Enoxaparin significantly reduced the early increase of von Willebrand factor over 48 hours compared with unfractionated heparin (+8.7% vs +93.9%; P<0.0001).
RCT (n=68)
randomized
Yes
Does enoxaparin reduce the early rise of von Willebrand factor and adverse clinical outcomes compared to unfractionated heparin in patients with unstable angina or non-Q-wave myocardial infarction?
In patients with unstable angina or non-Q-wave myocardial infarction, enoxaparin blunts the early rise of von Willebrand factor compared to unfractionated heparin, which correlates with improved clinical outcomes.
Absolute Event Rate: 8.7% vs 93.9%
p-value: p=<0.0001
BACKGROUND: The pathogenesis of unstable angina and non-Q-wave myocardial infarction is still poorly understood, and early evaluation of prognosis remains difficult. We therefore studied the predictive value of 5 biological indicators of inflammation, thrombogenesis, vasoconstriction, and myocardial necrosis, and we examined the effects of enoxaparin and unfractionated heparin on these markers after 48 hours of treatment. METHODS AND RESULTS: Sixty-eight patients with unstable angina or non-Q-wave myocardial infarction randomized in the international ESSENCE trial participated in this French substudy. C-reactive protein, fibrinogen, von Willebrand factor antigen, endothelin-1 and troponin I were measured on admission and 48 hours later. The composite end point of death, myocardial infarction, recurrent angina, or revascularization was significantly lower at 14 and 30 days of follow-up in patients allocated to enoxaparin compared with unfractionated heparin. All acute-phase reactant proteins were elevated on admission and increased further at 48 hours. Multivariate analysis demonstrated that the rise of von Willebrand factor over 48 hours was a significant and independent predictor of the composite end point at both 14 days and 30 days. Moreover the early increase of von Willebrand factor was more frequent and more severe with unfractionated heparin than with enoxaparin (mean change was +8.7+/-8.8% with enoxaparin versus +93.9+/-11.7% with unfractionated heparin, P<0.0001). The other clinical and biological variables did not predict outcome. CONCLUSIONS: In patients with unstable angina or non-Q-wave myocardial infarction, the acute-phase proteins increase over the first 2 days despite medical treatment. The early rise of von Willebrand factor is an independent predictor of adverse clinical outcome at 14 days and at 30 days. Enoxaparin provides protection as evidenced by the reduced release of von Willebrand factor, which represents a favorable prognostic finding.
Montalescot et al. (1998) conducted an RCT in unstable angina or non-Q-wave myocardial infarction (n=68). Enoxaparin vs. Unfractionated heparin was evaluated on Mean change in von Willebrand factor over 48 hours (p=<0.0001). Enoxaparin significantly reduced the early increase of von Willebrand factor over 48 hours compared with unfractionated heparin (+8.7% vs +93.9%; P<0.0001).