Oxidative stress and its association with coronary artery disease and different atherogenic risk factors

被引:131
作者
Vassalle, C [1 ]
Petrozzi, L [1 ]
Botto, N [1 ]
Andreassi, MG [1 ]
Zucchelli, GC [1 ]
机构
[1] CNR, Ist Fisiol Clin, Area Ric, I-56100 Pisa, Italy
关键词
atherosclerosis; coronary artery disease; isoprostane; oxidative stress; total antioxidant capacity;
D O I
10.1111/j.1365-2796.2004.01373.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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). Conclusion. 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.
引用
收藏
页码:308 / 315
页数:8
相关论文
共 20 条
  • [1] Aliev G, 2002, BRAIN PATHOL, V12, P21
  • [2] Coronary atherosclerosis and somatic mutations: an overview of the contributive factors for oxidative DNA damage
    Andreassi, MG
    [J]. MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH, 2003, 543 (01) : 67 - 86
  • [3] Free radicals in the physiological control of cell function
    Dröge, W
    [J]. PHYSIOLOGICAL REVIEWS, 2002, 82 (01) : 47 - 95
  • [4] Endothelial dysfunction: Clinical strategies for treating oxidant stress
    Fenster, BE
    Tsao, PS
    Rockson, SG
    [J]. AMERICAN HEART JOURNAL, 2003, 146 (02) : 218 - 226
  • [5] Ferrari C, 1996, ANNU REV FLUID MECH, V28, P1
  • [6] Oxidative stress and cardiovascular injury - Part II: Animal and human studies
    Griendling, KK
    FitzGerald, GA
    [J]. CIRCULATION, 2003, 108 (17) : 2034 - 2040
  • [7] Mitochondrial DNA damage and dysfunction associated with oxidative stress in failing hearts after myocardial infarction
    Ide, T
    Tsutsui, H
    Hayashidani, S
    Kang, DC
    Suematsu, N
    Nakamura, K
    Utsumi, H
    Hamasaki, N
    Takeshita, A
    [J]. CIRCULATION RESEARCH, 2001, 88 (05) : 529 - 535
  • [8] Antioxidants and oxidative stress in exercise
    Ji, LL
    [J]. PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE, 1999, 222 (03): : 283 - 292
  • [9] The molecular bases of Alzheimer's disease and other neurodegenerative disorders
    Maccioni, RB
    Muñoz, JP
    Barbeito, L
    [J]. ARCHIVES OF MEDICAL RESEARCH, 2001, 32 (05) : 367 - 381
  • [10] C-reactive protein, dietary n-3 fatty acids, and the extent of coronary artery disease
    Madsen, T
    Skou, HA
    Hansen, VE
    Fog, L
    Christensen, JH
    Toft, E
    Schmidt, EB
    [J]. AMERICAN JOURNAL OF CARDIOLOGY, 2001, 88 (10) : 1139 - 1142