CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Laurent Bonello, MD*,
Laurence Camoin-Jau, MD, PhD,
Arques Stephane, MD,
Paul Barragan, MD,
Francoise Dignat-George, PhD and
Franck Paganelli, MD
* Hopital universitaire nord de Marseille, Departement de cardiologie, Chemin des bourrely, Marseille, PACA 13015 France (Email: laurentbonello{at}yahoo.fr).
We thank Dr. Aradi and colleagues for their interest in our work (1). Our recently published trial is a pilot study that aimed to demonstrate that platelet monitoring of response to thienopyridines offers the promise of an improved outcome in patients undergoing percutaneous coronary intervention (PCI). Additional studies are needed to confirm those preliminary results and to determine which strategy of loading dose (LD) should be used. Thus, the present strategy of platelet reactivity (PR) monitoring and clopidogrel LD should not be used in clinical practice until further validation is reported.
As Dr. Aradi and colleagues highlighted, one potential limitation of the present strategy of clopidogrel LD adjustment is the time required to tailor the LD to platelet monitoring. However, it must be noted that most patients in the vasodilator-stimulated phosphoprotein-guided group had PCI after the second LD and therefore underwent PCI within 48 h of admission. The optimal delay between clopidogrel LD intakes should be defined by future studies to further reduce the time required for adjustment before PCI. Finally, a new P2Y12 adenosine diphosphate receptor that induces greater and faster PR inhibition may be particularly interesting in those subjects to limit the time required before PCI.
As stated by Dr. Aradi and colleagues, stable angina or low-risk acute coronary syndrome patients have a small risk of adverse events following PCI. However, reduced thrombotic events still occur in such patients. The clinical impact of clopidogrel in these low-risk patients is well established and therefore, the lack of efficacy of the drug may be as critical as in other settings (2,3). In addition, the link between PR and recurrent ischemic events after PCI is demonstrated in stable patients similarly to unstable patients (4). As pointed out by Dr. Aradi and colleagues, the peri-intervention level of PR inhibition may be more important than the time of clopidogrel loading. We believe that the teaching of our study is the clinical impact of a tailored dose of clopidogrel to obtain a sufficient degree of PR inhibition peri-intervention in order to decrease post-procedural thrombotic events. Accordingly, the number of acute events is low and may offer the possibility of post-intervention adjustment (1 acute stent thrombosis). Finally, the frequency of clopidogrel low response is by far less frequent in stable patients compared with unstable patients, which may account for their reduced rate of events. Furthermore, the low risk of thrombotic events after PCI may well be a limit to conduct specific studies on stable patients that would need a large number of patients to be properly powered. Finally, the low number of patients included in the present study prevents any subgroup analysis to assess the impact of LD adjustment in stable patients.
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References
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1. Bonello L, Camoin-Jau L, Arques S, et al. Adjusted clopidogrel loading doses according to vasodilator-stimulated phosphoprotein phosphorylation index decrease rate of major adverse cardiovascular events in patients with clopidogrel resistance: a multicenter randomized prospective study J Am Coll Cardiol 2008;51:1404-1411.[Abstract/Free Full Text]2. Steinhubl SR, Berger PB, Mann 3rd JT, et al. CREDO Investigators Clopidogrel for the Reduction of Events During Observation. Early and sustained dual oral antiplatelet therapy following percutaneous coronary intervention: a randomized controlled trial JAMA 2002;288:2411-2420.[Abstract/Free Full Text] 3. Bertrand ME, Legrand V, Boland J, et al. Randomized multicenter comparison of conventional anticoagulation versus antiplatelet therapy in unplanned and elective coronary stenting. The Full Anticoagulation Versus Aspirin and Ticlopidine (FANTASTIC) study. Circulation 1998;98:1597-1603.[Abstract/Free Full Text] 4. Barragan P, Bouvier JL, Roquebert PO, et al. Resistance to thienopyridines: clinical detection of coronary stent thrombosis by monitoring of vasodilator-stimulated phosphoprotein phosphorylation Catheter Cardiovasc Interv 2003;59:295-302.[CrossRef][Web of Science][Medline]
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Optimizing Clopidogrel Therapy Before Stent Implantation: Should Clinical Setting Be Taken Into Account?
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J. Am. Coll. Cardiol. 2008 52: 1349.
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