Platelets contribute to enhanced MCP-1 levels in patients with chronic heart failure.
BACKGROUND
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.


METHODS
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.


RESULTS
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.


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 sophisticated anti-platelet strategies may represent new therapeutic options in CHF.
Stumpf
C
C
Department of Cardiology, University of Erlangen-Nuremberg, Erlangen, Germany. ch.stumpf@web.de
Lehner
C
C
Raaz
D
D
Yilmaz
A
A
Anger
T
T
Daniel
W G
WG
Garlichs
C D
CD
D000368:Aged; D023201:CD40 Ligand / Q000097:blood; D002311:Cardiomyopathy, Dilated / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood*; D002908:Chronic Disease; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000209:etiology; D006801:Humans; D008297:Male; D015539:Platelet Activation
D018932:Chemokine CCL2; D023201:CD40 Ligand