title: Subcutaneous enoxaparin with early invasive strategy in patients with acute coronary syndromes.
abstract: BACKGROUND
  Subcutaneous enoxaparin during at least 48 hours provides adequate anticoagulation and good clinical results in patients with non-ST-segment elevation acute coronary syndromes undergoing percutaneous coronary intervention (PCI).
  
  
  METHODS
  In this nonrandomized retrospective study, we compared 347 patients with non-ST-segment elevation acute coronary syndromes who underwent rapid PCI after only 2 injections of subcutaneous enoxaparin (EI, n = 117) to those referred later to the catheterization laboratory with >or=3 injections (DI, n = 230). We measured anti-Xa at the time of PCI and evaluated bleeding and major ischemic events (death/myocardial infarction) at 30 days.
  
  
  RESULTS
  Patients in the EI group more frequently received glycoprotein IIb/IIIa inhibitors and clopidogrel preceding PCI than did patients in the DI group (58.1% vs 31.7%, P <.0001 for glycoprotein IIb/IIIa inhibitors and 68.4% vs 40.4% for clopidogrel pretreatment, P <.0001, respectively). The anti-Xa activity measured at the time of catheterization (0.92 +/- 0.04 U/mL vs 0.96 +/- 0.02 U/mL, EI vs DI, P =.25) and the injection-to-catheterization times (5.6 +/- 0.2 h vs 5.2 +/- 0.1 h, EI vs DI, P =.17) were similar in both groups. The 30-day bleeding rates of 1.7% and 4.8% in the EI and DI strategies were found to be equivalent with a significant non-inferiority test for the EI strategy (P <.05). There was a nonsignificant trend for less death or myocardial infarction at 30 days in the EI group compared to the DI group (4.3% vs 7.0%, non-inferiority test not significant).
  
  
  CONCLUSIONS
  A rapid invasive strategy with only 2 subcutaneous injections of enoxaparin provides similar levels of anticoagulation, and is associated with a favorable trend for ischemic events and with safety equivalent to a more prolonged "upstream" treatment with enoxaparin.
authors.affiliation: Department of Cardiology, Pitié-Salpêtrière Hospital, Paris, France.
authors.forename: J P
authors.initials: JP
authors.lastname: Collet
authors.forename: G
authors.initials: G
authors.lastname: Montalescot
authors.forename: J L
authors.initials: JL
authors.lastname: Golmard
authors.forename: M L
authors.initials: ML
authors.lastname: Tanguy
authors.forename: A
authors.initials: A
authors.lastname: Ankri
authors.forename: R
authors.initials: R
authors.lastname: Choussat
authors.forename: F
authors.initials: F
authors.lastname: Beygui
authors.forename: G
authors.initials: G
authors.lastname: Drobinski
authors.forename: N
authors.initials: N
authors.lastname: Vignolles
authors.forename: D
authors.initials: D
authors.lastname: Thomas
mesh_terms: D000704:Analysis of Variance; D000789:Angina, Unstable / Q000401:mortality / Q000628:therapy*; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D000925:Anticoagulants / Q000008:administration & dosage* / Q000009:adverse effects / Q000627:therapeutic use; D006328:Cardiac Catheterization; D000077144:Clopidogrel; D004334:Drug Administration Schedule; D017984:Enoxaparin / Q000008:administration & dosage* / Q000009:adverse effects / Q000627:therapeutic use; D006470:Hemorrhage / Q000139:chemically induced; D006801:Humans; D007279:Injections, Subcutaneous; D016015:Logistic Models; D008875:Middle Aged; D009203:Myocardial Infarction / Q000401:mortality / Q000628:therapy*; D017202:Myocardial Ischemia / Q000209:etiology; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D011292:Premedication / Q000009:adverse effects; D012189:Retrospective Studies; D012307:Risk Factors; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D000925:Anticoagulants; D017984:Enoxaparin; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000077144:Clopidogrel; D013988:Ticlopidine