The onset of cerebral ischaemia triggers a cascade of proinflammatory molecular 
and cellular events. Clinical studies suggest that the strength of this acute 
response is important in early and late clinical outcomes, early clinical 
worsening, and extent of brain damage. Variables that are predictors of adverse 
stroke outcome include erythrocyte sedimentation rate, and levels of C-reactive 
protein (CRP), interleukin-6, tumour necrosis factor-alpha and intercellular 
adhesion molecule-1. Current data indicate that inflammation serves to fuel 
atherosclerosis and can act as the link between atherosclerosis and 
atherothrombosis. Growing evidence indicates that platelets act as prominent 
players in the inflammatory component of these disease processes. Thus, upon 
activation, platelets release a series of cytokines and growth factors and 
express CD40 ligand, which interacts with the CD40 receptor on other major cell 
types involved in atherosclerosis/atherothrombosis. In healthy volunteers, CD40L 
expression in platelets is not significantly inhibited by acetylsalicylic acid 
(ASA) alone, but is inhibited after treatment with the ADP-receptor antagonist 
clopidogrel or with clopidogrel plus ASA. Of a range of potential inflammatory 
biomarkers that have been reported in the literature, the best studied is CRP. 
Such biomarkers may have clinical utility for refined identification of patients 
at high risk for atherothrombosis in different arterial beds and for monitoring 
of therapeutic agents in clinical trials.