Sean Cai1, Ron Wald1,2, Djeven P Deva3, Mercedeh Kiaii4, Ming-Yen Ng5, Gauri R Karur6, Oblugbenga Bello7, Zhuo Jun Li7, Jonathon Leipsic8, Laura Jimenez-Juan9, Anish Kirpalani3, Kim A Connelly1,7, Andrew T Yan10,11,12. 1. Department of Medicine, University of Toronto, Toronto, Canada. 2. Division of Nephrology, St Michael's Hospital, Toronto, Canada. 3. Department of Medical Imaging, St Michael's Hospital, University of Toronto, Toronto, Canada. 4. Division of Nephrology, St. Paul's Hospital, Vancouver, Canada. 5. Department of Diagnostic Radiology, The University of Hong Kong, Hong Kong, China. 6. Toronto Joint Department of Medical Imaging, University Health Network, Toronto, Canada. 7. Division of Cardiology, St. Michael's Hospital, 30 Bond Street, Donnelly 6-034, Toronto, ON, M5B 1W8, Canada. 8. Department of Medical Imaging, St Paul's Hospital, Vancouver, Canada. 9. Department of Medical Imaging, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Canada. 10. Department of Medicine, University of Toronto, Toronto, Canada. andrew.yan@unityhealth.to. 11. Department of Medical Imaging, St Michael's Hospital, University of Toronto, Toronto, Canada. andrew.yan@unityhealth.to. 12. Division of Cardiology, St. Michael's Hospital, 30 Bond Street, Donnelly 6-034, Toronto, ON, M5B 1W8, Canada. andrew.yan@unityhealth.to.
Abstract
BACKGROUND: Conversion from conventional hemodialysis (CHD) to in-centre nocturnal hemodialysis (INHD) is associated with left ventricular (LV) mass regression, but the underlying mechanisms are not fully understood. Using cardiac MRI (CMR), we examined the effects of INHD on epicardial adipose tissue (EAT) and paracardial adipose tissue (PAT), and the relationships between EAT, PAT and LV remodeling, biomarkers of nutrition, myocardial injury, fibrosis and volume. METHODS: We conducted a prospective multicenter cohort study of 37 patients transitioned from CHD to INHD and 30 patients on CHD (control). Biochemical markers and CMR were performed at baseline and 52 weeks. CMR images were analyzed by independent readers, blinded to order and treatment group. RESULTS: Among 64 participants with complete CMR studies at baseline (mean age 54; 43% women), there were no significant differences in EAT index (60.6 ± 4.3 mL/m2 vs 64.2 ± 5.1 mL/m2, p = 0.99) or PAT index (60.0 ± 5.4 mL/m2 vs 53.2 ± 5.9 mL/m2, p = 0.42) between INHD and CHD groups. Over 52 weeks, EAT index and PAT index did not change significantly in INHD and CHD groups (p = 0.21 and 0.14, respectively), and the changes in EAT index and PAT index did not differ significantly between INHD and CHD groups (p = 0.30 and 0.16, respectively). Overall, changes in EAT index inversely correlated with changes in LV end-systolic volume index (LVESVI) but not LV end-diastolic volume index (LVEDVI), LV mass index (LVMI), and LV ejection fraction (LVEF). Changes in PAT index inversely correlated with changes in LVESVI, LVMI and positively correlated with changes in LVEF. There were no correlations between changes in EAT index or PAT index with changes in albumin, LDL, triglycerides, troponin-I, FGF-23, or NT-proBNP levels over 52 weeks (all p > 0.30). CONCLUSIONS: INHD was not associated with any changes in EAT index and PAT index over 12 months. Changes in EAT index were not significantly associated with changes in markers of LV remodeling, nutrition, myocardial injury, fibrosis, volume status. In contrast, changes in PAT index, which paradoxically is expected to exert less paracrine effect on the myocardium, were correlated with changes in LVESVI, LVMI and LVEF. Larger and longer-term studies may clarify the role of PAT in cardiac remodeling with intensified hemodialysis. CLINICALTRIALS. GOV IDENTIFIER: NCT00718848.
BACKGROUND: Conversion from conventional hemodialysis (CHD) to in-centre nocturnal hemodialysis (INHD) is associated with left ventricular (LV) mass regression, but the underlying mechanisms are not fully understood. Using cardiac MRI (CMR), we examined the effects of INHD on epicardial adipose tissue (EAT) and paracardial adipose tissue (PAT), and the relationships between EAT, PAT and LV remodeling, biomarkers of nutrition, myocardial injury, fibrosis and volume. METHODS: We conducted a prospective multicenter cohort study of 37 patients transitioned from CHD to INHD and 30 patients on CHD (control). Biochemical markers and CMR were performed at baseline and 52 weeks. CMR images were analyzed by independent readers, blinded to order and treatment group. RESULTS: Among 64 participants with complete CMR studies at baseline (mean age 54; 43% women), there were no significant differences in EAT index (60.6 ± 4.3 mL/m2 vs 64.2 ± 5.1 mL/m2, p = 0.99) or PAT index (60.0 ± 5.4 mL/m2 vs 53.2 ± 5.9 mL/m2, p = 0.42) between INHD and CHD groups. Over 52 weeks, EAT index and PAT index did not change significantly in INHD and CHD groups (p = 0.21 and 0.14, respectively), and the changes in EAT index and PAT index did not differ significantly between INHD and CHD groups (p = 0.30 and 0.16, respectively). Overall, changes in EAT index inversely correlated with changes in LV end-systolic volume index (LVESVI) but not LV end-diastolic volume index (LVEDVI), LV mass index (LVMI), and LV ejection fraction (LVEF). Changes in PAT index inversely correlated with changes in LVESVI, LVMI and positively correlated with changes in LVEF. There were no correlations between changes in EAT index or PAT index with changes in albumin, LDL, triglycerides, troponin-I, FGF-23, or NT-proBNP levels over 52 weeks (all p > 0.30). CONCLUSIONS: INHD was not associated with any changes in EAT index and PAT index over 12 months. Changes in EAT index were not significantly associated with changes in markers of LV remodeling, nutrition, myocardial injury, fibrosis, volume status. In contrast, changes in PAT index, which paradoxically is expected to exert less paracrine effect on the myocardium, were correlated with changes in LVESVI, LVMI and LVEF. Larger and longer-term studies may clarify the role of PAT in cardiac remodeling with intensified hemodialysis. CLINICALTRIALS. GOV IDENTIFIER: NCT00718848.
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