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  • Title: Epicardial fat accumulation, cardiometabolic profile and cardiovascular events in patients with stages 3-5 chronic kidney disease.
    Author: Cordeiro AC, Amparo FC, Oliveira MA, Amodeo C, Smanio P, Pinto IM, Lindholm B, Stenvinkel P, Carrero JJ.
    Journal: J Intern Med; 2015 Jul; 278(1):77-87. PubMed ID: 25556720.
    Abstract:
    BACKGROUND: It has been hypothesized that epicardial adipose tissue (EAT) exerts pathogenic effects on cardiac structures. We analysed the associations between EAT and both cardiovascular (CV) disease risk factors and CV events in patients with chronic kidney disease (CKD). PATIENTS AND METHODS: We included 277 nondialysed patients [median age 61, interquartile range (IQR) 53-68 years; 63% men] with stages 3-5 CKD in this cross-sectional evaluation. EAT and abdominal visceral adipose tissue (VAT) were assessed by computed tomography. Patients were followed for median 32 (IQR 20-39) months, and the composite of fatal and nonfatal CV events was recorded. RESULTS: With increasing EAT quartiles, patients were older, had higher glomerular filtration rate, body mass index, waist, VAT and coronary calcification, higher levels of haemoglobin, triglycerides, albumin, C-reactive protein and leptin and higher prevalence of left ventricular hypertrophy and myocardial ischaemia; total and high-density lipoprotein cholesterol, 25-hydroxy-vitamin D and 1, 25-dihydroxy-vitamin D progressively decreased. Associations between EAT and cardiac alterations were not independent of VAT. During follow-up, 58 CV events occurred. A 1-SD higher EAT volume was associated with an increased risk of CV events in crude [hazard ratio (HR) 1.41, 95% confidence interval (CI) (1.12-1.78) and adjusted (HR 1.55, 95% CI 1.21-1.99) Cox models. However, adding EAT to a standard CV disease risk prediction model did not result in a clinically relevant improvement in prediction. CONCLUSION: Epicardial adipose tissue accumulation in patients with CKD increases the risk of CV events independent of general adiposity. This is consistent with the notion of a local pathogenic effect of EAT on the heart or heart vessels, or both. However, EAT adds negligible explanatory power to standard CV disease risk factors.
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