title: Anti-Xa activity relates to survival and efficacy in unselected acute coronary syndrome patients treated with enoxaparin.
abstract: BACKGROUND
  Low-molecular-weight heparin (LMWH) is recommended in the treatment of unstable angina (UA)/non-ST-segment-elevation myocardial infarction (NSTEMI), but no relationship has ever been shown between anticoagulation levels obtained with LMWH treatment and clinical outcomes.
  
  
  RESULTS
  In all, 803 consecutive patients with UA/NSTEMI were treated with subcutaneous enoxaparin and were followed up for 30 days. The recommended dose of enoxaparin of 1 mg/kg BID was used throughout the population except when physicians decided on dose reduction because of a history of a recent bleeding event or because of a high bleeding risk. Anti-factor Xa activity was >0.5 IU/mL in 93% of patients; subtherapeutic anti-Xa levels (<0.5 IU/mL) were associated with lower doses of enoxaparin. The 30-day mortality rate was significantly associated with low anti-Xa levels (<0.5 IU/mL), with a >3-fold increase in mortality compared with the patients with anti-Xa levels in the target range of 0.5 to 1.2 IU/mL (P=0.004). Multivariate analysis revealed low anti-Xa activity as an independent predictor of 30-day mortality at least as strong as age, left ventricular function, and renal function. In contrast, anti-Xa activity did not predict major bleeding complications within the range of anti-Xa levels observed in this study.
  
  
  CONCLUSIONS
  In this large unselected cohort of patients with UA/NSTEMI patients, low anti-Xa activity on enoxaparin treatment is independently associated with 30-day mortality, which highlights the need for achieving at least the minimum prescribed anti-Xa level of 0.5 IU/mL with enoxaparin whenever possible.
authors.affiliation: Institut de Cardiologie, Pitié-Salpêtrière Hospital, Paris, France. gilles.montalescot@psl.ap-hop-paris.fr
authors.forename: G
authors.initials: G
authors.lastname: Montalescot
authors.forename: J P
authors.initials: JP
authors.lastname: Collet
authors.forename: M L
authors.initials: ML
authors.lastname: Tanguy
authors.forename: A
authors.initials: A
authors.lastname: Ankri
authors.forename: L
authors.initials: L
authors.lastname: Payot
authors.forename: R
authors.initials: R
authors.lastname: Dumaine
authors.forename: R
authors.initials: R
authors.lastname: Choussat
authors.forename: F
authors.initials: F
authors.lastname: Beygui
authors.forename: V
authors.initials: V
authors.lastname: Gallois
authors.forename: D
authors.initials: D
authors.lastname: Thomas
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000188:drug therapy* / Q000401:mortality / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D000925:Anticoagulants / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D015415:Biomarkers; D006328:Cardiac Catheterization; D000077144:Clopidogrel; D015331:Cohort Studies; D003131:Combined Modality Therapy; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D004359:Drug Therapy, Combination; D017984:Enoxaparin / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D065427:Factor Xa Inhibitors; D005260:Female; D005500:Follow-Up Studies; D006470:Hemorrhage / Q000139:chemically induced / Q000453:epidemiology; D006801:Humans; D007527:Isoenzymes / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy* / Q000401:mortality / Q000628:therapy; D011446:Prospective Studies; D016019:Survival Analysis; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood
chemical_list: D000925:Anticoagulants; D015415:Biomarkers; D017984:Enoxaparin; D065427:Factor Xa Inhibitors; D007527:Isoenzymes; D019210:Troponin I; D000077144:Clopidogrel; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form; D013988:Ticlopidine