title: Dissecting the mechanisms of left ventricular diastolic dysfunction and inflammation in peritoneal dialysis patients.
abstract: OBJECTIVE
  Patients with symptoms of heart failure and preserved left ventricular (LV) systolic function are commonly encountered in clinical practice especially in peritoneal dialysis (PD) patients. We hypothesized that adiposity might influence LV diastolic function through systemic inflammation in this specific group.
  
  
  METHODS
  We designed a cross-sectional study in 173 prevalent PD patients. LV diastolic dysfunction was diagnosed by echocardiography. PD patient without LV diastolic dysfunction served as the control group. Serum inflammatory biomarkers were examined including tissue necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The location and amount of adipose tissue were assessed by computerized tomography (CT) at the level of the fourth lumbar vertebra.
  
  
  RESULTS
  Subjects with LV diastolic dysfunction had higher levels of the pro-inflammation cytokines and more visceral and peritoneal fat (all P<0.001) than control subjects. A significant correlation was found between visceral adipose tissue and pro-inflammatory cytokines (r = 0.70; P<0.001). Multivariable regression analysis found that the relationship between visceral adipose tissue and LV diastolic dysfunction became insignificant when either TNF-α or IL-6 were introduced into the model, although TNF-α and IL-6 were both significantly associated with LV diastolic dysfunction even after adjusting for visceral fat (OR = 1.51; 95% CI = 1.09-2.02; P = 0.033 and OR = 1.62; 95% CI = 1.09-1.82; P = 0.031, respectively).
  
  
  CONCLUSIONS
  Larger amounts of adipose tissue were associated with higher serum pro-inflammatory levels in PD patients, which might be related to the development of LV diastolic dysfunction. Modulating inflammatory reactions in PD patients can be a useful therapeutic approach for managing LV diastolic dysfunction.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, National Taiwan University College of Medicine and Hospital, Taipei, Taiwan.
authors.forename: Cho-Kai
authors.initials: CK
authors.lastname: Wu
authors.forename: Yin-Tsen
authors.initials: YT
authors.lastname: Huang
authors.forename: Heng-Hsu
authors.initials: HH
authors.lastname: Lin
authors.forename: Chung-Yi
authors.initials: CY
authors.lastname: Yang
authors.forename: Yu-Chung
authors.initials: YC
authors.lastname: Lien
authors.forename: Jen-Kuang
authors.initials: JK
authors.lastname: Lee
authors.forename: Jenq-Wen
authors.initials: JW
authors.lastname: Huang
authors.forename: Kuan-Yu
authors.initials: KY
authors.lastname: Hung
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D003430:Cross-Sectional Studies; D004452:Echocardiography; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation; D015850:Interleukin-6 / Q000097:blood; D050152:Intra-Abdominal Fat / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010530:Peritoneal Dialysis; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000150:complications / Q000503:physiopathology*
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha