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Oxidative stress and its association with coronary artery disease and different atherogenic risk factors
Author(s) -
Vassalle C.,
Petrozzi L.,
Botto N.,
Andreassi M. G.,
Zucchelli G. C.
Publication year - 2004
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.2004.01373.x
Subject(s) - medicine , oxidative stress , coronary artery disease , pathogenesis , endocrinology , endothelial dysfunction , cardiology , vascular disease , antioxidant , case control study , lipid peroxidation , gastroenterology , biology , biochemistry
. Objective. It is well known that free radicals contribute to endothelial dysfunction and are involved in the pathogenesis and development of cardiovascular diseases, such as atherosclerosis. The aim of this study was to provide evidence for enhanced oxidative stress in coronary artery disease (CAD). Methods. Plasma levels of 8‐isoprostane (8‐ epi PGF 2 α ), marker of lipid peroxidation, were measured in 68 subjects (age: 60 ± 2 years, mean ± SEM). Subjects included 30 healthy control subjects and 38 patients with angiographically proven CAD. In addition, the total antioxidant power (PAO) was evaluated in a subgroup (40 subjects, 12 healthy and 28 CAD). Results. Levels of 8‐ epi PGF 2 α increased with the number of affected vessels (one‐ and multi‐vessel disease versus control subjects, P < 0.001) and considering different risk determinants for atherosclerosis (i.e. hypertension, gender, hypercholesterolaemia, P < 0.01). In multivariate regression models the number of affected vessels was independently correlated with 8‐ epi PGF 2 α ( P < 0.05). PAO values significantly decreased with increased number of affected vessels ( P < 0.05) and in hypertensive patients when compared with those without hypertension ( P < 0.05). In multivariate regression models the number of affected vessels resulted an independent determinant for PAO ( P < 0.05). Concentration of 8‐ epi PGF 2 α and PAO also correlated with the number of cardiovascular risk factors ( P < 0.01 and P = 0.07, respectively). Conclusion. These findings indicate that elevated levels of plasma 8‐ epi PGF 2 α and reduced antioxidant capacity are associated with the extent and the severity of CAD and with the occurrence and number of different atherogenic risk factors. This observation may assist in providing more information as to how oxidative stress may predispose to atherogenesis and suggest attractive therapeutic strategies in the prevention and treatment of cardiovascular disease.