Abstract

BackgroundEpicardial fat, quantified in a single multi-slice computed tomography (MSCT) slice, is a reliable estimate of total epicardial fat volume (EFV). We sought to determine risk factors for EFV detected in a single-slice MSCT measurement (ssEFV) in pre-dialysis chronic kidney disease (CKD) patients. Our primary objective was to determine the association between ssEFV and coronary artery calcification (CAC).Methods94 pre-dialysis stage 3–5 CKD patients underwent MSCT to measure ssEFV and CAC. ssEFV was quantified at the level of the left main coronary artery. Measures of inflammation, traditional and kidney-related cardiovascular disease risk factors were collected.ResultsMean age: 63.7 ± 14 years, 56% male, 39% had diabetes, and mean eGFR: 25.1 ± 11.9 mL/min/1.73 m2. Mean ssEFV was 5.03 ± 2.4 cm3. By univariate analysis, body mass index (BMI) (r = 0.53; P = <0.0001), abdominal obesity (r = 0.51; P < 0.0001), high density lipoprotein (HDL) cholesterol (r = − 0.39; P = <0.0001), insulin resistance (log homeostasis model assessment of insulin resistance (log HOMA-IR)) (r = 0.38, P = 0.001), log interleukin-6 (IL-6) (r = 0.34; P = 0.001), and log urinary albumin to creatinine ratio (UACR) (r = 0.30, P = 0.004) demonstrated the strongest associations with ssEFV. Log coronary artery calcification (log CAC score) (r = 0.28, P = 0.006), and log fibroblast growth factor-23 (log FGF-23) (r = 0.23, P = 0.03) were also correlated with ssEFV. By linear regression, log CAC score (beta =0.40; 95% confidence interval (CI), 0.01-0.80; P = 0.045), increasing levels of IL-6 (beta = 0.99; 95% CI, 0.38 – 1.61; P = 0.002), abdominal obesity (beta = 1.86; 95% CI, 0.94 - 2.8; P < 0.0001), lower HDL cholesterol (beta = −2.30; 95% CI, – 3.68 to −0.83; P = 0.002) and albuminuria (log UACR, beta = 0.81; 95% CI, 0.2 to 1.4; P = 0.01) were risk factors for increased ssEFV.ConclusionsIn stage 3–5 CKD, coronary calcification and IL-6 and were predictors of ssEFV. Further studies are needed to clarify the mechanism by which epicardial fat may contribute to the pathogenesis of coronary disease, particularly in the CKD population.

Highlights

  • Epicardial fat, quantified in a single multi-slice computed tomography (MSCT) slice, is a reliable estimate of total epicardial fat volume (EFV)

  • Further studies are needed to clarify the mechanism by which epicardial fat may contribute to the pathogenesis of coronary disease, in the chronic kidney disease (CKD) population

  • Bivariate analysis was performed to evaluate the associations between single slice epicardial fat volume (ssEFV) and a priori chosen risk factors, including CAC, body mass index (BMI), abdominal obesity, homeostasis model assessment of insulin resistance (HOMA-IR), high-sensitivity C-reactive protein (hsCRP), IL-6, age, sex, hypertension, high density lipoprotein (HDL) cholesterol, low density lipoprotein cholesterol (LDL) cholesterol, total cholesterol, triglycerides, diabetes mellitus, smoking status and other kidney related cardiovascular disease (CVD) risk factors (albuminuria (UACR), fetuin, osteoprotegerin, FGF-23, intact parathyroid hormone (iPTH), 25- hydroxyvitamin D, and 1,25-Dihydroxyvitamin D levels

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Summary

Introduction

Epicardial fat, quantified in a single multi-slice computed tomography (MSCT) slice, is a reliable estimate of total epicardial fat volume (EFV). We sought to determine risk factors for EFV detected in a single-slice MSCT measurement (ssEFV) in pre-dialysis chronic kidney disease (CKD) patients. The metabolic syndrome is a risk factor for type 2 diabetes mellitus [1] and cardiovascular disease (CVD) [2], and is a risk factor for the development of incident chronic kidney disease (CKD) [3,4] This syndrome emphasizes the role of visceral abdominal adipose tissue in the pathogenesis of disease. Epicardial adipose tissue has been shown to correlate with coronary artery calcification (CAC) [11] and the metabolic syndrome [12]. Epicardial fat has not been quantified in the pre-dialysis CKD population nor its potential association with CAC or markers of inflammation

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