The use of unfractionated heparin, the traditional antithrombotic agent during percutaneous
coronary interventions (PCI), is associated with the risk of heparin-induced thrombocytopenia,
a rare but often fatal clinical condition. This article focuses on several issues
related to heparin-induced immune-mediated thrombocytopenia (HIT, type II) and alternative
modes of periprocedural anticoagulation in patients with suspected or known HIT.
The hypercoagulable state characterizing HIT, along with mechanical plaque disruption
resulting from PCI place patients with HIT at particular risk of thrombosis during
PCI. Given that a diagnosis of HIT precludes any further use of heparin, other treatment
modalities are essential. Direct thrombin inhibitors are the drugs of choice in this
challenging situation. These agents offer several advantages as anticoagulants for
patients with HIT: (1) the ability to inhibit both thrombin that is bound to fibrin
(clot-bound thrombin) and fluid-phase free thrombin; (2) rapid achievement of steady
state; and (3) no cross-reactivity with HIT antibodies. Recent data on the use of
bivalirudin, lepirudin, and argatroban in the setting of PCI in patients with HIT
are encouraging. Optimal dosing regimens for argatroban, lepirudin, and bivalirudin
should be further established in PCI patients.
KEYWORDS
Heparin - thrombocytopenia - direct thrombin inhibitors - heparin-induced thrombocytopenia
- HIT
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George D DangasM.D. Ph.D.
Cardiovascular Research Foundation
55 E. 59th Street, 6th Floor
New York, NY 10022
Email: gdangas@crf.org