Oxidative stress and its association with coronary artery disease and different atherogenic risk factors.
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-epiPGF(2alpha)), 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-epiPGF(2alpha) 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-epiPGF(2alpha) (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-epiPGF(2alpha) and PAO also correlated with the number of cardiovascular risk factors (P < 0.01 and P = 0.07, respectively).


CONCLUSIONS
These findings indicate that elevated levels of plasma 8-epiPGF(2alpha) 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.
Vassalle
C
C
CNR Institute of Clinical Physiology, Via Moruzzi 1, I-56100 Pisa, Italy. cristina.vassalle@ifc.cnr.it
Petrozzi
L
L
Botto
N
N
Andreassi
M G
MG
Zucchelli
G C
GC
D000975:Antioxidants / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D003324:Coronary Artery Disease / Q000378:metabolism*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D005260:Female; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000502:physiology*; D012307:Risk Factors
D000975:Antioxidants; D015415:Biomarkers; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost