title: Tumour necrosis factor-alpha in diastolic dysfunction.
abstract: BACKGROUND
  Active relaxation develops as a result of sequestration of calcium into the sarcoplasmic reticulum, and is controlled mainly by sarcoplasmic reticulum calcium ATPase (SERCA) and phospholamban.Tumour necrosis factor-alpha (TNF-alpha) downregulates both of these proteins, so it may play a role in the development of abnormal relaxation. However, a possible relationship between TNF-alpha and diastolic dysfunction has not been sufficiently evaluated in vivo. We investigated whether circulating levels of TNF-alpha increased in patients with relaxation abnormality.
  
  
  METHODS
  Forty hypertensive patients with normal left ventricular systolic function were enrolled in the study. Age-adjusted values of echocardiographically measured mitral inflow velocities, E-wave deceleration time and isovolemic relaxation time were used to define normal and abnormal relaxation. Twenty of the patients (mean age 59.2 +/- 10.6) had a relaxation abnormality (group I), and the twenty other patients (mean age 45.9 +/- 7.9) had a normal diastolic function (group II). TNF-alpha levels were measured by ELISA.
  
  
  RESULTS
  There were no significant differences between the two groups in terms of interventricular septal thickness, posterior wall thickness, left ventricular mass, ejection fraction, plasma creatinin level, and medication. Patients with a relaxation abnormality were older than those with a normal diastolic function (p < 0.001). TNF-alpha levels were similar in both groups (62.1 +/- 46.0 pg/ml for group I, and 48.7 +/- 51.4 pg/ml for group II, p = 0.089).
  
  
  CONCLUSIONS
  In this preliminary study, we demonstrated that TNF-alpha levels did not increase in patients with a relaxation abnormality. However, we think that a possible relationship between TNF-alpha and diastolic dysfunction should be clarified by further studies involving a larger number of patients with a wider spectrum of diastolic dysfunction.
authors.affiliation: Cardiology Department, Ankara University School of Medicine, Ankara, Turkey. mkilickap@yahoo.com
authors.forename: Mustafa
authors.initials: M
authors.lastname: Kilickap
authors.forename: Adalet
authors.initials: A
authors.lastname: Gurlek
authors.forename: Rabih
authors.initials: R
authors.lastname: Dandachi
authors.forename: Irem
authors.initials: I
authors.lastname: Dincer
authors.forename: Huseyin
authors.initials: H
authors.lastname: Tutkak
authors.forename: Dervis
authors.initials: D
authors.lastname: Oral
mesh_terms: D002135:Calcium-Binding Proteins / Q000378:metabolism; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D016022:Case-Control Studies; D003971:Diastole / Q000502:physiology*; D004452:Echocardiography; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D014409:Tumor Necrosis Factor-alpha / Q000009:adverse effects / Q000032:analysis*; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology*; D000099211:Phospholamban
chemical_list: D002135:Calcium-Binding Proteins; D000252:Calcium-Transporting ATPases; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D014409:Tumor Necrosis Factor-alpha; D000099211:Phospholamban