Stable phase post-MI patients have elevated VEGF levels correlated with inflammation markers, but not with atherosclerotic burden.

Stable phase post-MI patients have elevated VEGF levels correlated with inflammation markers, but not with atherosclerotic burden.
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DOI:
10.1186/1471-2261-14-166
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发表时间:
2014-11-22
影响因子:
2.1
通讯作者:
Šabovič M
Šabovič M
中科院分区:
医学4区
文献类型:
--
作者:
ErŽen B;Šilar M;Šabovič M

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血管内皮生长因子(VEGF)在心肌梗死(MI)后稳定期患者中的作用尚未探讨。因此,我们比较了心肌梗死后患者与健康对照组的VEGF值。此外,我们研究了VEGF的值是否与炎症标志物或动脉粥样硬化负担相关。招募41名男性患者(平均年龄44岁)在心肌梗死后稳定期(平均20.5个月),而25名健康年龄匹配的男性作为对照组。血浆中VEGF和几种炎症标志物的水平通过标准程序测量。动脉粥样硬化负担由冠状动脉粥样硬化的血管造影严重程度、内皮功能障碍(通过超声测量肱动脉血流介导的扩张来测量)、颈总动脉内膜-中膜厚度和踝-肱压力指数来确定。心肌梗死后患者的VEGF值与对照组相比显著升高(53.8±42.7 pg/ml vs. 36.3±8.9 pg/ml, p = 0.014)。VEGF升高与炎症分子白细胞介素6、白细胞介素8升高呈显著相关(r = 0.37, p = 0.017; r = 0.45, p = 0.003)。相比之下,尽管FMD和IMT在患者中明显受损,但VEGF与动脉粥样硬化负荷参数之间没有相关性。我们发现心肌梗死后稳定期血浆VEGF水平升高,且与炎症细胞因子相关,但与动脉粥样硬化负荷无关。因此,这表明VEGF水平的升高是持续炎症活动的一部分。由于这些患者的VEGF刺激炎症斑块的新生血管并诱导其不稳定,因此VEGF水平可能具有重要的负面预后价值。显然,需要进一步的研究来阐明VEGF作为预后标志物的作用。
The role of vascular endothelial growth factor (VEGF) in patients in the stable phase after myocardial infarction (MI) has not yet been explored. Therefore, we compared the values of VEGF in post-MI patients with those obtained in healthy controls. Furthermore, we investigated whether the values of VEGF correlate to either inflammation markers or the atherosclerotic burden. 41 male patients (on average 44 years old) in the stable phase after MI (on average 20.5 months after MI) were recruited, while 25 healthy age-matched males served as controls. Plasma levels of VEGF and several markers of inflammation were measured by standard procedures. The atherosclerotic burden was determined by the angiographic severity of coronary atherosclerosis, endothelial dysfunction (measured by ultrasound measurement of the flow mediated dilation of the brachial artery), the intima-media thickness of the common carotid artery and the ankle-brachial pressure index. VEGF values were significantly elevated in post-MI patients compared to the controls (53.8 ± 42.7 pg/ml vs. 36.3 ± 8.9 pg/ml, p = 0.014). The elevated VEGF values significantly correlated to the (increased) values of the inflammatory molecules interleukin 6 and 8 (r = 0.37, p = 0.017; and r = 0.45, p = 0.003; respectively). In contrast, no correlation was found between VEGF and the parameters of the atherosclerotic burden, although FMD and IMT were significantly impaired in patients. We found that plasma levels of VEGF are increased in the stable phase after MI and correlate with inflammation cytokines, but not with the atherosclerotic burden. Thus, this suggests that increased levels of VEGF are a part of ongoing inflammatory activity. Since VEGF in these patients stimulates neovascularization of inflamed plaques and induces their destabilization, the VEGF level can have an important negative prognostic value. Clearly, further studies are needed to clarify the role of VEGF as a prognostic marker.
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