Xoana Barros1,2, Timm Dirrichs3, Ralf Koos4, Sebastian Reinartz3, Nadine Kaesler5, Rafael Kramann5, Ulrich Gladziwa6, Markus Ketteler7, Jürgen Floege5, Nikolaus Marx8, José V Torregrosa9, András Keszei10, Vincent M Brandenburg8. 1. Department of Nephrology, University Hospital of the RWTH Aachen, Aachen, Germany. xoabaf@hotmail.com. 2. Department of Nephrology, Hospital Clinic, Carrer Villarroel 170, 08036, Barcelona, Spain. xoabaf@hotmail.com. 3. Department of Radiology, University Hospital of the RWTH Aachen, Aachen, Germany. 4. Department of Cardiology, Städtische Kliniken Mönchengladbach GmbH, Elisabeth-Krankenhaus Rheydt, Rheydt, Germany. 5. Department of Nephrology, University Hospital of the RWTH Aachen, Aachen, Germany. 6. Dialysis Center, Kuratorium für Heimdialyse (KfH), Würselen, Germany. 7. Department of Nephrology, Klinikum Coburg, Coburg, Germany. 8. Department of Cardiology, University Hospital of the RWTH Aachen, Aachen, Germany. 9. Department of Nephrology, Hospital Clinic, Carrer Villarroel 170, 08036, Barcelona, Spain. 10. Department of Medical Informatics, University Hospital of the RWTH Aachen, Aachen, Germany.
Abstract
BACKGROUND: Epicardial adipose tissue (EAT) is associated with coronary artery disease (CAD) in the general population. EAT is suggested to promote CAD by paracrine mechanisms and local inflammation. We evaluated whether in chronic hemodialysis (HD) patients EAT associates with CAD, how the amount of EAT develops over time, and if EAT independently predicts the mortality risk. METHODS: Post-hoc analysis of a prospective study in 59 chronic HD patients who underwent non-enhanced multi-slice computed tomography (MSCT) at baseline. Thirty-seven patients underwent another MSCT after 24 ± 5 months. We measured EAT volume (cm³) and Agatston calcification scores of coronary arteries (CAC) and aortic valves (AVC). All-cause mortality was assessed after a follow-up of 88 months (IQR 52-105). RESULTS: Baseline EAT was 128.2 ± 60.8 cm³ and significantly higher than in a control group of non-renal patients (94 ± 46 cm³; p < 0.05). Median Agatston score for CAC was 329 (IQR 23-1181) and for AVC was 0 (IQR 0-25.3) in HD patients. We observed significant positive correlations between baseline EAT and age (r = 0.386; p = 0.003), BMI (r = 0.314; p = 0.016), CAC (r = 0.278; p = 0.03), and AVC (r = 0.282; p = 0.03). In multivariate analysis, age, BMI and AVC remained as significant predictors of EAT (p < 0.01). Calcification scores significantly increased over 2 years; in contrast EAT change was not significant (+11 %, IQR -10 to 24 %; p = 0.066). The limited patient number in the present study precludes analysis of the EAT impact upon survival. CONCLUSION: EAT correlated significantly with cardiovascular calcification in long-term HD patients. Mean EAT did not significantly change over 2 years.
BACKGROUND: Epicardial adipose tissue (EAT) is associated with coronary artery disease (CAD) in the general population. EAT is suggested to promote CAD by paracrine mechanisms and local inflammation. We evaluated whether in chronic hemodialysis (HD) patients EAT associates with CAD, how the amount of EAT develops over time, and if EAT independently predicts the mortality risk. METHODS: Post-hoc analysis of a prospective study in 59 chronic HDpatients who underwent non-enhanced multi-slice computed tomography (MSCT) at baseline. Thirty-seven patients underwent another MSCT after 24 ± 5 months. We measured EAT volume (cm³) and Agatston calcification scores of coronary arteries (CAC) and aortic valves (AVC). All-cause mortality was assessed after a follow-up of 88 months (IQR 52-105). RESULTS: Baseline EAT was 128.2 ± 60.8 cm³ and significantly higher than in a control group of non-renal patients (94 ± 46 cm³; p < 0.05). Median Agatston score for CAC was 329 (IQR 23-1181) and for AVC was 0 (IQR 0-25.3) in HDpatients. We observed significant positive correlations between baseline EAT and age (r = 0.386; p = 0.003), BMI (r = 0.314; p = 0.016), CAC (r = 0.278; p = 0.03), and AVC (r = 0.282; p = 0.03). In multivariate analysis, age, BMI and AVC remained as significant predictors of EAT (p < 0.01). Calcification scores significantly increased over 2 years; in contrast EAT change was not significant (+11 %, IQR -10 to 24 %; p = 0.066). The limited patient number in the present study precludes analysis of the EAT impact upon survival. CONCLUSION: EAT correlated significantly with cardiovascular calcification in long-term HDpatients. Mean EAT did not significantly change over 2 years.
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