| Background and Objective Acute Coronary Syndrome (Acute coronary syndrome, ACS) is due to a variety of factors which lead to vascular endothelial injury and atherosclerotic plaque ulceration, bleeding, induced platelet activation, adhesion, aggregation, and then the process of thrombosis. There are different degrees of imbalance of coagulation, anticoagulation and fibrinolysis system in patients with ACS,which may be manifested as apparent hypercoagulable state, prothrombotic state (prethrombotic state, PTS) or thrombosis, and secondary hyperfibrinolysis. Therefore, the strengthening of anti-platelet and anticoagulant therapy is the basic treatment of patients with ACS. Results from a number of large-scale clinical trials have showed that:for patients with high-risk ACS undergoing percutaneous coronary intervention (PCI), effective anti-platelet and anticoagulant treatment can prevente acute stent thrombosis and other adverse events. By blocking the final pathway of platelet aggregation, new anti-platelet drug GPⅡb/Ⅲa receptor antagonist tirofiban hydrochloride can play a powerful and rapid roal in inhibiting platelet aggregation and then reduce the incidence of major adverse cardiac events. In this process, however, there are relatively few researches on whether tirofiban can significantly influence the coagulation and anticoagulation system, such as antithrombinⅢ(ATⅢ) and activated clotting time(ACT). Furthermore, the present viewpoints about this are different. Therefore, this study was designed to initially explore the changes of coagulation and anticoagulation system in patients with high-risk ACS and whether and how tirofiban impact them by observing different time points'platelet aggregation rate (PAR), activated clotting time (ACT) and plasma levels of AT III before and after PCI, and then evaluate its efficacy to guide clinical practice. Patients and Methods After risk stratification, seventy patients with high-risk ACS undergoing PCI were randomly devided into the tirofiban group and the control group. In the tirofiban group there are 36 cases, which involved 25 males and 11 females, aged 35 to 70 years with the mean age 60.6±8.5 years. In the control group there are 34 cases, which involved 24 males and 10 females, aged 42 to 72 years old, with an average of 58.9±8.3 years. PAR, ACT and ATIII levels before PCI,12 hours, 36 hours and 48 hours after PCI were tested, compared and analyzed between the two groups to explore whether tirofiban can impact those parameters.Results(1) comparison of general state and baseline data between the two groups:There were no significant differences in age, sex, complicating diseases, vascular lesion and stenting characteristics (P>0.05).(2) comparison of platelet aggregation rate (PAR):PAR after PCI in the tirofiban group changed significantly, between the two groups, different time points, the interaction between groups and different time points were statistically significant (P <0.01); Compared with that before PCI, PAR of 12 and 36 hours after PCI in the tirofiban group were significantly decreased (4.15±5.61% vs 37.87±20.13%, 9.57±7.66% vs 37.87±20.13%, both P<0.05), however, after stopping tirofiban 12 hours, namely 48 hours after PCI, PAR rapidly rebound to baseline level. PAR of 12, 36 and 48 hours after PCI in the control group all had no significant change compared with that before PCI(both P>0.05). Comparison of PAR at the same time points between the two groups showed that there were no significant difference between PAR before PCI and 48 hours after PCI(P>0.05); however, PAR of 12 and 36 hours after PCI were significantly lower than that of.the control group respectively(4.15±5.61% vs 41.69±18.90%,9.57±7.66% vs 39.54±23.37%), the difference were statistically significant (both P<0.05). (3) Comparison of activated clotting time (ACT) between the two groups:treatment effect(whether adminstrating tirofiban or not) between the two groups showed no significant difference (F= 0.569 P> 0.05), repeated measurements of different time points within the two groups showed statistically significant difference (F= 16.059, P <0.05), and there was also no statistically difference, with the interaction between the two groups·different time points (F= 0.367, P> 0.05). ACT of 12,36 and 48 hours after PCI compared with those before PCI in the two groups all increased significantly(P all<0.05).(4) Changes of plasma antithrombinⅢ(ATⅢ) in both groups:it showed no difference between the treatment effect (F= 0.816 P> 0.05), repeated measurements of different time points within the two groups were significantly different (F=21.004 P< 0.05),·different points in time between the two groups no statistically significant difference between the interaction (F= 1.088 P> 0.05), and there was also no statistically difference with the interaction between the two groups·different time points (F= 1.088 P> 0.05). Plasma ATⅢlevels of 12,36and 48 hours after PCI decreased significantly compared with those before PCI in both groups(P all<0.05). The ATⅢlevel of 48 hours after PCI in the tirofiban group was higher than those 12 and 36 hours after PCI(166±69 vs 144±58 mg/L,166±69 vs 132±56mg/L, both P<0.05), but still significantly lower than that before PCI(166±69 vs 238±65 mg/L,P<0.05).(5)Correlation analysis of ACT values and ATⅢlevel in both groups:ACT values of 12,36 and 48 hours showed significant positive correlation with ATⅢlevels at the same points in both groups. The coefficient were r=0.889, P<0.01; r= 0.812, P <0.01; r= 0.690, P<0.01 in the tirofiban group and r= 0.793, P<0.01; r= 0.855, P <0.01; r= 0.742, P<0.01 in the control group respectively.Conclusions (1) Tirofiban can inhibit platelet aggregation rapidly and powerfully in patients with high-risk ACS immediately after PCI.(2) ATⅢsignificantly decreased after PCI in patients with ACS, the anticoagulation effect of anticoagulants such as heparin are subject to certain restrictions, therefore, it is easy to emerge thrombotic complications.(3) Tirofiban can significantly decrease platelet aggregation rate, strengthen the anti-platelet effect, however, it nearly do not directly influence ATⅢlevel and ACT value.(4) In patients with ACS after PCI, it is important to strengthen the anti-platelet therapy, at the same time, for patients with thrombosis, we should consider the possibility of secondary thrombogenesis caused by decrease or deficiency of ATⅢ. Meanwhile, perhaps it is more effective to complement ATⅢagents or administer direct thrombin inhibitors which do not depend on ATⅢto make effects.
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