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Platelet CD62 expression and PDGFAB secretion in patients undergoing PTCA and treatment with abciximab
1Institute of Clinical Pharmacology, Medical School of the J.W. Goethe University, Frankfurt am Main, Germany. graff@em.uni-frankfurt.de
Insights
Abciximab significantly reduced platelet aggregation and GPIIb/IIIa binding in coronary patients. However, platelet secretion markers CD62 and PDGF showed only slight reductions, with no direct correlation observed.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Pharmacology
Background:
- Platelet activation is crucial in coronary artery disease.
- GPIIb/IIIa inhibitors like abciximab are used to prevent thrombotic events.
- Understanding the impact of abciximab on platelet activation markers is essential.
Purpose of the Study:
- To investigate the correlation between CD62 expression and PDGF secretion in coronary patients treated with abciximab.
- To assess the effect of abciximab on platelet activation markers and function.
Main Methods:
- Flow cytometry was used to measure fibrinogen binding and CD62 expression on platelets.
- Platelet aggregation was assessed using ADP and collagen.
- Platelet-derived growth factor (PDGF) release was measured by immunoassay in nine coronary patients undergoing angioplasty and treated with abciximab, aspirin, and heparin.
Main Results:
- Abciximab significantly reduced fibrinogen binding and platelet aggregation in response to ADP and collagen.
- CD62 expression showed a slight but significant decrease over time during abciximab treatment.
- Platelet-derived growth factor (PDGF) release was not significantly affected by abciximab therapy.
Conclusions:
- Abciximab effectively inhibits GPIIb/IIIa binding and platelet aggregation.
- CD62 expression and PDGF release are only minimally affected by abciximab.
- No direct correlation was found between CD62 expression and PDGF release under abciximab treatment.
Aims:
To investigate a correlation of the platelet activation marker CD62 and secretion of the growth factor PDGF from platelets in coronary patients under therapy with the GPIIb/IIIa-inhibitor abciximab.
Methods:
Flow cytometric assessment of fibrinogen binding (GPIIb/IIIa-binding site) and CD62 expression, as well as PDGF release of human platelets (immunoassay) and platelet aggregation with 20 microM ADP and 2 microg ml(-1) collagen were evaluated in nine patients with stable coronary artery disease. Patients were undergoing elective balloon angioplasty and were treated with aspirin (100 mg day(-1)), heparin (ACT < 220 s) and abciximab (bolus and infusion over 12 h). Blood samples were obtained before initiation of abciximab therapy (under aspirin and heparin) (I), 3 h after angioplasty under abciximab (II) and 12 h after termination of abciximab infusion (III).
Results:
Compared with sample I before abciximab therapy, fibrinogen binding was reduced to 37% (+/- 34 s.d., P < 0.05) (II) and 55% (+/- 40 s.d., P < 0.05) (III). Reduced fibrinogen binding also led to a significant reduction of the aggregation response to ADP (down to 37% +/- 20) and collagen (down to 0%). Mean fluorescence intensity of CD62-expression was 78 units (+/- 20 s.d.) (I), 72 units (+/- 14 s.d.) (II) and 64 units (+/- 12 s.d., P < 0.05) (III). PDGF release from isolated, washed platelets was 99 (+/- 33 s.d.) ng/10(9) platelets at (I), 82 (+/- 31 s.d.) ng/10(9) platelets and 96 (+/- 30 s.d.) ng/10(9) platelets.
Conclusions:
The results indicate that despite a strong reduction of GPIIb/IIIa-binding and platelet aggregation, CD62 as a marker of platelet secretion and the secretion product PDGF were only slightly reduced under abciximab treatment. No direct correlation between CD62 expression and PDGF release could be demonstrated.
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