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CLINICAL RESEARCH: ACUTE CORONARY SYNDROMES

Administration of eptifibatide to acute coronary syndrome patients receiving enoxaparin or unfractionated heparin

Effect on platelet function and thrombus formation

Eli I. Lev, MD^*, David Hasdai, MD^*, Erez Scapa, MD, Ana Tobar, MD, Abid Assali, MD^*, Judith Lahav, PhD, Alexander Battler, MD^*, Juan J. Badimon, PhD^|| and Ran Kornowski, MD^*,*

^* Cardiology Department, Rabin Medical Center, Israel (affiliated with the Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel)
Department of Medicine "H," Rabin Medical Center, Israel (affiliated with the Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel)
Pathology Department, Rabin Medical Center, Israel (affiliated with the Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel)
Coagulation Laboratory, Rabin Medical Center, Israel (affiliated with the Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel)
^|| Cardiovascular Biology Research Laboratory, the Cardiovascular Institute, Mount Sinai Medical Center, New York, New York, USA

Manuscript received August 19, 2003; accepted September 16, 2003.

^* Reprint requests and correspondence: Dr. Ran Kornowski, Cardiology Department, Rabin Medical Center, 39 Jabotinski St. Petah-Tikva, 49100, Israel.
rkornowski{at}clalit.org.il

OBJECTIVES: The goal of this study was to compare the antithrombotic effects of enoxaparin versus unfractionated heparin (UFH) when combined with eptifibatide in acute coronary syndrome (ACS) patients.

BACKGROUND: An increasing number of high-risk ACS patients are treated with low-molecular-weight heparin and a glycoprotein (GP) IIb/IIIa inhibitor. There is a paucity of data regarding the antithrombotic properties of such a combination as compared with UFH and GP IIb/IIIa inhibitors.

METHODS: Twenty-six ACS patients scheduled to undergo coronary angiography were treated with subcutaneous enoxaparin (n = 13) or intravenous UFH (n = 13). All patients received eptifibatide just before coronary angiography. Antithrombotic effects were assessed as changes in platelet-thrombus formation using the Badimon ex vivo perfusion chamber. Perfusions were carried out at a high shear rate (HSR) and a low shear rate (LSR). Patients underwent two perfusion studies: at baseline (under enoxaparin or UFH) and 10 min after the eptifibatide bolus. Platelet function was evaluated by ADP-induced platelet aggregation and the rapid platelet function analyzer.

RESULTS: Both therapeutic combinations achieved a marked reduction in platelet aggregation after eptifibatide (83% to 89.7% reduction in the enoxaparin-eptifibatide group and 77.8% to 85.5% reduction in the UFH-eptifibatide group, inter-group differences not significant). Both groups also demonstrated marked reductions in thrombus formation, but the reductions achieved in the enoxaparin-eptifibatide group were significantly higher than those achieved in the UFH-eptifibatide group (HSR: 75.6% reduction vs. 63.9%, respectively, p = 0.01; LSR: 79.7% reduction vs. 66.1%, respectively, p = 0.0001).

CONCLUSIONS: The combination of eptifibatide with enoxaparin appears to have a more potent antithrombotic effect than that of eptifibatide and UFH in the doses tested.

Abbreviations and Acronyms   ACS = acute coronary syndrome   ACT = activated clotting time   aPTT = activated partial thromboplastin time   GP = glycoprotein   HSR = high shear rate   LMWH = low-molecular-weight heparin   LSR = low shear rate   MI = myocardial infarction   PCI = percutaneous coronary intervention   RPFA = rapid platelet function analyzer   TAT = thrombin antithrombin complex   UFH = unfractionated heparin