PUMA
Istituto di Fisiologia Clinica     
Campolo J., Caruso R., De Maria R., Parolini M., Oliva F., Roubina E., Cighetti G., Frigerio M., Vitali E., Parodi O. Aminothiol redox alterations in patients with chronic heart failure of ischaemic or non-ischaemic origin. In: Journal of Cardiovascular Medicine, vol. 8 pp. 1024 - 1028. Lippincott Williams & Wilkins, 2007.
 
 
Abstract
(English)
Objective Oxidative stress plays a role in the progression of chronic heart failure (CHF), but whether and how ischaemic heart disease (IHD) or non-IHD aetiology may account for differential redox alterations is currently unclear. We assessed the relation between thiol redox state and lipid peroxidation, as a marker of oxidative stress, in patients with CHF of ischaemic or non-ischaemic origin. Methods Blood reduced glutathione, plasma total and reduced cysteine, cysteinylglycine, homocysteine, glutathione, plasma a-tocopherol, ascorbic acid, and free malondialdehyde were assessed in 43 CHF heart transplant candidates (24 IHDand 19 non-IHD) and 30 controlsmatched 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 antioxidant 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.
Subject aminothiols
chronic heart failure
lipid peroxidation
oxidative stress


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