Safety and Efficacy Comparison of Platelet Glycoprotein IIb/IIIa Antagonist in Treating STEMI Patients by Intracoronary-intravenous Administration and Intravenous Administration:A Meta-analysis / 中国循环杂志

Objective: To compare the safety and efifcacy of platelet glycoprotein IIb/IIIa antagonist in treating STEMI patients by intracoronary-intravenous administration and intravenous administration. Methods: We searched PubMed, Embase, Cochrane library, CNKI, VIPH and Wanfang database, the retrieval stopped at 2014-03. According to 5.0.2 Cochrane handbook, 2 scientists collected 2494 STEMI patients treated by IIb/IIIa antagonist from 20 references, and they were divided into 2 groups. Combination group, the patients received intracoronary, then intravenous administration, n=1258 and Intravenous group, the patients receive only intravenous administration, n=1236. RevMan 5.0 software was used for Meta-analysis. Results: At 1 month after PCI treatment, compared with Intravenous group, the Combination group had better conditions of TIMI 3, TMP 3, ST segment recovery, MACE occurrence and MI area changes, all P0.05. Conclusion: Intracoronary-intravenous administration of platelet glycoprotein IIb/IIIa antagonist had the better effect for treating STEMI patients without increasing the side effects of post-operative bleeding and thrombocytopenia.

EDTA Inhibits the Binding of Clone 96.2C1, an Anti-CD41a Monoclonal Antibody, to the Platelets and Addition of Heparin and CaCl2 to the Antibody Neutralizes the EDTA-induced Inhibitory Effect

BACKGROUND: The binding of some monoclonal antibodies platelet glycoprotein (GP) IIb/IIIa, which is frequently used for flow cytometric immnophenotyping, is known to be inhibited by EDTA. To select the ideal antibodies to be included in the 'Acute Leukemia Panel' for immunophenotyping of acute leukemia, we compared the inhibitory effect of EDTA on the binding of 5 different clones of monoclonal antibodies to platelet GP IIb/IIIa. We also discovered a simple method to neutralize this inhibitory effect. METHODS: Flow cytometric measurement of the number of platelet GP IIb/IIIa binding sites with different anticoagulants was performed using a panel of 5 clones of monoclonal antibodies against CD41 (clone PM6/248), CD41a (clone 96.2C1 & clone HIP8), CD41b (clone HIP2) and CD61 (clone VI-PL2), and the results are expressed as the mean equivalent soluble fluorochrome (MESF) values. RESULTS: The MESF value of the EDTA platelets stained with anti-CD41a, clone 96.2C1 antibody showed a significantly lower value than the MESF of platelets anticoagulated with heparin or citrate (P<0.001). The inhibitory effect of EDTA on the binding of anti-CD41a, clone 96.2C1 antibody to the platelets was neutralized by addition of heparin and CaCl2. The mean MESF value of EDTA platelets stained with anti-CD41a, clone 96.2C1 antibody was significantly increased by the addition of heparin and CaCl2 (P=0.0001). CONCLUSION: The false-negative results of the binding of anti-CD41a, clone 96.2C1 antibody to the platelets seem to be due to the calcium chelating property of EDTA, and the addition of CaCl2 and heparin could be used as an easy compensatory measure for the inhibitory effect of EDTA on other antibodies as well.

Increased Activation of Platelet Glycoprotein IIb/IIIa in Hypercholesterolemic Patients

BACKGROUND: Platelet function is directly influenced by lipoproteins, and platelets from hypercholesterolemic patients display increased reactivity which is related to initiation, progression, and development of thromboembolic complications in atherosclerosis. But the exact mechanism of this effect is unclear. METHODS: In this study, total and activated numbers of platelet glycoprotein (Gp) IIb/IIIa were evaluated in twenty patients (7 men; age, 55.4+/-8.7 years) with hypercholesterolemia (plasma total cholesterol level over 240 mg/dL and normal triglyceride level) and twenty one subjects (8 men; 51.1+/-13.7 years) with normal plasma cholesterol and triglyceride levels. Flow cytometry was used to detect the binding of fluorescein isothiocyanate (FITC)-conjugated anti-CD41 or PAC1 to platelet Gp IIb/IIIa in whole blood. When whole blood was incubated with PAC1, platelets were also activated with adenosine diphosphate (ADP) or thrombin. RESULTS: PAC1 was more bound to unstimulated platelets from patients with hypercholesterolemia (p<0.005), and binding of PAC1 correlated significantly with plasma total cholesteol (r=0.48, p=0.002) and LDL-cholesterol (r=0.47, p=0.002) levels. Binding of PAC1 to unstimulated platelets increased as binding of anti-CD41 increased (r=0.40, p=0.01). On multivariate linear regression analysis, plasma total cholesterol level and binding of anti-CD41 were independent variables that determined binding of PAC1. After ADP- or thrombin-stimulation, binding of PAC1 to platelets and percentage of antibody positive cells were also greater in patients with hypercholesterolemia (p<0.05). There was a significant positive correlation between mean platelet volume and binding of anti-CD41 to unstimulated platelets (r=0.46, p<0.0050), but the latter was not different between hypercholesterolemia and control groups. CONCLUSION: Unstimulated platelets from patients with hypercholesterolemia had similar total number of Gp IIb/IIIa to those from control subjects, but had more activated Gp IIb/IIIa. After ADP- or thrombin-stimulation, platelet Gp IIb/IIIa was also more activated under hypercholesterolemia.