Association of Aortic Valve Calcification and Epicardial Fat Volume

Transcription

1 Association of Aortic Valve Calcification and Epicardial Fat Volume Poster No.: C-2540 Congress: ECR 2015 Type: Scientific Exhibit Authors: S. Reinartz, C. K. Kuhl, N. Marx, V. Brandenburg, R. Koos, T. Dirrichs; Aachen/DE Keywords: DOI: Cardiac, CT, Comparative studies, Calcifications / Calculi, Connective tissue disorders /ecr2015/C-2540 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 8

2 Aims and objectives Epicardial adipose tissue (EAT) has emerged as an important factor of coronary artery atherosclerosis (1,2) due to its endocrine potential, including secretion of several proinflammatory mediators. The pathogenesis of aortic valve calcification (AVC) shares many similarities with atherosclerosis (3-4). The relationship between AVC and EAT ist still unknown. To find out whether they are associated was aim of this study. Methods and materials Cross-sectional study on 139 patients ( Table 1 on page 2 ) with echocardiographically proven AVC was performed. For quantification of AVC and EAT, all patients underwent non contrast-enhanced ECG-triggered Dual Source CT from the pulmonary bifurcation to the diaphragm. Standard reconstruction using cardiac field of view and reconstruction kernel for quantifying coronary calcification (B35F) with 3 mm slice thickness was used. EAT is defined as fat located above the epicardium and surrounded by the pericardium (5) and harbours the coronaries. Thererfore EAT was assumed having densities between -200 to -40 HU (5) and is quantified by counting pixels matching these densities in this space ( Fig. 1 on page 3 ). AVC was measured by using the Agaston method (6,7) applied on the aortic valve calcifications with the same dataset. EAT in patients with AVC (studygroup) was compared to values obtained in a younger control population (n=30, Table 1 on page 2 ) without relevant coronary or aortic valve calcification. We stratified patients with AVC in a low (n = 69) and high calcification (n = 70) group using AVC median. Images for this section: Page 2 of 8

3 Table 1: Patients characteristics of the study and control group regarding cardiovascular risk factors. Page 3 of 8

4 Fig. 1: ECG-triggered Dual Source CT with manually marked epicardial fat tissue (margenta) indicating density values between -200 and -40 Hounsfield. Reconstruction: Field of view: 180 sqcm, Kernel: B35f Page 4 of 8

5 Results Mean AVC score in the study group was 1408 ± Patients with AVC showed significantly higher EAT (163 ± 65 ccm) as compared to our control group without relevant coronary or valvular calcification (94 ± 46 ccm3, p< 0.001; Fig. 2 on page 5 ). This effect was evident in gender specific analysis, too (p<0.05). Epicardial fat volume was significantly smaller (151 ± 50 ccm) in the low calcification group than in the high calcification group (175 ± 76 cm, p=0.03, Fig. 3 on page 5 ). Images for this section: Fig. 2: Box plot of EAT Volume regarding men and women in study and control group showing significant (gender) specific differences in EAT-Volume between groups (p<0.001, gender specific: p<0.05) Page 5 of 8

6 Fig. 3: Box plot of EAT Volume regarding high calcification (n=70) and low calcification group (n=69) respectively control population (n=30) showing significant (p=0.03) differences. Page 6 of 8

7 Conclusion Patients with AVC showed significantly increased EAT compared to a younger reference population without relevant coronary or valvular calcification. Furthermore, our data demonstrate a moderate association between the severity of AVC and EAT indicating a possible role of epicardial adipose tissue in the valvular calcification process. Personal information Sebastian D. Reinartz, Department of Diagnostic and Interventional Radiology, University Hospital, RWTH-Aachen, Germany; sreinartz@ukaachen.de References 1. Mazurek T, Human epicardial adipose tissue is a source of inflammatory mediators. Circulation. 2003;108: Mahabadi AA, Association of Epicardial Fat With Cardiovascular Risk Factors and Incident Myocardial Infarction in the General Population: The Heinz Nixdorf Recall Study. Journal of the American College of Cardiology. 2013; 61: Greif M, Pericardial adipose tissue determined by dual source ct is a risk factor for coronary atherosclerosis. Arterioscler Thromb Vasc Biol. 2009:781e Kunita E, Prognostic value of coronary artery calcium and epicardial adipose tissue assessed by non-contrast cardiac computed tomography. Atherosclerosis. 2014; 233: Page 7 of 8

8 5. Marwan M, Quantification of epicardial fat by computed tomography: why, when and how? Journal of Cardiovascular Computed Tomography. 2013; 7: Agatston A, Quantification of coronary artery calcium using ultrafast computed tomography, Journal American College of cardiology, 1990; Koos R, Quantification of aortic valve calcification using multislice spiral computed tomography: comparizon with atomic absorbtion spectroscopy, Invest Radiol 2006, Page 8 of 8