Smoking, atherothrombosis and clopidogrel
- 1William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, London, UK
- 2National Heart and Lung Institute, Imperial College, London, UK
- Correspondence to Professor Timothy David Warner, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, UK; t.d.warner{at}qmul.ac.uk
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Contributors The authors have contributed equally to the production of this commentary.
- antiplatelet treatment
- endothelin
- endothelium
- free radicals
- NSAIDS
- platelet activation
- venous thromboembolism
Smoking is well understood to increase the risk of atherothrombotic events by some two to threefold.1–3 Putting it another way, in 2003 the SCORE project estimated that over a period of 10 years smokers compared with non-smokers have approximately twice the risk of a fatal cardiovascular event.4 Set against this elevation in risk, it was reported in the mid-1980s that there was a smokers' paradox, in that smoking appeared to confer a reduced mortality following an acute myocardial infarction.5 It was also noted, in accordance with the suggestions from studies such as SCORE, that smokers tended to be 10 years or so younger and such variables could account for the difference seen. A more recent analysis has concluded that reports of the smokers' paradox appear largely confined to the 1980s and 1990s, at which time fibrinolysis was the generally employed approach for reperfusion, whereas the paradox is not seen in more contemporary studies when patients are routinely treated with early invasive management.6
A more recent smokers' paradox has been the observation that the response to clopidogrel is enhanced in smokers over non-smokers.7 This taps into current interest …
