Heparin or enoxaparin anticoagulation for primary percutaneous coronary intervention.
OBJECTIVE
The aim of this study was to compare efficacy and safety outcomes among patients receiving enoxaparin or unfractionated heparin (UFH) while undergoing percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI).


BACKGROUND
Primary PCI (pPCI) for ST elevation has traditionally been supported by UFH. The low molecular weight heparin enoxaparin may provide better outcomes when used for pPCI.


METHODS
Consecutive eligible patients (580) undergoing pPCI enrolled in the prospective electronic Pitié-Salpêtrière registry of ischemic coronary syndromes (e-PARIS) registry were grouped according to whether they received UFH or enoxaparin as the sole anticoagulant. Logistic regression modeling, propensity-weighted adjustment, and sensitivity analyses were used to evaluate efficacy and safety endpoints for enoxaparin vs. UFH.


RESULTS
Enoxaparin was administered to 346 patients and UFH to 234 without ACT or anti-Xa guided dose adjustment. PCI was performed through the radial artery in 90%, with frequent (75%) use of GPIIb/IIIa antagonists. Patients receiving enoxaparin were more likely to be therapeutically anticoagulated during the procedure (68% vs. 50%, P < 0.0001) and were less likely to experience death or recurrent myocardial infarction (MI) in hospital (adjusted OR 0.28 95% CI (0.12-0.68) or by 30 days (adjusted OR 0.35 95% CI 0.16-0.81). All cause mortality was also reduced in hospital (adjusted OR 0.32, 95% CI (0.12-0.85) and to 30 days (adjusted OR 0.40 95% CI 0.17-0.99). Other ischemic endpoints were similarly reduced with enoxaparin. Thrombolysis in myocardial infarction (TIMI) major bleeding events were numerically fewer among patients receiving enoxaparin (1.2% vs. 2.6%, P = 0.2).


CONCLUSIONS
In patients with STEMI presenting for PCI, enoxaparin was associated with a reduction in all ischemic complications, more frequent therapeutic anticoagulation, and no increase in major bleeding when compared against unfractionated heparin. © 2010 Wiley-Liss, Inc.
Brieger
David
D
Department of Cardiology, Concord Hospital, University of Sydney, Sydney, Australia.
Collet
Jean-Philippe
JP
Silvain
Johanne
J
Landivier
Antoine
A
Barthélémy
Olivier
O
Beygui
Farzin
F
Bellemain-Appaix
Anne
A
Mercadier
Anne
A
Choussat
Remi
R
Vignolles
Nicolas
N
Costagliola
Dominique
D
Montalescot
Gilles
G
D000368:Aged; D000704:Analysis of Variance; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects / Q000401:mortality; D000925:Anticoagulants / Q000009:adverse effects / Q000627:therapeutic use*; D016009:Chi-Square Distribution; D017984:Enoxaparin / Q000009:adverse effects / Q000627:therapeutic use*; D005260:Female; D006470:Hemorrhage / Q000139:chemically induced / Q000517:prevention & control; D006493:Heparin / Q000009:adverse effects / Q000627:therapeutic use*; D017052:Hospital Mortality; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000401:mortality / Q000628:therapy*; D016017:Odds Ratio; D010297:Paris; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D057216:Propensity Score; D011446:Prospective Studies; D012042:Registries; D018570:Risk Assessment; D012307:Risk Factors; D055502:Secondary Prevention; D013997:Time Factors; D016896:Treatment Outcome
D000925:Anticoagulants; D017984:Enoxaparin; D010975:Platelet Aggregation Inhibitors; D006493:Heparin