{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,13]],"date-time":"2026-04-13T16:20:07Z","timestamp":1776097207370,"version":"3.50.1"},"reference-count":60,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2015,1,21]],"date-time":"2015-01-21T00:00:00Z","timestamp":1421798400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001807","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa do Estado de S\u00e3o Paulo","doi-asserted-by":"crossref","award":["2010\/16593-2"],"award-info":[{"award-number":["2010\/16593-2"]}],"id":[{"id":"10.13039\/501100001807","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Adib Jatene Foundation and the Swedish Research Council"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Intern Med"],"published-print":{"date-parts":[[2015,7]]},"abstract":"Abstract<\/jats:title>Background<\/jats:title>It has been hypothesized that epicardial adipose tissue (EAT<\/jats:styled-content>) exerts pathogenic effects on cardiac structures. We analysed the associations between EAT<\/jats:styled-content> and both cardiovascular (CV<\/jats:styled-content>) disease risk factors and CV<\/jats:styled-content> events in patients with chronic kidney disease (CKD<\/jats:styled-content>).<\/jats:p><\/jats:sec>Patients and methods<\/jats:title>We included 277 nondialysed patients [median age 61, interquartile range (IQR) 53\u201368\u00a0years; 63% men] with stages 3\u20135 CKD<\/jats:styled-content> in this cross\u2010sectional evaluation. EAT<\/jats:styled-content> and abdominal visceral adipose tissue (VAT<\/jats:styled-content>) were assessed by computed tomography. Patients were followed for median 32 (IQR<\/jats:styled-content> 20\u201339) months, and the composite of fatal and nonfatal CV<\/jats:styled-content> events was recorded.<\/jats:p><\/jats:sec>Results<\/jats:title>With increasing EAT<\/jats:styled-content> quartiles, patients were older, had higher glomerular filtration rate, body mass index, waist, VAT<\/jats:styled-content> and coronary calcification, higher levels of haemoglobin, triglycerides, albumin, C\u2010reactive protein and leptin and higher prevalence of left ventricular hypertrophy and myocardial ischaemia; total and high\u2010density lipoprotein cholesterol, 25\u2010hydroxy\u2010vitamin D and 1, 25\u2010dihydroxy\u2010vitamin D progressively decreased. Associations between EAT<\/jats:styled-content> and cardiac alterations were not independent of VAT<\/jats:styled-content>. During follow\u2010up, 58 CV<\/jats:styled-content> events occurred. A 1\u2010SD<\/jats:styled-content> higher EAT<\/jats:styled-content> volume was associated with an increased risk of CV<\/jats:styled-content> events in crude [hazard ratio (HR<\/jats:styled-content>) 1.41, 95% confidence interval (CI<\/jats:styled-content>) (1.12\u20131.78) and adjusted (HR<\/jats:styled-content> 1.55, 95% CI<\/jats:styled-content> 1.21\u20131.99) Cox models. However, adding EAT<\/jats:styled-content> to a standard CV<\/jats:styled-content> disease risk prediction model did not result in a clinically relevant improvement in prediction.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>Epicardial adipose tissue accumulation in patients with CKD<\/jats:styled-content> increases the risk of CV<\/jats:styled-content> events independent of general adiposity. This is consistent with the notion of a local pathogenic effect of EAT<\/jats:styled-content> on the heart or heart vessels, or both. However, EAT<\/jats:styled-content> adds negligible explanatory power to standard CV<\/jats:styled-content> disease risk factors.<\/jats:p><\/jats:sec>","DOI":"10.1111\/joim.12344","type":"journal-article","created":{"date-parts":[[2015,1,5]],"date-time":"2015-01-05T07:23:18Z","timestamp":1420442598000},"page":"77-87","source":"Crossref","is-referenced-by-count":40,"title":["Epicardial fat accumulation, cardiometabolic profile and cardiovascular events in patients with stages 3\u20135 chronic kidney disease"],"prefix":"10.1111","volume":"278","author":[{"given":"A. C.","family":"Cordeiro","sequence":"first","affiliation":[{"name":"Division of Renal Medicine and Baxter Novum Department of Clinical Science Intervention and Technology Karolinska Institutet Stockholm Sweden"},{"name":"Department of Hypertension and Nephrology Dante Pazzanese Institute of Cardiology S\u00e3o Paulo Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"F. 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