[8-hydroxy-2'-deoxyguanosine and lipid peroxidation in patients with heart failure].

نویسندگان

  • Miguel Rivera
  • Esther Roselló-Lletí
  • Fernando García de Burgos
  • Vicente Bertomeu
  • Rafael Payá
  • Raquel Cortés
  • Luís Martínez-Dolz
  • Alejandro Jordán
  • Jose L Pérez-Boscá
  • Antonio Salvador
  • Francisco Marín
  • Francisco Sogorb
  • Ricardo Valero
  • Vicente Miró
  • Manuel Portolés
چکیده

INTRODUCTION AND OBJECTIVES Heart failure is associated with increased free radical production, which leads to a state of oxidative stress. Known markers of oxidative stress include 8-hydroxy-2'-deoxyguanosine, which reflects oxidative damage to DNA, and lipid peroxidation, which can be used to quantify damage to lipid-rich structures. The aims of this study were to compare 8-hydroxy-2'-deoxyguanosine and lipid peroxidation levels in heart failure patients and healthy subjects and to assess how these levels are influenced by heart failure etiology. METHODS The study included 78 patients (57 male, age 64 [14] years) with heart failure and 12 control subjects. Patients completed a questionnaire and were graded according to the New York Heart Association classification. Doppler echocardiography was performed and blood samples were obtained. 8-hydroxy-2'-deoxyguanosine and lipid peroxidation levels were determined. RESULTS Significant differences were observed between patients and control subjects in 8-hydroxy-2'-deoxyguanosine and lipid peroxidation levels, at 0.34 (0.54) ng/mL vs 0.04 (0.07) ng/mL (P<.05), and 18 (10) microM vs 8 (3) microM (P<.01), respectively. Subsequent analysis showed that heart failure etiology had a significant effect on the levels of the two markers (P<.05), which were highest in patients with hypertensive cardiomyopathy. CONCLUSIONS Levels of 8-hydroxy-2'-deoxyguanosine and lipid peroxidation were higher in heart failure patients than in control subjects. The most significant increases were found in patients with hypertensive cardiomyopathy.

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عنوان ژورنال:
  • Revista espanola de cardiologia

دوره 59 11  شماره 

صفحات  -

تاریخ انتشار 2006