Aminothiol redox alterations in patients with chronic heart failure of ischaemic or non-ischaemic origin

Objective Oxidative stress plays a role in the progression of chronic heart failure (CHF), but whether and how ischaemic heart disease (HD) or non-IHD aetiology may account for differential redox alterations is currently unclear. We assessed the relation between thiol redox state and lipid peroxiclation, as a marker of oxidative stress, in patients with CHF of ischaernic or non-ischaernic origin. Methods Blood reduced glutathione, plasma total and reduced cysteine, cysteinylglycine, homocysteine, glutathione, plasma et-tocopherol, ascorbic acid, and free malondialdehyde were assessed in 43 CHF heart transplant candidates (24 IHD and 19 non-IHD) and 30 controls matched for age, gender and number of atherosclerotic risk factors. Results Reduced cysteine was increased in CHF patients compared with controls. The highest levels were found in IHD versus non-IHD patients versus controls. Malondialdehyde levels were significantly higher in IHD patients than in controls, whereas antioxiclant vitamins did not differ among the three groups. Conclusions Specific abnormalities in the thiol pattern are associated with heart failure aetiology in CHF patients. Our findings point to the possible role of reduced cysteine in the progression of chronic IHD to heart failure status, as an additional pro-oxidant stimulus for worsening oxidative stress.