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      Pericardial fat volume and coronary risk factors as predictors of non-calcified coronary plaque presence among patients with coronary calcium score = 0

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          Abstract

          Introduction

          There is scarce data linking pericardial fat volume (PFV) and classical coronary risk factors with non-calcified plaque presence among patients with CAC = 0 in the literature.

          Material and method

          A total of 811 patients with chest pain suggestive of angina underwent CT coronary angiography for the assessment of coronary artery disease were collected. Of these, 417 with CAC = 0 were included in the analysis.

          Result

          Patients with non-calcified plaque were older (54 ± 9 versus 50 ± 10, P = 0.01) and had a higher prevalence of diabetes mellitus (31% versus 17%, P = 0.02), high BMI (29.9 versus 28.3, P = 0.04), and increased PFV (123 cm 3 versus 99 cm 3, P < 0.01) compared to patients without plaque. In multivariate regression analysis, high BMI[OR(CI) = 1.1(1–1.3), P = 0.02] was an independent predictor of non-calcified coronary plaque presence among patients with CAC = 0 after adjustment to variables with P < 0.05 in the univariate analysis.

          Conclusion

          In patients with a CAC score of 0, advanced age, diabetes mellitus, increased PFV, and high BMI were all associated with the presence of non-calcified plaque. After multivariate adjustment, increased BMI remained a significant independent predictor for non-calcified plaque presence.

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          Most cited references14

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          The double role of epicardial adipose tissue as pro- and anti-inflammatory organ.

          Obesity is associated with low grade inflammation. Whether this is just an adaptive response to excess adiposity to maintain a normal oxygen supply or a chronic activation of the innate immune system is still unknown. Recent research has focused on the origin of the inflammatory markers in obesity and the extent to which adipose tissue has a direct effect. The production of adipokines by visceral adipose tissue is of particular interest since their local secretion by visceral fat depots may provide a novel mechanistic link between obesity and the associated vascular complications. Growing evidences suggest that the epicardial adipose tissue, the visceral fat depot located around the heart, may locally interact with myocardium and coronary arteries. Epicardial fat is a source of adiponectin and adrenomedullin, adipokines with anti-inflammatory properties, and several proinflammatory cytokines as well as Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin 1 (IL1), IL-1 h, Interleukin (IL6), Monocyte Chemoattractive Protein-1 (MCP-1), Nerve Growth Factor (NGF), resistin, Plasminogen Activator Inhibitor-1 (PAI-1), and free fatty acids. Epicardial adipose tissue could locally modulate the heart and vasculature, through paracrine secretion of pro- and anti-inflammatory cytokines, thereby playing a possible role in the adiposity-related inflammation and atherosclerosis. On the other hand, epicardial fat could exert a protective effect through adiponectin and adrenomedullin secretion as response to local or systemic metabolic or mechanical insults. Future studies will continue to provide new and fascinating insights into the double role of epicardial adipose tissue in the development of cardiovascular pathology and/or in protecting the heart and arteries.
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            Epicardial Adipose Tissue Contributes to the Development of Non-Calcified Coronary Plaque: A 5-Year Computed Tomography Follow-up Study

            Aim: Epicardial adipose tissue (EAT) has been suggested as a contributing factor for coronary atherosclerosis based on the previous cross-sectional studies and pathophysiologic background. However, a causal relationship between EAT and the development of non-calcified coronary plaque (NCP) has not been investigated. Methods: A total of 122 asymptomatic individuals (age, 56.0 ± 7.6 years; male, 80.3%) without prior history of coronary artery disease (CAD) or metabolic syndrome and without NCP or obstructive CAD at baseline cardiac computed tomography (CT) were enrolled. Repeat cardiac CT was performed with an interval of more than 5 years. Epicardial fat volume index (EFVi; cm3/m2) was assessed in relation to the development of NCP on the follow-up CT where the results were classified into “calcified plaque (CP),” “no plaque,” and “NCP” groups. Results: On the follow-up CT performed with a median interval of 65.4 months, we observed newly developed NCP in 24 (19.7%) participants. Baseline EFVi was significantly higher in the NCP group (79.9 ± 30.3 cm3/m2) than in the CP group (63.7 ± 22.7 cm3/m2; P = 0.019) and in the no plaque group (62.5 ± 24.7 cm3/m2; P = 0.021). Multivariable logistic regression analysis demonstrated that the presence of diabetes (OR, 9.081; 95% CI, 1.682–49.034; P = 0.010) and the 3rd tertile of EFVi (OR, 4.297; 95% CI, 1.040–17.757; P = 0.044 compared to the 1st tertile) were the significant predictors for the development of NCP on follow-up CT. Conclusions: Greater amount of EAT at baseline CT independently predicts the development of NCP in asymptomatic individuals.
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              Noncalcified atherosclerotic plaque burden at coronary CT angiography: a better predictor of ischemia at stress myocardial perfusion imaging than calcium score and stenosis severity.

              The purpose of this study was to examine the relation between the coronary CT angiographic findings of calcified and noncalcified plaque burden and stenosis severity and the myocardial perfusion imaging finding of ischemia. Seventy-two patients (41 men, 31 women; mean age, 56 years) underwent coronary CT angiography and stress-rest SPECT myocardial perfusion imaging. Calcium scoring was performed. Coronary CT angiograms were analyzed for stenosis and noncalcified or mixed plaque. A plaque analysis tool was used to calculate the volume of noncalcified plaque components. SPECT images were analyzed for perfusion defects. Data were analyzed per patient and per vessel. A total of 53 purely noncalcified, 50 mixed, and 201 purely calcified plaques were detected. Forty-five stenoses were rated > or = 50%, 19 of those being > or = 70%. Myocardial perfusion imaging depicted perfusion defects in 37 vessels (13%) in 24 patients (18 reversible, 19 fixed defects). Vessels with > or = 50% stenosis had significantly (p = 0.0009) more perfusion defects in their supplied territories (11 with, 22 without perfusion defects) than did vessels without significant lesions (26 with, 229 without perfusion defects). In vessel-based analysis, the sensitivity of coronary CT angiography in prediction of any perfusion defect on myocardial perfusion images was 30% with 91% specificity, 33% positive predictive value, and 90% negative predictive value. Between vessels with and those without perfusion defects, there was no significant difference in Agatston or calcium volume score (p = 0.25), but there was a significant difference in noncalcified plaque volume (44 +/- 77 vs 19 +/- 58 mm(3); p = 0.03). Multiple stepwise regression analysis showed noncalcified plaque volume was the only significant predictor of ischemia (p = 0.01). At coronary CT angiography, noncalcified plaque burden is a better predictor of the finding of myocardial ischemia at stress myocardial perfusion imaging than are calcium score and degree of stenosis.
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                Author and article information

                Contributors
                Journal
                Indian Heart J
                Indian Heart J
                Indian Heart Journal
                Elsevier
                0019-4832
                2213-3763
                Jan-Feb 2024
                19 December 2023
                : 76
                : 1
                : 51-53
                Affiliations
                [a ]Radiology Department, Medicine College, University of Kufa, Najaf, Iraq
                [b ]Internal Medicine Department, Medicine College, University of Kufa, P.O. 21, Kufa, Najaf, Iraq
                [c ]Al-Sader Teaching Medical City, Najaf Health Directorate, Najaf, Iraq
                Author notes
                []Corresponding author. husseinaf.alnaffakh@ 123456uokufa.edu.iq
                Article
                S0019-4832(23)00475-3
                10.1016/j.ihj.2023.12.006
                10943564
                38128878
                798b1860-6aeb-4d35-9e6c-835f80a3c92b
                © 2023 Cardiological Society of India. Published by Elsevier, a division of RELX India, Pvt. Ltd.

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 10 August 2023
                : 5 November 2023
                : 15 December 2023
                Categories
                Research Brief

                coronary,non-calcified plaque,pericardial fat
                coronary, non-calcified plaque, pericardial fat

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