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Platelet CD62 expression and PDGFAB secretion in patients undergoing PTCA and treatment with abciximab

  1. J. Graff1,
  2. D. Andries1,
  3. M. Elsner2,
  4. D. Westrup4,
  5. S. Bassus3,
  6. N. Franz1,
  7. U. Klinkhardt1,
  8. S. Harder1

Article first published online: 24 JAN 2002

DOI: 10.1046/j.1365-2125.2001.01392.x

Issue

British Journal of Clinical Pharmacology

British Journal of Clinical Pharmacology

Volume 51, Issue 6, pages 577–582, June 2001

Additional Information

How to Cite

Graff, J., Andries, D., Elsner, M., Westrup, D., Bassus, S., Franz, N., Klinkhardt, U. and Harder, S. (2001), Platelet CD62 expression and PDGFAB secretion in patients undergoing PTCA and treatment with abciximab. British Journal of Clinical Pharmacology, 51: 577–582. doi: 10.1046/j.1365-2125.2001.01392.x

Author Information

  1. 1

    Institute of Clinical Pharmacology,

  2. 2

    Department of Cardiology,

  3. 3

    Center for Physiology, Medical School of the J.W. Goethe University, Frankfurt am Main and

  4. 4

    Deutsche Klinik für Diagnostik, Wiesbaden, Germany

* Dr med. Jochen Graff, Institute of Clinical Pharmacology, University Hospital, Frankfurt/Main, Theodor Stern Kai 7, D-60590 Frankfurt am Main, Germany. Tel.: 069/6301–7622; Fax: 069/6301 7636; E-mail: graff@em.uni-frankfurt.de

Publication History

  1. Issue published online: 24 JAN 2002
  2. Article first published online: 24 JAN 2002
  3. Received 14 January 2000,accepted 16 February 2001.

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Keywords:

  • abciximab;
  • P-selectin;
  • platelet derived growth factor

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 µm ADP and 2 µg 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/109 platelets at (I), 82 (± 31 s.d.) ng/109 platelets and 96 (± 30 s.d.) ng/109 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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