This study suggests that tirofiban infusion suppresses the elevation of soluble cell adhesion molecule levels in patients with unstable AP. Such patients were selected because it was expected that inflammatory activities would be triggered in their vascular systems.
The importance of inflammation in acute coronary syndromes is well established. It is known that GP IIb/IIIa antagonists inhibit platelet activation by blocking the fibrinogen binding receptor . However, can the clinical improvements demonstrated in multi-central studies be attributed solely to inhibition of platelet activation?
Platelets play an important role not only in the coagulation system but also in the inflammatory response [16–18]. Platelet activation can increase inflammation through several mechanisms. Platelets release a wide range of growth factors and inflammatory mediators from intracellular storage organelles. Products of activation may aid neutrophil accumulation and enhance inflammation. Activated leukocytes and platelets potentate each others' effects. The important mediators released by platelets are P-selectin (CD62p), CD40p, platelet activating factor, macrophage chemotactic factor-1, interleukin-1, thrombospondin and fibronectin. These mediators are rapidly expressed by activated platelets [19–24].
Inhibition of platelet function by specific GP IIb/IIIa antagonists may decrease plateletmediated inflammation. Tirofiban may not only inhibit platelet activation but also suppress inflammatory processes [25, 26]. This effect is not cross-reactivity; it can explain the antiinflammatory properties of tirofiban.
In a group (IA) of high risk patients with unstable AP, the high baseline levels of some cell adhesion molecules (sICAM-1, sVCAM-1), significantly decrease after adding tirofiban to the usual treatment of intravenous unfractionated heparin, aspirin and others. In patients with UAP but lower risk, the baseline values of sICAM-1 and sVCAM-1, although higher than those of the Groups II and III, were not affected by the treatment, that not includes tirofiban.
Inflammation, especially platelet-mediated, may be suppressed and the ischemic end-point will be reduced after GP IIb/IIIa antagonist therapy.