Leukocyte-platelet adhesion was significantly increased in patients with AMI compared to elective PTCA controls (77 vs 35 fluorescence channels; P=.003), inducing inflammatory cytokine expression.
Observational (n=40)
Does leukocyte-platelet adhesion increase inflammatory cytokine expression in patients with acute myocardial infarction?
Leukocyte-platelet adhesion is increased in acute myocardial infarction and directly induces inflammatory cytokine expression, highlighting a cellular mechanism for post-infarction inflammation.
Absolute Event Rate: 77% vs 35%
p-value: p=.003
BACKGROUND: Activated platelets tether and activate myeloid leukocytes. To investigate the potential relevance of this mechanism in acute myocardial infarction (AMI), we examined cytokine induction by leukocyte-platelet adhesion and the occurrence of leukocyte-platelet conjugates in patients with AMI. METHODS AND RESULTS: We obtained peripheral venous blood samples in 20 patients with AMI before and daily for 5 days after direct percutaneous transluminal coronary angioplasty (PTCA) and in 20 patients undergoing elective PTCA. Throughout the study period, CD41 immunofluorescence of leukocytes (flow cytometry) revealed increased leukocyte-platelet adhesion in patients with AMI compared with control patients (mean +/- SE of fluorescence channels before PTCA: 77 +/- 16 versus 35 +/- 9; P = .003). In vitro, thrombin-stimulated fixed platelets bound to neutrophils and monocytes. Within 2 hours, this resulted in increased mRNA for interleukin (IL),1 beta, IL-8, and monocyte chemoattractant protein (MCP)-1 in unfractionated leukocytes. After 4 hours, IL-1 beta and IL-8 concentration of the cell-free supernatant had increased by 268 +/- 36% and 210 +/- 7%, respectively, and cellular MCP-1 content had increased by 170 +/- 8%. Addition of activated platelets to adherent monocytes had a similar effect and was associated with nuclear factor-kappa B activation. Inhibition of binding by anti-P selectin antibodies reduced the effect of activated platelets on cytokine production. CONCLUSIONS: In patients with AMI, leukocyte-platelet adhesion is increased. Binding of activated platelets induces IL-1 beta, IL-8, and MCP-1 in leukocytes. Our findings suggest that leukocyte-platelet adhesion contributes to the regulation of inflammatory responses in AMI.
Neumann et al. (1997) conducted an observational in Acute myocardial infarction (n=40). Acute myocardial infarction vs. Elective PTCA was evaluated on Leukocyte-platelet adhesion (mean CD41 immunofluorescence channels) (p=.003). Leukocyte-platelet adhesion was significantly increased in patients with AMI compared to elective PTCA controls (77 vs 35 fluorescence channels; P=.003), inducing inflammatory cytokine expression.