Smoking is known to produce hyper reactive platelets but smoking also enhances action of clopidogrel.. Read more. Syndicated from HOTM.
Much has been said repeatedly, that smoking is a no, no, and bad for just about every aspect of our health. And that is true. Smoking obviously does more harm than good. Recently, I read an interesting article on a potential benefit of smoking. In the Aug 12th issue of the J of the American College of Cardiology, Dr Bliden and colleagues from the Sinai Thrombosis Research Center, Baltimore, published their findings in a small study of 259 patients, smokers who were on plavix to see the effects of smoking on platelet function, in these patients. They found that smoking seem to induce some enzymes in the CYP450 system, specifically CYP1A2, to enhance the conversion of clopidogrel to its active metabolite, thereby enhancing the action of clopidogrel. Interesting. In other words, smokers who are also on clopidogrel, have enhance platelet inhibition and so less thrombotic tendency. Apparently, when they reviewed the literature, they found that there was already a hint of this in the larger clopidogrel studies like CREDO, CLARITY, etc. However, I must caution that this is not a prospective randomised study and the numbers are small. Although it may be hypothesis generating and something for us to study further, who smokers should not think that their blood is thinner and so they are less likely to have heart attacks. THAT IS NOT WHAT I MEAN. It is possible that smokers on Plavix, maybe less likely to have a thrombotic event. I think that this theory, merits further study. Be that as it may, we cannot go out there and tell patients with DES to continue smoking and taking plavix, in the hope that they get less DES stent thrombosis. That is an obvious NO,NO. Whatever it is, patients with thrombotic diseases or vascular disease should stop smoking to prevent vascular events, Plavix or not.
The second point that I wish to raise is that Plavix is a pro-drug that needs to be activated via the CYP450 pathway, thereby making it vulnerable to all kinds of potential drug-drug interaction. Omeperazole for example may slow down the activation of Plavix, thereby causing it to be less effective. This is important because, we often use Plavix as an alternative to aspirin, after aspirin gastritis in some patients. Sometimes in this context, we also give them Omeperazole. We must then remember that the Plavix may not act so well.
Much has been said repeatedly, that smoking is a no, no, and bad for just about every aspect of our health. And that is true. Smoking obviously does more harm than good. Recently, I read an interesting article on a potential benefit of smoking. In the Aug 12th issue of the J of the American College of Cardiology, Dr Bliden and colleagues from the Sinai Thrombosis Research Center, Baltimore, published their findings in a small study of 259 patients, smokers who were on plavix to see the effects of smoking on platelet function, in these patients. They found that smoking seem to induce some enzymes in the CYP450 system, specifically CYP1A2, to enhance the conversion of clopidogrel to its active metabolite, thereby enhancing the action of clopidogrel. Interesting. In other words, smokers who are also on clopidogrel, have enhance platelet inhibition and so less thrombotic tendency. Apparently, when they reviewed the literature, they found that there was already a hint of this in the larger clopidogrel studies like CREDO, CLARITY, etc. However, I must caution that this is not a prospective randomised study and the numbers are small. Although it may be hypothesis generating and something for us to study further, who smokers should not think that their blood is thinner and so they are less likely to have heart attacks. THAT IS NOT WHAT I MEAN. It is possible that smokers on Plavix, maybe less likely to have a thrombotic event. I think that this theory, merits further study. Be that as it may, we cannot go out there and tell patients with DES to continue smoking and taking plavix, in the hope that they get less DES stent thrombosis. That is an obvious NO,NO. Whatever it is, patients with thrombotic diseases or vascular disease should stop smoking to prevent vascular events, Plavix or not.
The second point that I wish to raise is that Plavix is a pro-drug that needs to be activated via the CYP450 pathway, thereby making it vulnerable to all kinds of potential drug-drug interaction. Omeperazole for example may slow down the activation of Plavix, thereby causing it to be less effective. This is important because, we often use Plavix as an alternative to aspirin, after aspirin gastritis in some patients. Sometimes in this context, we also give them Omeperazole. We must then remember that the Plavix may not act so well.
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