Ikonomidis Ignatios, Stamatelopoulos Kimon, Lekakis John, Vamvakou Georgia D, Kremastinos Dimitrios Th
2nd Cardiology Department, University of Athens, Attikon Hospital, Perikleous 19, N. Chalkidona, Athens 14343, Greece.
Atherosclerosis. 2008 Jul;199(1):3-11. doi: 10.1016/j.atherosclerosis.2008.02.019. Epub 2008 Feb 29.
Current thinking supports the notion that several inflammatory proteins intervene with endothelium and haemostatic factors leading to plaque formation and rupture. Of these, C-reactive protein (CRP), monocyte/macrophage colony-stimulating factor (MCSF) and interleukin-6 (IL-6) promote atherogenesis by inducing monocyte-macrophage activation, foam cell formation, platelet activation, tissue factor expression, release of other procoagulant cytokines or downregulation of atheroprotective cytokines such as interleukin 10 and transforming growth factor b-1 (TGFb-1). CRP, MSCF and IL-6 are interrelated and have been found in increased blood concentrations in CAD. Increased levels of CRP and IL-6 predict a higher cardiovascular event rate in the general population and in addition to high MCSF or low TGFb-1 predict adverse outcome in CAD patients independently of traditional risk factors. Moreover, in CAD patients, the predictive value of MCSF is additive and beyond that of CRP suggesting the need of a "multimarker approach" in assessing cardiovascular risk. Accumulating evidence supports the utility of non-invasive markers of subclinical atherosclerosis, namely carotid intimal media thickness, flow mediated dilatation of the brachial artery, augmentation index or pulse wave velocity, in the prediction of cardiovascular risk particularly in primary prevention settings. The combination of these non-invasive tests has been shown to improve their prognostic accuracy compared to each other alone. Although several therapeutic strategies like vaccination against antigens promoting atherogenesis, cyclooxygenase inhibitors, statins, and ACE inhibitors may reduce the levels of these inflammatory markers and improve the non-invasive markers of subclinical atherosclerosis, the impact on cardiovascular risk resulting from these changes is unknown. The combination of an established inflammatory marker such as CRP or a vascular marker such as IMT with novel biochemical and vascular markers of cardiovascular disease may offer additive prognostic information for adverse outcome.
目前的观点支持这样一种看法，即几种炎症蛋白会干扰内皮细胞和止血因子，从而导致斑块形成和破裂。其中，C反应蛋白（CRP）、单核细胞/巨噬细胞集落刺激因子（MCSF）和白细胞介素-6（IL-6）通过诱导单核细胞-巨噬细胞活化、泡沫细胞形成、血小板活化、组织因子表达、释放其他促凝血细胞因子或下调诸如白细胞介素10和转化生长因子β-1（TGFβ-1）等抗动脉粥样硬化细胞因子来促进动脉粥样硬化的发生。CRP、MSCF和IL-6相互关联，并且已发现它们在冠心病患者血液中的浓度会升高。CRP和IL-6水平升高预示着普通人群中较高的心血管事件发生率，此外，高MCSF或低TGFβ-1水平独立于传统危险因素之外还预示着冠心病患者的不良预后。此外，在冠心病患者中，MCSF的预测价值具有叠加性，且超过CRP，这表明在评估心血管风险时需要采用“多标志物方法”。越来越多的证据支持亚临床动脉粥样硬化的非侵入性标志物，即颈动脉内膜中层厚度、肱动脉血流介导的扩张、增强指数或脉搏波速度，在预测心血管风险方面的实用性，尤其是在一级预防环境中。与单独使用这些非侵入性检测方法相比，联合使用这些检测方法已被证明可以提高其预后准确性。尽管几种治疗策略，如针对促进动脉粥样硬化发生的抗原进行疫苗接种、环氧化酶抑制剂、他汀类药物和血管紧张素转换酶抑制剂，可能会降低这些炎症标志物的水平并改善亚临床动脉粥样硬化的非侵入性标志物，但这些变化对心血管风险的影响尚不清楚。将一种已确立的炎症标志物如CRP或一种血管标志物如内膜中层厚度与新型心血管疾病生化和血管标志物相结合，可能会为不良预后提供叠加的预后信息。
