Vassalle C, Petrozzi L, Botto N, Andreassi M G, Zucchelli G C
CNR Institute of Clinical Physiology, Via Moruzzi 1, I-56100 Pisa, Italy.
J Intern Med. 2004 Oct;256(4):308-15. doi: 10.1111/j.1365-2796.2004.01373.x.
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).
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).
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).
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.
众所周知，自由基会导致内皮功能障碍，并参与心血管疾病如动脉粥样硬化的发病机制和发展过程。本研究的目的是为冠状动脉疾病（CAD）中氧化应激增强提供证据。
在68名受试者（年龄：60±2岁，均值±标准误）中测量了脂质过氧化标志物8-异前列腺素（8-epiPGF(2α)）的血浆水平。受试者包括30名健康对照者和38名经血管造影证实患有CAD的患者。此外，在一个亚组（40名受试者，12名健康者和28名CAD患者）中评估了总抗氧化能力（PAO）。
8-epiPGF(2α)水平随着受累血管数量的增加而升高（单支血管病变和多支血管病变与对照者相比，P<0.001），并且考虑动脉粥样硬化的不同风险决定因素时（即高血压、性别、高胆固醇血症，P<0.01）也是如此。在多变量回归模型中，受累血管数量与8-epiPGF(2α)独立相关（P<0.05）。PAO值随着受累血管数量的增加而显著降低（P<0.05），并且与无高血压患者相比，高血压患者的PAO值也降低（P<0.05）。在多变量回归模型中，受累血管数量是PAO的独立决定因素（P<0.05）。8-epiPGF(2α)浓度和PAO也与心血管危险因素的数量相关（分别为P<0.01和P = 0.07）。
这些发现表明，血浆8-epiPGF(2α)水平升高和抗氧化能力降低与CAD的范围和严重程度以及不同致动脉粥样硬化危险因素的发生和数量相关。这一观察结果可能有助于提供更多关于氧化应激如何易导致动脉粥样硬化发生的信息，并为心血管疾病的预防和治疗提出有吸引力的治疗策略。
