Sung Min Ko1, Chao Zhang2, Zhengjia Chen2, Luis D'Marco3,4, Antonio Bellasi5,6, Arthur E Stillman7, Geoffrey Block8, Paolo Raggi9,10. 1. Department of Radiology, Konkuk University Medical Center, Konkuk University School of Medicine, 4-12 Hwayang-dong, Gwangjin-gu, Seoul, 143-729, Korea. 2. Department of Biostatistics and Bioinformatics, Emory University, Atlanta, GA, USA. 3. Hospital Residència Sant Camil, Ronda Sant Camil, 08810, Sant Pere de Ribes, Catalunya, Spain. 4. Clínica Puerto Ordaz, Unidad Avanzada de Investigación y Diagnostico Ecográfico y Renal, Puerto Ordaz, 8050, Venezuela. 5. Sant' Anna Hospital, Como, Italy. 6. University of Milan, Milan, Italy. 7. Division of Cardiothoracic Imaging, Department of Radiology, Emory University, Atlanta, GA, USA. 8. Denver Nephrology, Denver, CO, USA. 9. Division of Cardiothoracic Imaging, Department of Radiology, Emory University, Atlanta, GA, USA. raggi@ualberta.ca. 10. Mazankowski Alberta Heart Institute, University of Alberta School of Medicine, 8440-112 Street, Suite 4A7.050, Edmonton, AB, T6G2B7, Canada. raggi@ualberta.ca.
Abstract
BACKGROUND: In the general population and in hemodialysis patients epicardial adipose tissue (EAT) has been associated with increased mortality and cardiovascular events. Weight loss and lipid lowering therapies reduced EAT in the general population. It is unknown whether sevelamer, a phosphate (Pi) binder that lowers cholesterol and reduces inflammation in dialysis patients also affects EAT progression. METHODS: Post-hoc analysis of a randomized trial of sevelamer (SVL) versus calcium-based Pi binders (CPiB) in incident hemodialysis patients. EAT was measured on cardiac computed tomography scans performed at enrollment, 6, 12 and 18 months from baseline. RESULTS: Of 109 patients, 54 received SVL and 55 CPiB; the median LDL change was -16.4 % (IQR: -67.5, 142.3 %) and 12.1 % (IQR: -51.9, 193.8 %) with SVL and CPiB respectively (p < 0.001). At baseline EAT correlated significantly with gender, body mass index and total coronary artery calcium score (all p < 0.02). At the end of follow-up, EAT progressed significantly from baseline in the CPiB treated patients but not in the SVL treated patients [median increase 9.1 % (p = 0.005) vs 3.9 % (p = 0.25)]. However, there was no significant difference in the degree of progression between treatment groups (p = 0.34). There was no correlation between LDL or CRP change and EAT change. There were insufficient events in either arm to assess the impact of EAT change on mortality. CONCLUSION:EAT progression from baseline was significantly smaller with SVL than with CPiB, although the difference between treatments was not statistically significant, probably due to the small sample size. Change in serum lipids and markers of inflammation did not predict EAT progression.
RCT Entities:
BACKGROUND: In the general population and in hemodialysis patients epicardial adipose tissue (EAT) has been associated with increased mortality and cardiovascular events. Weight loss and lipid lowering therapies reduced EAT in the general population. It is unknown whether sevelamer, a phosphate (Pi) binder that lowers cholesterol and reduces inflammation in dialysis patients also affects EAT progression. METHODS: Post-hoc analysis of a randomized trial of sevelamer (SVL) versus calcium-based Pi binders (CPiB) in incident hemodialysis patients. EAT was measured on cardiac computed tomography scans performed at enrollment, 6, 12 and 18 months from baseline. RESULTS: Of 109 patients, 54 received SVL and 55 CPiB; the median LDL change was -16.4 % (IQR: -67.5, 142.3 %) and 12.1 % (IQR: -51.9, 193.8 %) with SVL and CPiB respectively (p < 0.001). At baseline EAT correlated significantly with gender, body mass index and total coronary artery calcium score (all p < 0.02). At the end of follow-up, EAT progressed significantly from baseline in the CPiB treated patients but not in the SVL treated patients [median increase 9.1 % (p = 0.005) vs 3.9 % (p = 0.25)]. However, there was no significant difference in the degree of progression between treatment groups (p = 0.34). There was no correlation between LDL or CRP change and EAT change. There were insufficient events in either arm to assess the impact of EAT change on mortality. CONCLUSION: EAT progression from baseline was significantly smaller with SVL than with CPiB, although the difference between treatments was not statistically significant, probably due to the small sample size. Change in serum lipids and markers of inflammation did not predict EAT progression.
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