So far, only one LMWH has demonstrated superior results to UFH when treating UA. A meta-analysis of data from 5 major trials (ESSENCE, TIMI 11B, FRIC, FRISC, and FRAXIS) showed that enoxaparin gives better results than UFH for treating all groups of UA/NQWMI patients with regard to the composite end point of death, MI, and the need for revascularization, without increasing the risk of major bleeding (63). The meta-analysis showed that neither dalteparin nor nadroparin were superior to UFH for treating ACS patients, although equivalence was demonstrated with dalteparin in the FRIC study (48). Moreover, a direct comparison of the efficacy and safety of enoxaparin and tinzaparin in the EVET study (55) showed that enoxaparin is more effective in reducing both the incidence of recurrent angina at 7 d and the need for revascularization at 30 d in UA/NQWMI patients. This benefit is achieved without increasing bleeding complications. The multicenter, ARMADA study (64) evaluated the effects of enoxaparin, dal-teparin, and UFH on von Willebrand factor and platelet activation (both predictors of adverse outcome) in UA/NQWMI patients. In agreement with earlier studies, enoxa-parin and dalteparin blunted the rise of von Willebrand factor when compared with UFH, although the greater effect of enoxaparin on this factor was not confirmed. At 30 d, the incidences of clinical events were 13.0 and 18.8% for enoxaparin and dalteparin, respectively, compared to 27.7% for UFH. The study also showed that platelet GPIb/IX receptor (von Willebrand receptor) expression might also be associated with outcome in this patient group and that the highest GPIb/IX receptor expression was seen with enoxaparin. In addition, differential effects on tissue factor were also noted.
Montalescot et al. (65) have hypothesized that the control of von Willebrand factor, in light of its being a predictor of clinical outcome in UA, may relate to the effectiveness of anticoagulation, and that the degree of control may differ between the anticoagulants evaluated in UA. To test their hypothesis, they studied 154 patients with UA or NQWMI enrolled in a variety of clinical trials assessing anticoagulant treatments. In these studies, UFH, enoxaparin, and dalteparin were used to treat patients for a minimum of 48 h. Their findings confirmed that in patients with UA, a rise in von Willebrand factor over the initial 48 h is associated with impaired outcome at 30 d. They found that the early rise in von Willebrand factor seen in UA patients treated with UFH is less if treatment is undertaken with enoxaparin. However, such an early rise in von Willebrand factor was found to be minimally reduced by dalteparin. The authors concluded that this may be an explanation for the superiority noted with enoxaparin in clinical trials.
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