Stumpf C, Lehner C, Raaz D, Yilmaz A, Anger T, Daniel W G, Garlichs C D
Department of Cardiology, University of Erlangen-Nuremberg, Erlangen, Germany.
Heart. 2008 Jan;94(1):65-9. doi: 10.1136/hrt.2007.115006. Epub 2007 Jun 17.
Increasing scientific data suggest a role for inflammation in chronic heart failure (CHF), but up to now the exact mechanisms are still not clear. Recently, platelets were identified as inducing inflammation partly by releasing cytokines. This new aspect necessitates further studies about the contribution of platelets for the inflammatory setting of CHF.
50 CHF patients (mean 66.9 (SD 12.6) years, mean EF 22.1% (SD 9.1)) and 25 healthy controls (mean 63.6 (SD 10.2) years) were examined. MCP-1 serum levels were measured via EIA, expression of platelet CD154 by flow cytometry. In in-vitro experiments activated platelets were cocultured with human umbilical vein endothelial cells (HUVEC) in the presence and absence of anti-CD154 antibodies. MCP-1 in the supernatants was measured by EIA.
CHF patients showed significantly enhanced MCP-1 levels (median: 191.8; 25th centile: 153.7; 75th centile: 227.1 pg/ml vs median: 101.0; 25th centile: 86.7; 75th centile: 117.5 pg/ml, p<0.001). MCP-1 levels positively correlated with severity of CHF. In the cell coculture model activated platelets were able to significantly induce MCP-1 release from HUVEC in a CD154-dependent manner. Furthermore, CHF patients showed enhanced platelet CD154 expression with a positive correlation with MCP-1 levels. Aspirin therapy had no influence on either CD154 expression or MCP-1 levels.
Platelets can contribute to enhanced MCP-1 levels in CHF. MCP-1 is markedly elevated in serum of CHF patients showing a direct correlation with the severity of symptoms and the degree of left ventricular dysfunction. Further studies are required to test whether MCP-1 blocking or sophisticated anti-platelet strategies may represent new therapeutic options in CHF.
越来越多的科学数据表明炎症在慢性心力衰竭（CHF）中发挥作用，但迄今为止确切机制仍不清楚。最近，血小板被确定为部分通过释放细胞因子诱导炎症。这一新情况使得有必要进一步研究血小板在CHF炎症环境中的作用。
对50例CHF患者（平均年龄66.9（标准差12.6）岁，平均射血分数22.1%（标准差9.1））和25名健康对照者（平均年龄63.6（标准差10.2）岁）进行检查。通过酶免疫测定法测量血清MCP-1水平，采用流式细胞术检测血小板CD154的表达。在体外实验中，将活化的血小板与人脐静脉内皮细胞（HUVEC）在有和没有抗CD154抗体的情况下共同培养。通过酶免疫测定法测量上清液中的MCP-1。
CHF患者的MCP-1水平显著升高（中位数：191.8；第25百分位数：153.7；第75百分位数：227.1 pg/ml，而对照组中位数：101.0；第25百分位数：86.7；第75百分位数：117.5 pg/ml，p<0.001）。MCP-1水平与CHF严重程度呈正相关。在细胞共培养模型中，活化的血小板能够以CD154依赖的方式显著诱导HUVEC释放MCP-1。此外，CHF患者血小板CD154表达增强，与MCP-1水平呈正相关。阿司匹林治疗对CD154表达或MCP-1水平均无影响。
血小板可导致CHF患者MCP-1水平升高。CHF患者血清中MCP-1明显升高，与症状严重程度和左心室功能障碍程度直接相关。需要进一步研究以测试阻断MCP-1或完善的抗血小板策略是否可能成为CHF的新治疗选择。
