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J Am Coll Cardiol, 1999; 34:1420-1426
© 1999 by the American College of Cardiology Foundation
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CLINICAL STUDIES

Effect of glycoprotein IIb/IIIa receptor blockade on platelet-leukocyte interaction and surface expression of the leukocyte integrin Mac-1 in acute myocardial infarction

Franz-Josef Neumann, MDa, Dietlind Zohlnhöfer, MDa, Leila Fakhoury, MDa, Ilka Ott, MDa, Meinrad Gawaz, MDa and Albert Schömig, MDa

a Deutsches Herzzentrum and 1. Medizinische Klinik der Technischen Universität München, Munich, Germany

Manuscript received January 14, 1999; revised manuscript received May 20, 1999, accepted June 28, 1999.

Reprint requests and correspondence: Dr. Franz-Josef Neumann, Deutsches Herzzentrum an der Technischen Universität, Lazarettstr. 36, 81636 München, Germany.
neumann{at}dhm.mhn.de

OBJECTIVES

This prospective randomized study investigated platelet-induced upregulation of Mac-1 on monocytes and its inhibition by glycoprotein (GP) IIb/IIIa blockage in patients with acute myocardial infarction (AMI).

BACKGROUND

In experimental AMI, Mac-1 on leukocytes is the pivotal adhesion molecule for detrimental inflammatory responses. In vitro, platelet adhesion to monocytes upregulates Mac-1.

METHODS

Patients undergoing stenting in AMI within 48 h after onset of symptoms were randomly assigned to receive either standard-dose heparin (n = 50) or abciximab plus low-dose heparin (n = 50). In serial blood samples, we assessed platelet-monocyte interaction and Mac-1 surface expression by triple color immunofluorescence flow cytometry.

RESULTS

Compared with platelet-negative monocytes, Mac-1 surface expression on monocytes with attached platelets was upregulated (median fluorescence intensity [interquartile range]: 259 [179 to 367] vs. 135 [78 to 195] arbitrary units, p < 0.001). As an indicator of platelet-monocyte interaction, mean fluorescence of the platelet marker GP Ib{alpha} in the monocytes population decreased after abciximab, although it remained unaffected by heparin alone. Abciximab achieved this effect by a reduction in platelet mass attached to monocytes (GP Ib{alpha} fluorescence intensity of heterotypic aggregates at 24 h [arbitrary units]: 187 [143 to 236] after abciximab vs. 228 [156 to 332] after heparin, p = 0.02), whereas it did not affect the percentage of monocytes with adherent platelets. Reduction of platelet-monocyte interaction resulted in decreased Mac-1 surface expression (fluorescence intensity at 24 h [arbitrary units]: 116 [68 to 153] after abciximab vs. 162 [117 to 239] after heparin, p = 0.001).

CONCLUSIONS

In patients with AMI, platelet-leukocyte interactions modulate Mac-1 expression on monocytes. Glycoprotein IIb/IIIa blockade is a therapeutic option to interfere with this mechanism.

Abbreviations and Acronyms
  AMI = acute myocardial infarction
  FITC = fluoresceine isothiocyanate
  GP = glycoprotein
  mAbs = monoclonal antibodies
  PBS = phosphate buffered saline
  PE = phycoerythrine
  PSGL = P-selectin glycoprotein ligand




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