Background Increasing scientific data suggests a role for inflammation in chronic heart failure (CHF), but up to now the exact mechanisms are still not clear. Recently, platelets were identified to induce inflammation partly by releasing cytokines. This new aspect necessitates further studies about the contribution of platelets for the inflammatory setting of CHF.
Methods 50 CHF patients (66.9 + 12.6 years, mean EF 22.1+9.1 %) and 25 healthy controls (63.6±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.
Results CHF patients showed significantly enhanced MCP-1 levels (median: 191.8; 25th: 153.7; 75th: 227.1 pg/mL vs. median: 101.0 25th: 86.7; 75th: 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 neither an influence on CD154 expression nor on MCP-1 levels.
Conclusions 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 distinguished anti-platelet strategies may represent new therapeutic options in CHF.
- chronic heart failure
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