title: Accumulation of epicardial fat rather than visceral fat is an independent risk factor for left ventricular diastolic dysfunction in patients undergoing peritoneal dialysis.
abstract: BACKGROUND
  Symptoms of heart failure with preserved left ventricular systolic function are common among patients undergoing peritoneal dialysis (PD). Epicardial fat (EpF) is an ectopic fat depot with possible paracrine or mechanical effects on myocardial function. The aim of our current study is to assess the association between EpF and Left ventricular diastolic dysfunction (LVDD) in patients undergoing PD and to clarify the relationships among EpF, inflammation, and LVDD in this population.
  
  
  METHODS
  This was a cross-sectional study of 149 patients with preserved left ventricular systolic function who were undergoing PD. LVDD was diagnosed (according to the European Society of Cardiology guidelines) and EpF thickness measured by echocardiography. The patients without LVDD were used as controls. The serum inflammatory biomarker high-sensitivity C-reactive protein (hsCRP) was measured. The location and amount of adipose tissue were assessed by computed tomography (CT) at the level of the fourth lumbar vertebra.
  
  
  RESULTS
  Subjects with LVDD had higher levels of hsCRP, more visceral and peritoneal fat, and thicker EpF (all p < 0.001) than controls. Visceral adipose tissue, hsCRP, and EpF all correlated significantly (p < 0.05) with LVDD. Multivariate regression analysis rendered the relationship between visceral adipose tissue and LVDD insignificant, whereas EpF was the most powerful determinant of LVDD (odds ratio = 2.41, 95% confidence interval = 1.43-4.08, p < 0.01). EpF thickness also correlated significantly with the ratio of transmitral Doppler early filling velocity to tissue Doppler early diastolic mitral annular velocity (E/e'; r = 0.27, p < 0.01).
  
  
  CONCLUSIONS
  EpF thickness is significantly independently associated with LVDD in patients undergoing PD and may be involved in its pathogenesis.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, National Taiwan University College of Medicine and Hospital No, 7, Chung-Shan South Road Taipei 100, Taipei, Taiwan. chokaiwu@yahoo.com.tw.
authors.forename: Heng-Hsu
authors.initials: HH
authors.lastname: Lin
authors.forename: Jen-Kuang
authors.initials: JK
authors.lastname: Lee
authors.forename: Chung-Yi
authors.initials: CY
authors.lastname: Yang
authors.forename: Yu-Chung
authors.initials: YC
authors.lastname: Lien
authors.forename: Jenq-Wen
authors.initials: JW
authors.lastname: Huang
authors.forename: Cho-Kai
authors.initials: CK
authors.lastname: Wu
mesh_terms: D050154:Adiposity; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D003971:Diastole; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D050152:Intra-Abdominal Fat / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016014:Linear Models; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016017:Odds Ratio; D010496:Pericardium / Q000000981:diagnostic imaging / Q000503:physiopathology*; D010530:Peritoneal Dialysis / Q000009:adverse effects*; D011237:Predictive Value of Tests; D012307:Risk Factors; D013318:Stroke Volume; D014057:Tomography, X-Ray Computed; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D016277:Ventricular Function, Left
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D002097:C-Reactive Protein