Secondary Logo

Journal Logo

Institutional members access full text with Ovid®

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

Campolo, Jonica; Caruso, Raffaele; De Maria, Renata; Parolini, Marina; Oliva, Fabrizio; Roubina, Elena; Cighetti, Giuliana; Frigerio, Maria; Vitali, Ettore; Parodi, Oberdan

Journal of Cardiovascular Medicine: December 2007 - Volume 8 - Issue 12 - p 1024–1028
doi: 10.2459/JCM.0b013e3281053a63
Original articles
Buy

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 α-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 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.

aCNR Clinical Physiology Institute of Milan, Cardiology Department, Niguarda Ca' Granda Hospital, Milan, Italy

bCardiology Department, Niguarda Ca' Granda Hospital, Milan, Italy

cDepartment of Preclinical Sciences, LITA Vialba, University of Milan, Milan, Italy

Received 4 October, 2006

Revised 7 February, 2007

Accepted 12 February, 2007

Correspondence to Prof Oberdan Parodi, CNR Clinical Physiology Institute of Milan, Cardiology Department, Niguarda Ca' Granda Hospital, Piazza Ospedale Maggiore 3, 20162 Milan, Italy Tel: +39 02 6473407; fax: +39 02 66116990; e-mail: ifcnig@tin.it

© 2007 Italian Federation of Cardiology. All rights reserved.