title: Relationship between oxidative stress and systolic dysfunction in patients with hypertrophic cardiomyopathy.
abstract: BACKGROUND
  Progression of hypertrophic cardiomyopathy (HCM) to left ventricular dilatation and systolic dysfunction sometimes occurs. However, the mechanism is not known. We examined whether oxidative stress was elevated in myocardia of HCM patients and whether the levels were correlated with left ventricular dilatation and systolic dysfunction.
  
  
  RESULTS
  Endomyocardial biopsy samples obtained from the right ventricular side of the septum of 31 patients with HCM, and 10 control subjects were studied immunohistochemically for the expression of 4-hydroxy-2-nonenal (HNE)-modified protein, which is a major lipid peroxidation product. Expression of HNE-modified protein was found in all myocardial biopsy samples from patients with HCM. Expression was distinct in the cytosol of cardiomyocytes. The expression levels in patients with HCM were significantly increased compared with those in control subjects (P = .0005). The expression levels in patients with HCM were correlated with left ventricular end-diastolic diameter (r = 0.483, P = .0053) and end-systolic diameter (r = 0.500, P = .0037) determined by echocardiography. The expression levels were inversely correlated with left ventricular ejection fraction determined by left ventriculography (r = -0.640, P = .0001).
  
  
  CONCLUSIONS
  Oxidative stress was elevated in myocardia of HCM patients and the levels were correlated with left ventricular dilatation and systolic dysfunction. Oxidative stress is involved in the pathogenesis of heart failure in patients with HCM.
authors.affiliation: Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
authors.forename: Kazufumi
authors.initials: K
authors.lastname: Nakamura
authors.forename: Kengo Fukushima
authors.initials: KF
authors.lastname: Kusano
authors.forename: Hiromi
authors.initials: H
authors.lastname: Matsubara
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Nakamura
authors.forename: Aya
authors.initials: A
authors.lastname: Miura
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Nishii
authors.forename: Kimikazu
authors.initials: K
authors.lastname: Banba
authors.forename: Satoshi
authors.initials: S
authors.lastname: Nagase
authors.forename: Katsumasa
authors.initials: K
authors.lastname: Miyaji
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Morita
authors.forename: Hironori
authors.initials: H
authors.lastname: Saito
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Emori
authors.forename: Tohru
authors.initials: T
authors.lastname: Ohe
mesh_terms: D000447:Aldehydes / Q000378:metabolism; D001706:Biopsy; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications / Q000503:physiopathology*; D016022:Case-Control Studies; D004452:Echocardiography; D005260:Female; D006333:Heart Failure / Q000209:etiology; D006801:Humans; D007150:Immunohistochemistry; D015227:Lipid Peroxidation; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D013318:Stroke Volume / Q000502:physiology; D013599:Systole / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000150:complications* / Q000503:physiopathology
chemical_list: D000447:Aldehydes; C027576:4-hydroxy-2-nonenal