LETTER TO THE EDITOR
Reply
Gilles Montalescot, MDa
a Department of Cardiology, Centre Hospitalier, Universitaire Pitie-Salpetriere, 47 Boulevard de l’Hopital, 75013 Paris France
gilles.montalescot{at}psl.ap-hop-paris.fr
Interestingly, Dr. Hödl has focused his attention only on the two low molecular weight heparin (LMWH) treatments, whereas four anticoagulant treatments were examined in our study. Clearly, Dr. Hödl drew more definite conclusions than we did between the two LMWHs, because we were cautious enough not to compare dalteparin to enoxaparin (see Fig. 1 in Ref. 1), and we only compared each new anticoagulant treatment (enoxaparin, dalteparin, PEG-hirudin) to the standard of care—unfractionated heparin (UH) (1). Also, UH was the control arm in all the randomized studies in which our patients were included. Moreover, Dr. Hödl did not consider our warning (pg. 113 of Ref. 1) stating that "the main limitation of our study is the lack of randomization among the four treatment groups."
Dr. Hödl discussed post hoc analyses but forgot to mention and to refer to the first demonstration of von Willebrand factor (vWf) as a prognosis factor of outcome in unstable angina with a significantly better effect of enoxaparin compared to UH in controlling the release of vWf. These data were obtained in a prespecified substudy of the ESSENCE trial performed in several French centers; in a double-blind fashion, patients were randomized to receive either enoxaparin or UH. All clinical events were adjudicated by the end point committee of the ESSENCE trial; the substudy was designed and conducted prospectively, and all samples from all centers were analyzed in a blinded fashion in a central laboratory (2). Dr. Hödl suggests using data from the randomized FRIC trial opposing dalteparin to UH, which was published in 1997 (3); we would be very happy to collaborate with him on this great idea and test the vWf hypothesis in the FRIC population. Paradoxically, Dr. Hödl also states that the "proper" way to analyze our data would have been to pool all the data obtained with the two different LMWHs; major chemical, biological and clinical differences exist between these LMWHs, and there has been much debate on this issue. We believe that pooling these data would have generated many more letters to the editor!
There are few biological markers of prognosis in unstable angina. Our recent studies have focused attention on vWf as a new marker of potential interest in acute coronary syndromes. It appeared consistently as a predictive factor of outcome, and we believe it deserves attention and further evaluation in large studies. Our most recent publication demonstrated that the new anticoagulants tested in unstable angina behave better than UH with regards to vWf release. We agree it should also be confirmed. Step-by-step we are progressing in the understanding of the role of vWf in the prognosis of unstable angina, and the time has come for head-to-head comparisons between the new anticoagulant treatments. In that regard, the ARMADA study has now been completed and we will share the data very soon. I am sure that Dr. Hödl will appreciate the results.
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References
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1. Montalescot G, Collet JP, Lison L, et al. Effects of various anticoagulant treatments on von Willebrand factor release in unstable angina. J Am Coll Cardiol. 2000;36:110–114[Abstract/Free Full Text]
2. Montalescot G, Philippe F, Ankri A, et al. Early increase of von Willebrand factor predicts adverse outcome in unstable coronary artery disease: beneficial effects of enoxaparin. Circulation. 1998;98:287–289[Free Full Text]
3. Klein W, Buchwald A, Hillis SE, et al. Comparison of low-molecular-weight heparin with unfractionated heparin acutely and with placebo for 6 weeks in the management of unstable coronary artery disease. Fragmin in unstable coronary artery disease study (FRIC). Circulation. 1997;96:61–68[Abstract/Free Full Text]
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