Summary
Inflammation is central to the pathogenesis and progression of atherosclerosis and
thrombosis, the underlying cause of major cardiovascular disease. Platelets, in addition
to their role in haemostasis, play a key role in both thrombus formation and inflammation
following vascular injury, especially atherosclerotic lesions. An increasing body
of evidence suggests that inhibition of platelet function can modulate inflammatory
markers, particularly those associated with activated platelets, such as CD40 ligand,
P-selectin, and C-reactive protein. The currently available antiplatelet agents aspirin,
clopidogrel, prasugrel, abciximab, and eptifibatide have shown varying effects on
inflammatory markers. These effects seem to be mostly indirect, i.e. mediated primarily
through reduced platelet activation that results in reduced inflammatory marker expression.
However, there is some evidence that suggests direct effects (i.e. those independent
of platelets) may also play a role in modulating inflammatory markers. Evidence linking
inflammation and thrombosis supports the hypothesis that agents with both anti-inflammatory
and antiplatelet effects may reduce vascular inflammation and limit acute and long-term
thrombotic events. An assessment of the involvement of inflammatory mediators in atherosclerosis
may provide further insight into important predictive markers of cardiovascular outcomes
that may also serve as potential therapeutic targets. This review examines the evidence
for and potential clinical relevance of the effects of antiplatelet therapy on inflammatory
markers.
Keywords
Antiplatelet therapy - thrombosis - inflammation - platelets