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Department of Anesthesiology, Erasme Hospital, Brussels, Belgium
To the Editor:
I read with great interest the paper of Vaughn et al (1) who presented the PFA® (platelet function analyser) as a device sensitive and useful in the evaluation of platelet inhibition seen with clopidogrel. This is not true. There is good evidence to indicate that the thienopyridines clopidogrel and ticlopidine has similar platelet inhibitory effects (2,3) . A literature search on the National Library of Medicine’s Medline system was performed for the following terms: PFA, clopidogrel, ticlopidine. Two well-conducted studies were identified. Fischetti et al and Kottke-Marchant et al determined platelet function with use of the PFA® in patients receiving aspirin+ticlopidine+heparin (4,5) and glycoprotein inhibitor abciximab (4). In their studies, the PFA® was not significantly affected by ticlopidine when given in conjunction with aspirin. These findings contrasted with earlier observations from ADP-induced platelet aggregation which was significantly inhibited by aspirin+ticlopidine compared to aspirin alone (6,7) . The PFA® is a test cartridge system. The collagen/ADP cartridge has a high local concentration of ADP (50µg adenosine-5’-diphosphate) and this may explain the lack of ticlopidine effect on the PFA® (4). Evidence about the performance of the PFA® in predicting platelet dysfunction associated with clopidogrel therapy is lacking.
References
Department of Anesthesiology, University of Mississippi School of Medicine, Jackson, Mississippi
In Response:
We appreciate Dr. Fattorutto’s interest in our case report and his passion in his opinions. Unfortunately, however, we fail to understand on what basis he draws the conclusion that the PFA-100 is insensitive to platelet dysfunction induced by clopidogrel. Indeed, the studies cited by Dr. Fattorutto support the use of the PFA-100 for this very purpose.
In the Fischetti study (1) the authors do not address the clinical applicability of the PFA-100 as a tool, but rather use it to investigate the phenomenon of platelet aggregation following coronary angioplasty. Fischetti, et al. demonstrate that ticlopidine’s effects on platelet aggregability are detected by the PFA-100. Similarly, the Kottke-Marchant study (2) also examines platelet function in the setting of coronary angioplasty. Although this study is a closer evaluation of the PFA-100 itself, it does not examine the role of ticlopidine as a sole agent to decrease platelet aggregability. To view this study as an indictment of the PFA-100 in this regard is less than objective.
The PFA-100 has not been specifically studied as a tool to assess clopidogrel-induced platelet dysfunction in an ambulatory setting. The vast preponderance of investigation, however, supports the use of the technology as a sensitive and specific tool for the detection of drug-induced platelet dysfunction, including that caused by the thienopyridines (3).
References
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