Platelet-derived chemokine RANTES may be a sign of restenosis after percutaneous coronary intervention in patients with stable angina pectoris

Platelet-derived chemokine RANTES may be a sign of restenosis after percutaneous coronary intervention in patients with stable angina pectoris
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DOI:
10.1080/09537100600759618
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发表时间:
2006-01
期刊:
影响因子:
3.3
通讯作者:
N. Inami;S. Nomura;K. Manabe;Y. Kimura;T. Iwasaka
N. Inami;S. Nomura;K. Manabe;Y. Kimura;T. Iwasaka
中科院分区:
医学3区
文献类型:
--
作者:
N. Inami;S. Nomura;K. Manabe;Y. Kimura;T. Iwasaka

文献摘要

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炎症在经皮冠状动脉介入治疗(PCI)后再狭窄的发生中起着致病作用。我们测量并比较了 PCI 后正常 T 细胞表达和分泌的激活调节 (RANTES)、单核细胞趋化肽-1 (MCP-1)、可溶性 (s) P-选择素和 sL-选择素水平升高的比率。对接受 PCI 并在 6 个月随访时重复进行血管造影的 52 名患者(43 名男性和 9 名女性,年龄 63 ± 10 岁)在 PCI 之前、之后 1、3 和 7 天测量了趋化因子和可溶性标志物的血浆水平。 16 名 (31%) 患者发生再狭窄。在再狭窄组中观察到 sL-选择素显着且呈时间依赖性增加。然而,有或没有再狭窄时,MCP-1 水平没有显着差异。再狭窄组的 sP-选择素水平在 PCI 后 3 天出现短暂升高。有或没有再狭窄的患者之间的 RANTES 水平在基线时没有差异。然而,在非再狭窄组中观察到 RANTES 水平显着且随时间变化,并且再狭窄患者与无再狭窄患者相比,RANTES 水平升高的比例具有统计学意义。这些结果表明,劳累性心绞痛患者 PCI 术后再狭窄的发生可能与 PCI 术后早期的白细胞激活有关。此外,血小板衍生趋化因子RANTES可能是稳定型心绞痛患者PCI术后再狭窄的标志。
Inflammation plays a pathogenic role in the development of restenosis after percutaneous coronary intervention (PCI). We measured and compared the ratio of elevated levels of regulated on activation normally T-cell expressed and secreted (RANTES), monocytic chemotactic peptide-1 (MCP-1), soluble (s) P-selectin and sL-selectin after PCI. Plasma levels of chemokines and soluble markers were measured before, 1, 3 and 7 days after PCI in 52 patients (43 males and nine females, aged 63 ± 10 years) who underwent PCI and who had repeated angiograms at a 6-month follow-up. Restenosis occurred in 16 (31%) patients. A significant and time-dependent increase in sL-selectin was observed in the restenosis group. However, there were no significant differences in MCP-1 levels with or without restenosis. sP-selectin levels in the restenosis group exhibited a transient elevation at 3 days after PCI. RANTES levels were no different at baseline between patients with or without restenosis. However, a significant and time-dependent decrease in RANTES levels were observed in the non-restenosis group, and patients with restenosis compared with patients without restenosis had a statistically significant ratio of elevated levels of RANTES. These findings suggest that restenosis development after PCI in patients with effort angina pectoris may involve leukocyte activation at an early period after PCI. In addition, platelet-derived chemokine RANTES may be a sign of restenosis after PCI in patients with stable angina pectoris.