Degree of anticoagulation after one subcutaneous and one subsequent intravenous booster dose of enoxaparin: implications for patients with acute coronary syndromes undergoing early percutaneous coronary intervention.

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Many cardiologists continue to be reluctant to utilize low-molecular-weight heparin in the treatment of patients with non-ST-segment-elevation acute coronary syndrome because they are concerned about how to manage such patients if they have received only one dose of subcutaneous enoxaparin and are then taken within hours of such treatment to the cardiac catheterization laboratory for percutaneous coronary intervention (PCI). Although we and others have recommended that such patients who have received only one subcutaneous enoxaparin dose receive an intravenous 0.3 mg/kg enoxaparin "booster" dose immediately prior to PCI, there are little actual data to support this recommendation. 20 middle-aged subjects were treated with 1 mg/kg subcutaneously-administered enoxaparin and then 6 hours later with a "booster" dose of 0.3 mg/kg intravenously-administered enoxaparin. Anti-Xa levels, as well as ENOX Times, were assessed at baseline, at 2, 4 and 6 hours after the initial SC dose, and at 5 min, 1 and 2 hours after the IV booster dose. At 2 and 6 hours after the initial subcutaneous enoxaparin dose, thirty-five percent of patients had anti-Xa levels below 0.6 IU/mL; twenty percent and ten percent had anti-Xa levels below 0.5 IU/mL at 2 and 6 hours after the initial subcutaneous dose, respectively. After the IV booster dose, all patients had anti-Xa levels in the therapeutic range during the 5 minutes to 2 hours during which blood samples were obtained. There was no significant "overshoot" with this booster dose above what is considered to be the upper therapeutic range. ENOX times showed an overall moderate correlation with anti-Xa levels. A strategy of administering a 0.3 mg/kg IV booster dose to patients who have received only one subcutaneous dose of enoxaparin and then undergo PCI within the first 2-6 hours of such treatment reliably leads to anti-Xa levels in the therapeutic range.