Friday, June 22, 2012


I read with great interest this article coming out of Baltimore, USA, which seemed to suggest an advantage for smokers in treatment of CAD.
Dr Paul Gurbel and colleagues from Sinai Hospital Baltimore, did a re-analysis of the big 6 plavix ( clorpidogrel ) trial in the 90s and 2000s. These included the Caprie, Credo, Cure, Clarity, Charisma, and the Current Oasis 7 trials. They examined these trials from the point of view of comparing the responses of smokers with non-smokers.
Their findings are published in the June 20th, issue of the Journal of the American Medical Association.
They found that during the trial, if they sub-analyse, those who were still smoking at the time of the trial had a better clopidogrel effects when compared to non-smokers. In fact, the clopidogrel effects were largely negated, if you were not smoking, and were no better then aspirin alone.
This findings is a little odd, and yet was quite consistent across the big 6 trials. Is it true that smokers are better protected by clopidogrel and that with non-smokers, we may have to increase the dose or change to another drug? However, as a clinician, I do not see more coronary thrombosis or stent thrombosis in non-smokers. I give them the same plavix ( clopidogrel ).
Obviously, we are not advocating that we should ask CAD patients to start smoking in order to be better protected. The researchers made it a point to this categorically. They just wish us to know this statistical fact and begin to trail and understand why. It is more for further research sake.
I also have the funny notion that this maybe another discrepancy between statistical fact and clinical truth. Say what you like, my non-smokers with DES ( drug eluting stents ), do not get more stent thrombosis. In fact stent thrombosis is so rare now with us, with the second generation DES.
However, I felt that this Plavix Paradox should be documented and perhaps further research done.

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