The role of platelets CD40 ligand (CD154) in acute coronary syndromes
Abstract
Background
Despite of the proof of the biological function of CD154 on platelets, there has been little information about its role either in patients with stable angina or in those with acute coronary syndrome (ACS).
Objective
This study aimed to investigate the expression of CD154 on platelets and its role in ACS.
Methods
The study included 50 patients with ACS (24 patients with acute myocardial infarction (AMI) and 26 patients with unstable angina (UA)), 20 patients with stable angina (SA) and 18 healthy volunteers. CD154 and CD62 expression on platelets were analyzed by flow cytometry. Their relations to the clinical and laboratory data were assessed in the studied group.
Results
Patients with AMI and UA had higher levels of platelets CD154 and CD62 as compared to those with SA and among patients with AMI, UA and SA versus healthy volunteers. Platelets CD154 showed significant positive correlations with the studied pro-inflammatory markers (Ox-LDL, CRP and fibrinogen), segmental wall motion score and the studied risk factors. There were significant negative correlations between platelet CD154 and serum nitric oxide among patients.
Conclusions
CD154 may be used as a marker of thrombo-embolic events. Nitric oxide may have an anti-atherogenic effect. There is an association between platelet activation and severity of coronary artery disease among patients with ACS.
Abbreviations: ACS, Acute coronary syndrome, ECs, endothelial cells, SMCs, smooth muscle cells, CD40L, CD40 ligand, CAD, coronary artery disease, AMI, acute myocardial infarction, UA, unstable angina, SA, stable angina, BMI, body mass index, WHR, waist hip ratio, SWMSI, segmental wall motion score index, C-RP, C-reactive protein, Ox-LDL, oxidized low density lipoprotein level, NO, serum nitric oxide, GMFI, geometric mean fluorescence intensity
Keywords: Acute Coronary Syndrome, CD154, Flow Cytometry, Platelets
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PII: S0049-3848(09)00311-9
doi:10.1016/j.thromres.2009.06.028
© 2009 Elsevier Ltd. All rights reserved.
