title: Left ventricular dysfunction in Klinefelter syndrome is associated to insulin resistance, abdominal adiposity and hypogonadism.
abstract: OBJECTIVE
  Epidemiological data suggest there is an increased risk of dying from heart disease among patients with Klinefelter syndrome (KS). Due to high prevalence of hypogonadism and metabolic syndrome, we speculated that patients with KS may have subclinical changes in the left ventricular function. Therefore, the aim was to assess left ventricular long axis function by tissue Doppler echocardiography in patients with KS and relate these findings to the metabolic status and testosterone levels.
  
  
  METHODS
  Cross-sectional study. Out-patient clinic.
  
  
  METHODS
  We investigated 25 unselected patients with KS, recruited from endocrine and fertility clinics. Twenty-five age-matched males served as controls.
  
  
  METHODS
  Left ventricular systolic long axis function (velocities and strain rate) assessed by tissue Doppler echocardiography related to free testosterone, fasting values of plasma glucose, insulin, homeostasis model assessment (HOMA)-index, cholesterol and triglycerides in addition to dual energy X-ray absorptiometry (DEXA) scan derived assessment of truncal body fat.
  
  
  RESULTS
  The long axis function was significantly reduced in patients with KS (peak systolic velocities 4.4 +/- 1.3 vs. 5.3 +/- 1.0 cm/s, P < 0.01 and strain rate -1.3 +/- 0.3 vs.-1.6 +/- 0.3 s(-1), P < 0.01). However, the ventricular dysfunction was mainly attributed KS patients with metabolic syndrome. The peak systolic velocities were significantly correlated to truncal body fat (r = -0.72, P < 0.01) and free testosterone (r = 0.63, P < 0.01), but uncorrelated to plasma glucose, insulin and HOMA-index.
  
  
  CONCLUSIONS
  Systolic long axis function is decreased in patients with KS and metabolic syndrome. The decrease in myocardial systolic function was significantly related to truncal body fat and hypogonadism, but not correlated to insulin sensitivity.
authors.affiliation: Department of Cardiology, Aarhus University Hospital, Skejby, Denmark. holmark@ki.au.dk
authors.forename: N H
authors.initials: NH
authors.lastname: Andersen
authors.forename: A
authors.initials: A
authors.lastname: Bojesen
authors.forename: K
authors.initials: K
authors.lastname: Kristensen
authors.forename: N H
authors.initials: NH
authors.lastname: Birkebaek
authors.forename: J
authors.initials: J
authors.lastname: Fedder
authors.forename: P
authors.initials: P
authors.lastname: Bennett
authors.forename: J S
authors.initials: JS
authors.lastname: Christiansen
authors.forename: C H
authors.initials: CH
authors.lastname: Gravholt
mesh_terms: D050153:Abdominal Fat / Q000378:metabolism / Q000473:pathology*; D050154:Adiposity / Q000502:physiology*; D000328:Adult; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D006801:Humans; D007006:Hypogonadism / Q000150:complications* / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology; D007333:Insulin Resistance / Q000502:physiology; D007713:Klinefelter Syndrome / Q000150:complications* / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D013739:Testosterone / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000150:complications* / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology; D055815:Young Adult
chemical_list: D013739:Testosterone