Medizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität München, Munich, Germany.
J Am Coll Cardiol. 2010 Feb 16;55(7):637-42. doi: 10.1016/j.jacc.2009.07.073.
We sought to assess whether emotional stress-induced acute coronary syndrome (ACS) is mediated by increased inflammatory and vasoconstrictive mediators.
The World Cup soccer 2006 has been shown to provoke levels of stress sufficient to increase the incidence of ACS. However, the mechanisms by which stress translates into vascular injury up to plaque rupture still remain elusive.
Serum levels of soluble CD40L (sCD40L), soluble vascular cell adhesion molecule (sVCAM)-1, monocyte chemoattractant protein (MCP)-1, tumor necrosis factor (TNF)-alpha, high-sensitivity C-reactive protein (hsCRP), regulated on activation, normal T-cell expressed and secreted (RANTES), and endothelin (ET)-1 were determined in patients who experienced an ACS during World Cup matches, in ACS reference patients (not associated with emotional stress), and in healthy volunteers. Correlations and receiver-operating characteristic curves were calculated to develop multivariable analysis and to investigate the diagnostic value of each parameter.
The sCD40L, sVCAM-1, MCP-1, TNF-alpha, and ET-1 were significantly higher in study patients compared with the reference group. The hsCRP was similar in both groups, whereas RANTES was decreased in study patients. A positive correlation was found between ET-1 and soccer-induced enhanced levels of sCD40L, sVCAM-1, MCP-1, and TNF-alpha. Receiver-operating characteristic analysis displayed high performance of both MCP-1 and ET-1 as a measure to discriminate between stress-induced ACS and ACS controls.
Stress-induced ACS is associated with a profound increase of inflammatory and vasoconstrictive mediators. The evaluation of a targeted drug delivery, such as anti-inflammatory agents, ET-1 receptor antagonists, or inhibition of endothelin-converting enzyme is warranted to reduce stress-mediated cardiovascular morbidity.
我们旨在评估情绪应激诱发的急性冠状动脉综合征（ACS）是否通过增加炎症和血管收缩介质来介导。
2006 年世界杯足球赛已被证明足以引起应激水平升高，从而增加 ACS 的发生率。然而，应激如何转化为血管损伤，直至斑块破裂的机制仍不清楚。
在世界杯比赛期间发生 ACS 的患者、与情绪应激无关的 ACS 参考患者（reference patients）和健康志愿者中，测定血清可溶性 CD40L（sCD40L）、可溶性血管细胞黏附分子（sVCAM）-1、单核细胞趋化蛋白（MCP）-1、肿瘤坏死因子（TNF）-α、高敏 C 反应蛋白（hsCRP）、调节激活正常 T 细胞表达和分泌（RANTES）和内皮素（ET）-1 的水平。计算相关性和接收者操作特征曲线以进行多变量分析，并研究每个参数的诊断价值。
与参考组相比，研究患者的 sCD40L、sVCAM-1、MCP-1、TNF-α和 ET-1 明显升高。两组的 hsCRP 相似，而研究患者的 RANTES 降低。ET-1 与足球引起的 sCD40L、sVCAM-1、MCP-1 和 TNF-α的增强水平之间存在正相关。接收者操作特征分析显示 MCP-1 和 ET-1 作为区分应激性 ACS 和 ACS 对照的指标具有较高的性能。
应激诱发的 ACS 与炎症和血管收缩介质的明显增加有关。需要评估靶向药物输送，如抗炎药、ET-1 受体拮抗剂或内皮素转换酶抑制剂，以减少应激介导的心血管发病率。
