| Objective: To study the effects of platelet glycoprotein(GP) IIb/IIIa receptor antagonist tirofiban on blood serum soluble CD40 ligand(sCD40L) and high sensitivety C react protein(hs-CRP) perioperative intervention in acute myocardial infarction (AMI), and to investigate the role of inflammation on AMI and the influence of GP IIb/IIIa receptor antagonist on the inflammatory reaction and the stability of plaque. It also probed the significance of changes in sCD40L through the research of the relevance of sCD40L and hs-CRP.Methods: Selecting 20 non-coronary heart disease adults for control group, 20 stability angina pectoris(SAP) patients, 80 AMI patients divided into conventional therapy group and tirofiban group stochastically, and treating 120 subjects with A, B, C, D groups respectively: control group(group A: n=20), SAP group(group B: n=20), conventional therapy group: treated without tirofiban (group C: n=40), tirofiban group: treated with tirofiban(group D: n=40).Both group C and group D underwent percutaneous coronary intervention (PCI) . Except for group A, group B received secondary prevention of coronary heart disease treatment, group C and group D accepted antiplatelet, anticoagulant therapy and or thrombolysis therapy. Group D: tirofiban was initiated 6 hours before PCI according to the standard dose (tirofiban was administered intravenously with a loading dose of 10μg/kg for 3 minutes, followed by infusion of 0. 15μg/(kg. min). Maintained infusion was given for 36 hours after PCI) . All SAP and AMI patients who were selected were collected venous blood 5ml as soon as possible. AMI patients were collected blood sample again 24 hours after PCI. We measured the density of serum sCD40L and hs-CRP, then compared the difference of sCD40L and hs-CRP among different groups. To investigate the relationship of inflammationgs and AMI, explore the influcence of GPIIb/IIIa receptor antagonist tirofiban on the inflammatory reaction and the stability of artery atheromatous plaque. Both group C and group D was following up 30 days after PCI, and observed the major adverse cardiac events(MACE) during 30 days.Results: 1.The level of the serum sCD40L and hs-CRP in AMI patients was significantly higher than that in group B and group A (p < 0. 01). The serum sCD40L in group B was higher than that in group A, but there was no difference between group B and group A of sCD40L (p>0. 05), and there was obvious difference of the density of the serum hs-CRP between group B and group A (p < 0.05). 2. Comparisons of sCD40L and hs-CRP between C and D group before operation: there was no difference between group C and group D of the two markers (p > 0. 05), however, not only in group C but also in group D the level of sCD40L and hs-CRP 24 hours after PCI was obviously higher than that preoperation (p<0. 01), and the level of sCD40L and hs-CRP degrade obviously 24 hours after operation in group D (p < 0.01). 3. The straight linear relevance analysis showed that the sCD40L and hs-CRP were relevant. The relevance of sCD40L and hs-CRP r=0.894(p < 0. 05). 4. During the follow-up of 30 days after PCI, MACE were significantly less frequent in group D than group C(p< 0. 05). 5. No serious hemorrhage was observed in both group C and group D during in-hospital, however, more patients with minor hemorrhage and thrombocytopenia in group D(15% vs 2.5%, p<0. 05).Conclusion: 1. Inflammation reaction exists in the development of AMI. The elevated sCD40L and hs-CRP may be the activating signs of coronary artery disease. The high level of sCD40L may represent instability of the plaque.The serum sCD40L and hs-CRP have some relevance. sCD40L can be used as markers of inflammation as serum hs-CRP. They have some predictive value for the development of AMI. 2. The level of sCD40L and hs-CRP 24 hours after PCI was obviously higher than that preoperation. This may be concerned with the enhanced local inflammatory reaction or partial tear of the intima after PCI. Therefore, it is necessary that strengthens anti-inflammatory treatment after PCI. 3. GPII b/IIIa receptor antagonist can improve the infarct-related artery TIMI flow of AMI patients, reduce the occurrence of MACE. 4. GPIIb/IIIa receptor antagonist tirofiban can degrade the levels of serum sCD40L and hs-CRP. Tirofiban not only inhibits platelet aggregation, but also may contribute to the stability of atherosclerotic plaque, nonspecific anti-inflammatory action is independent of the anti-platelet effect. They provide theoretical basis for identifying the unstable plaque in clinical and applying GP IIb/IIIa receptor antagonist preoperative intervention for AMI.
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