Evidence of oxidative stress in chronic heart failure in humans

Abstract

Chronic heart failure (CHF) due to coronary artery disease (CAD) has been shown to be associated with increased plasma thiobarbituric reactive substances (TBARS) and reduced plasma thiol (PSH) concentrations, suggesting oxidative stress (OS). The aims of the present studies were (a) to determine whether OS is due to CAD or CHF per se and (b) to determine if a wider range of more specific markers of OS are abnormal in CHF. In the first study, two groups of patients (n = 15 each) were compared. Group 1 (11 male, mean age 56 years) had CHF due to CAD and group 2 (12 male, mean age 53 years) had non-CAD CHF. Median plasma TBARS in controls was 7.6 nmol . ml⁻¹ , 10.0 nmol . m⁻¹ in group 1 and 9.3 nmol. ml⁻¹ in group 2 (P < 0.01 both groups vs control). Median PSH was 505 384 and 364 nmol. ml⁻¹ (P < 0.05 and P < 0.01 vs control) respectively. Fifty-three patients with CHF were recruited in the second study. Malondialdehyde and PSH were 10.3 and 409 nmol. ml⁻¹ respectively, compared to control values of 7.9 and 560 nmol. ml^.1 (both P < 0.001). The median values for the following additional measures of OS in controls and patients were: erythrocyte superoxide dismustase 131 vs 114 U . l⁻¹ (P = 0.005); caeruloplasmin oxidase 97 vs 197 U. l⁻¹ (P < 0.01); erythrocyte glutathione 1.56 nmol . ml⁻¹ vs 1.77 nmol . ml⁻¹ (P < 0.02); plasma conjugated dienes 0.28 vs 0.33 optical density units (P = ns). Chronic heart failure, regardless of aetiology, is associated with abnormalities of a range of markers of OS.