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(Circulation. 2000;101:e241.)
© 2000 American Heart Association, Inc.

Circulation Electronic Pages

Thrombocytopenia and Glycoprotein IIb/IIIa Inhibitors: Causation or Association?

Michael Poullis, BSc (Hons), MBBS, FRCS (Eng)

Department of Cardiothoracic Surgery National Heart and Lung Institute, Imperial College of Science, Technology, and Medicine, Hammersmith Hospital, Du Cane Road, East Acton, London W12 0NN, United Kingdom, mpoullis@rpms.ac.uk

Iqbal Malik, BSc(Hons), MBBS, MRCP

Department of Cardiology National Heart and Lung Institute

	Introduction

 
To the Editor:

Trials of glycoprotein IIb/IIIa inhibitors (GPI) in acute coronary syndromes (ACS) reveal that thrombocytopenia occurs with an incidence of up to 3.7%.¹ McClure et al² confirm the association of thrombocytopenia and ACS and correlate this with adverse bleeding and ischemic events. However, unlike previous studies, they found no association between GPI and thrombocytopenia.³ Understanding the mechanism of thrombocytopenia may aid in resolving this discrepancy.

The method of platelet count determination may help identify the mechanism of the thrombocytopenia. Platelet counts are determined by techniques that rely on their size. A gate is set, above which platelets are not included in the count, even when present. This forms the basis for detecting microaggregation.⁴ Many modern hematological analyzers provide a size histogram for platelets that extends beyond the counting gate. This enables "true" thrombocytopenia to be differentiated from "microaggregation thrombocytopenia."

Microaggregation is important because unstable angina can cause platelet activation via P-selectin and other inflammatory mediators. Thus, the thrombocytopenia may represent an extensive inflammatory response causing secondary platelet activation.

Thrombocytopenia per se (eg, idiopathic thrombocytopenia) does not increase the incidence of acute coronary events, but it does increase bleeding complications. However, thrombocytopenia in the presence of microaggregation (eg, thrombotic thrombocytopenia purpura and antiphospholipid syndrome) is associated with both bleeding and thrombotic complications, including acute coronary events.

Possible mechanisms of GPI-induced thrombocytopenia include the following: (1) the inhibition of megakaryocytes expressing glycoprotein IIb/IIIa receptors⁵ (this is unlikely because platelet half-life is 10 days and ACS thrombocytopenia usually occurs within 48 . . . [Full Text of this Article]