Glenn N Levine1, Tracy Ferrando. 1. Department of Medicine, Baylor College of Medicine and Section of Cardiology, Houston V.A. Medical Center, Houston, TX 77030, USA. glevine@bcm.tmc.edu
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: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. CONCLUSIONS: 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.
Authors: Dean J Kereiakes; James Tcheng; Edward T A Fry; Deepak L Bhatt; Gideon Bosker; Jose G Diez; James J Ferguson; Glenn N Levine; Gary L Schaer; James Zidar Journal: J Invasive Cardiol Date: 2003-09 Impact factor: 2.022
Authors: J P Collet; G Montalescot; L Lison; R Choussat; A Ankri; G Drobinski; I Sotirov; D Thomas Journal: Circulation Date: 2001-02-06 Impact factor: 29.690
Authors: J Hirsh; T E Warkentin; S G Shaughnessy; S S Anand; J L Halperin; R Raschke; C Granger; E M Ohman; J E Dalen Journal: Chest Date: 2001-01 Impact factor: 9.410
Authors: Rémi Choussat; Gilles Montalescot; Jean Philippe Collet; Eric Vicaut; Annick Ankri; Vanessa Gallois; Gérard Drobinski; Ivan Sotirov; Daniel Thomas Journal: J Am Coll Cardiol Date: 2002-12-04 Impact factor: 24.094
Authors: C P Cannon; W S Weintraub; L A Demopoulos; R Vicari; M J Frey; N Lakkis; F J Neumann; D H Robertson; P T DeLucca; P M DiBattiste; C M Gibson; E Braunwald Journal: N Engl J Med Date: 2001-06-21 Impact factor: 91.245
Authors: James J Ferguson; Elliott M Antman; Eric R Bates; Marc Cohen; Nathan R Every; Robert A Harrington; Carl J Pepine; Pierre Theroux Journal: Am Heart J Date: 2003-10 Impact factor: 4.749
Authors: Nick R Bijsterveld; Arno H Moons; Joost C M Meijers; Marcel Levi; Harry R Büller; Ron J G Peters Journal: J Am Coll Cardiol Date: 2003-08-06 Impact factor: 24.094
Authors: Robert C Welsh; Cynthia M Westerhout; Christopher E Buller; Blair O'Neill; Phillip Gordon; Paul W Armstrong Journal: J Thromb Thrombolysis Date: 2012-07 Impact factor: 2.300
Authors: Jack L Martin; Edward T A Fry; Todd Martin; Trevor H Atherley; Seth S Martin; Marvin J Slepian Journal: J Thromb Thrombolysis Date: 2009-03-17 Impact factor: 2.300