. Chiu C.A. Lu L.F. Chung F.M. Shin S.J. Lee Y.J. Increased epicardial adipose tissue (EAT) volume in type 2 diabetes mellitus and association with metabolic syndrome and severity of coronary atherosclerosis.Clin Endocrinol (Oxf). 2009; 70: 876-882Crossref PubMed Scopus (176) Google Scholar, 26Yerramasu A. Dey D. Venuraju S. Anand D.V. Atwal S. Corder R. Berman D.S. Lahiri A. Increased volume of epicardial fat is an independent risk factor for accelerated progression of sub-clinical coronary atherosclerosis.Atherosclerosis. 2012; 220: 223-230Abstract Full Text Full Text PDF PubMed Scopus (179) Google Scholar Gorter et al,27Gorter P.M. de Vos A.M. van der G.Y. Stella P.R. Doevendans P.A. Meijs M.F. Prokop M. Visseren F.L. Relation of epicardial and pericoronary fat to coronary atherosclerosis and coronary artery calcium in patients undergoing coronary angiography.Am J Cardiol. 2008; 102: 380-385Abstract Full Text Full Text PDF PubMed Scopus (219) Google Scholar when analyzing the EAT volumes in patients with angina pectoris and a body mass index <27 kg/m2, found that increased EAT was related to more severe coronary atherosclerosis and CAC. This relation was not observed in patients with a high body mass index. However, others have reported an association for EAT volume only with the presence of coronary atherosclerosis, not with its severity,22Djaberi R. Schuijf J.D. van Werkhoven J.M. Nucifora G. Jukema J.W. Bax J.J. Relation of epicardial adipose tissue to coronary atherosclerosis.Am J Cardiol. 2008; 102: 1602-1607Abstract Full Text Full Text PDF PubMed Scopus (152) Google Scholar nor did they find an association between ultrasound-measured EAT and the presence or severity of angiographic coronary artery disease.28Chaowalit N. Somers V.K. Pellikka P.A. Rihal C.S. Lopez-Jimenez F. Subepicardial adipose tissue and the presence and severity of coronary artery disease.Atherosclerosis. 2006; 186: 354-359Abstract Full Text Full Text PDF PubMed Scopus (139) Google Scholar In the present pooled cohort, univariate analysis revealed a significant, albeit weak, correlation between EAT and minimal coronary resistance, suggesting that EAT might be linked only remotely to vasomotor microvascular dysfunction. These results are in line with previous studies that have revealed either a weak or even an absent relation between epicardial fat and vasomotor dysfunction in healthy controls or patients with various stages of coronary artery disease.25Bucci M. Joutsiniemi E. Saraste A. Kajander S. Ukkonen H. Saraste M. Pietila M. Sipila H.T. Teras M. Maki M. Airaksinen K.E. Hartiala J. Knuuti J. Iozzo P. Intrapericardial, but not extrapericardial, fat is an independent predictor of impaired hyperemic coronary perfusion in coronary artery disease.Arterioscler Thromb Vasc Biol. 2011; 31: 211-218Crossref PubMed Scopus (27) Google Scholar, 29Gaborit B. Kober F. Jacquier A. Moro P.J. Flavian A. Quilici J. Cuisset T. Simeoni U. Cozzone P. Alessi M.C. Clement K. Bernard M. Dutour A. Epicardial fat volume is associated with coronary microvascular response in healthy subjects: a pilot study.Obesity (Silver Spring). 2012; 20: 1200-1205Crossref PubMed Scopus (23) Google Scholar Using a method comparable to that used in the present study, Bucci et al25Bucci M. Joutsiniemi E. Saraste A. Kajander S. Ukkonen H. Saraste M. Pietila M. Sipila H.T. Teras M. Maki M. Airaksinen K.E. Hartiala J. Knuuti J. Iozzo P. Intrapericardial, but not extrapericardial, fat is an independent predictor of impaired hyperemic coronary perfusion in coronary artery disease.Arterioscler Thromb Vasc Biol. 2011; 31: 211-218Crossref PubMed Scopus (27) Google Scholar also found a weak correlation between perfusion reserve and epicardial fat. Excluding patients without obstructive coronary artery disease, however, abolished this association.25Bucci M. Joutsiniemi E. Saraste A. Kajander S. Ukkonen H. Saraste M. Pietila M. Sipila H.T. Teras M. Maki M. Airaksinen K.E. Hartiala J. Knuuti J. Iozzo P. Intrapericardial, but not extrapericardial, fat is an independent predictor of impaired hyperemic coronary perfusion in coronary artery disease.Arterioscler Thromb Vasc Biol. 2011; 31: 211-218Crossref PubMed Scopus (27) Google Scholar The largest cohort examined to date was obtained from the Multi-Ethnic Study of Atherosclerosis (MESA) study, which only revealed an effect of EAT on perfusion reserve in asymptomatic women, indicating a possible gender effect. Correction of the flow reserve for baseline hemodynamic conditions subsequently attenuated this association.30Brinkley T.E. Jerosch-Herold M. Folsom A.R. Carr J.J. Hundley W.G. Allison M.A. Bluemke D.A. Burke G.L. Szklo M. Ding J. Pericardial fat and myocardial perfusion in asymptomatic adults from the Multi-Ethnic Study of Atherosclerosis.PLoS One. 2011; 6: e28410Crossref PubMed Scopus (11) Google Scholar The primary objective of the present study, however, was to analyze the effect of DM on the relation between EAT and perfusion parameters. This subgroup analysis did not establish any such relation, although it became appreciable stronger in patients without DM and remained significant after correction for traditional cardiovascular risk factors. This finding is of importance, because omitting DM participants significantly diminished the statistical power with regard to the sample size, yet more clearly revealed a relation between vasomotor function and EAT volume. Apparently, DM induces “statistical noise” pertaining to this association, and this indirectly implies that EAT has a less profound effect on the myocardial perfusion reserve in patients with DM. The lack of any relation between EAT and the myocardial perfusion parameters in the patients with DM underscores this notion, although the small sample size of patients with DM warrants caution in the inferences that can be drawn. Altogether, however, these data suggest that a direct relation does not exist between EAT and myocardial perfusion in those with DM and hints toward a more complex multifactorial pathophysiology of vasomotor control owing to this metabolic perturbation. The study limitations include the cross-sectional study design, which did not allow inference of causal associations. This also resulted in a skewed distribution of the patients with and without DM and suboptimal characterization of the longevity and level of control of DM. Second, although care was taken to exclude obstructive coronary artery disease using quantitative cardiac positron emission tomography, a small number of patients with hemodynamically significant lesions might have been included.3Danad I. Raijmakers P.G. Appelman Y.E. Harms H.J. de H.S. van den Oever M.L. Heymans M.W. Tulevski I.I. van K.C. Hoekstra O.S. Lammertsma A.A. Lubberink M. van Rossum A.C. Knaapen P. Hybrid imaging using quantitative H215O PET and CT-based coronary angiography for the detection of coronary artery disease.J Nucl Med. 2013; 54: 55-63Crossref PubMed Scopus (92) Google Scholar Third, the present study focused merely on the EAT volume and did not take into account its function (e.g., by studying circulating adipokines secreted by EAT). Notwithstanding these limitations, the present results provide novel insights and could act as an incentive to further explore the role of EAT accumulation and function in the pathophysiology of coronary vasomotor dysfunction in patients with and without DM. The authors have no conflicts of interest to disclose." @default.
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• W2078588918 title "Effect of Type 2 Diabetes Mellitus on Epicardial Adipose Tissue Volume and Coronary Vasomotor Function" @default.
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• W2078588918 cites W2028675920 @default.
• W2078588918 cites W2029378482 @default.
• W2078588918 cites W2037579622 @default.
• W2078588918 cites W2046003362 @default.
• W2078588918 cites W2046838549 @default.
• W2078588918 cites W2053427294 @default.
• W2078588918 cites W2053642000 @default.
• W2078588918 cites W2058267199 @default.
• W2078588918 cites W2059141130 @default.
• W2078588918 cites W2063209936 @default.
• W2078588918 cites W2072194913 @default.
• W2078588918 cites W2073713188 @default.
• W2078588918 cites W2080205213 @default.
• W2078588918 cites W2083947509 @default.
• W2078588918 cites W2094311032 @default.
• W2078588918 cites W2104600471 @default.
• W2078588918 cites W2109975725 @default.
• W2078588918 cites W2119693754 @default.
• W2078588918 cites W2131519487 @default.
• W2078588918 cites W2132401137 @default.
• W2078588918 cites W2144403818 @default.
• W2078588918 cites W2145387017 @default.
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