as measured through the activated partial thromboplas- tin time (aPTT). Institutions vary considerably regarding reference values and dose adjustment procedures. Sev- eral approaches have been used to counteract this limi- tation, either by more frequent aPTT monitoring or by adopting a single nomogram for dose adjustment. Despite such approaches and the availability of state-of- the-art devices for aPTT measurement, several studies during the last 5 years have consistently showed that less than 55% of the population treated with UFH achieve a specified target aPTT level, usually after at least 48 hours of therapy. 4 Several studies have shown the clinical efficacy of low- molecular-weight heparin. Gurfinkel et al 5 published the first clinical evidence that low-molecular-weight heparin could be more effective than conventional therapy with UFH. These findings on safety and efficacy have been tested and validated with enoxaparin in the Efficacy and Unfractionated heparin (UFH) has been the treatment of choice for patients with an acute coronary syndrome for almost 20 years. 1 Its combination with aspirin repre- sents a rational therapeutic approach to the thrombotic process underlying unstable angina (UA) and non-Q- wave myocardial infarction. 2,3 Yet the use of UFH has a number of drawbacks, most important of which is the difficulty in obtaining a target level of anticoagulation, From the a Favaloro Foundation, Buenos Aires, and b Brigham and Women’s Hospi- tal, Boston. Supported by a research grant from Rhône-Poulenc Rorer (Collegeville, Pa), now Aventis Pharma. Submitted February 11, 2000; accepted July 5, 2000. Reprint requests: Gerardo E. Bozovich, MD, Coronary Unit, Favaloro Foundation, Av Belgrano 1746, 1093 Buenos Aires, Argentina. E-mail: bozovich@impsat1.com.ar Copyright © 2000 by Mosby, Inc. 0002-8703/2000/$12.00 + 0 4/1/109921 doi:10.1067/mhj.2000.109921 Acute Ischemic Heart Disease Superiority of enoxaparin versus unfractionated heparin for unstable angina/non-Q-wave myocardial infarction regardless of activated partial thromboplastin time Gerardo E. Bozovich, MD, a Enrique P. Gurfinkel, MD, PhD, b Elliott M. Antman, MD, b Carolyn H. McCabe, BS, b and Branco Mautner, MD, a for the TIMI 11B investigators Buenos Aires, Argentina, and Boston, Mass Background Whether the clinical superiority of enoxaparin versus unfractionated heparin (UFH) depends on a more stable antithrombotic effect or the proportion of patients not reaching the therapeutic level with UFH has not been addressed. Methods All patients participating in the Thrombolysis In Myocardial Infarction 11B trial who received UFH and had sufficient activated partial thromboplastin time (aPTT) data (n = 1893) were compared with patients who received enoxa- parin (n = 1938). Patients receiving UFH were divided into 3 categories depending on mean aPTT values throughout 48 hours: subtherapeutic, for those in whom the average aPTT fell below 55 seconds; therapeutic, between 55 and 85 sec- onds; and supratherapeutic, longer than 85 seconds. Events and bleeding rates were determined at 48 hours. Results A small portion of patients (6.7%) had a subtherapeutic average aPTT value (n = 127). Forty-seven percent of patients (n = 891) fell within the therapeutic range, and 46% were in the supratherapeutic level (n = 875). Event rates were 7.0% in the UFH group versus 5.4% with enoxaparin (P = .039). Events rates were higher in every aPTT strata compared with enoxaparin and statistically significant in the supratherapeutic group (odds ratio 0.65; 95% confidence interval, 0.47- 0.89). Major bleeding rates were 0%, 0.6%, and 0.9% for the subtherapeutic, target, and supratherapeutic strata, respec- tively, and 0.8% with enoxaparin. Minor hemorrhages occurred in 5.1% of patients receiving enoxaparin versus 3.9%, 2%, and 2.3%, respectively, for the UFH subgroups (P < .001 for all UFH groups vs enoxaparin). Conclusions Enoxaparin showed a better clinical profile compared with every level of anticoagulation with UFH. Potential mechanisms for enoxaparin superiority are stable antithrombotic activity, lack of rebound thrombosis, and intrinsic superiority. (Am Heart J 2000;140:637-42.)