title: Does oxidative stress modulate left ventricular diastolic function in asymptomatic subjects with hereditary hemochromatosis?
abstract: BACKGROUND
  Little is known about the early mechanisms mediating left ventricular (LV) diastolic dysfunction in patients with hereditary hemochromatosis (HH). However, the increased oxidative stress related to iron overload may be involved in this process, and strain rate (SR), a sensitive echocardiography-derived measure of diastolic function, may detect such changes.
  
  
  OBJECTIVE
  we evaluated the relationship between left ventricular diastolic function measured with tissue Doppler SR and oxidative stress in asymptomatic HH subjects and control normal subjects.
  
  
  METHODS
  Ninety-four consecutive visits of 43 HH subjects, age 30-74 (50 +/- 10, mean +/- SD), and 37 consecutive visits of 21 normal volunteers, age 30-63 (48 +/- 8), were evaluated over a 3-year period. SR was obtained from the basal septum in apical four-chamber views. All patients had confirmed C282Y homozygosity, a documented history of iron overload, and were New York Heart Association functional class I. Normal volunteers lacked HFE gene mutations causing HH.
  
  
  RESULTS
  In the HH subjects, the SR demonstrated moderate but significant correlations with biomarkers of oxidative stress; however, no correlations were noted in normal subjects. The biomarkers of iron overload per se did not show significant correlations with the SR.
  
  
  CONCLUSIONS
  Although our study was limited by the relatively small subject number, these results suggest that a possible role of oxidative stress to affect LV diastolic function in asymptomatic HH subjects and SR imaging may be a sensitive measure to detect that effect.
authors.affiliation: Cardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. shizukya@uc.edu
authors.forename: Yukitaka
authors.initials: Y
authors.lastname: Shizukuda
authors.forename: Charles D
authors.initials: CD
authors.lastname: Bolan
authors.forename: Dorothy J
authors.initials: DJ
authors.lastname: Tripodi
authors.forename: Vandana
authors.initials: V
authors.lastname: Sachdev
authors.forename: Tammy T
authors.initials: TT
authors.lastname: Nguyen
authors.forename: Gilberto
authors.initials: G
authors.lastname: Botello
authors.forename: Yu-Ying
authors.initials: YY
authors.lastname: Yau
authors.forename: Stanislav
authors.initials: S
authors.lastname: Sidenko
authors.forename: Ernst
authors.initials: E
authors.lastname: Inez
authors.forename: Mir I
authors.initials: MI
authors.lastname: Ali
authors.forename: Myron A
authors.initials: MA
authors.lastname: Waclawiw
authors.forename: Susan F
authors.initials: SF
authors.lastname: Leitman
authors.forename: Douglas R
authors.initials: DR
authors.lastname: Rosing
mesh_terms: D000328:Adult; D000368:Aged; D054459:Elasticity Imaging Techniques; D005260:Female; D006432:Hemochromatosis / Q000150:complications* / Q000175:diagnosis / Q000235:genetics*; D000071020:Hemochromatosis Protein; D015395:Histocompatibility Antigens Class I / Q000235:genetics*; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000235:genetics*; D008875:Middle Aged; D018384:Oxidative Stress / Q000235:genetics*; D013318:Stroke Volume; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000209:etiology* / Q000235:genetics*
chemical_list: C103673:HFE protein, human; D000071020:Hemochromatosis Protein; D015395:Histocompatibility Antigens Class I; D008565:Membrane Proteins