The landmark statin trials showed a significant reduction in morbidity and
mortality associated with ischemic heart disease. However, it may not be wi
dely appreciated that smoking had a marked adverse effect on outcome in the
se trials. In both the primary and secondary prevention setting, the effect
of smoking was broadly similar. Smoking markedly increased the risk of eve
nts in the placebo and treatment groups. For example, in the primary preven
tion trials, this risk was 74-86% higher when smokers were compared with no
nsmokers in the placebo groups. The corresponding figures for the secondary
prevention trials were 23-61%. The risk of events in untreated nonsmokers
was of a similar order to that seen in smokers taking statins. Although sta
tin treatment was associated with a significant reduction in events in smok
ers, the best outcome was observed in nonsmokers treated with statins (prim
ary prevention: lovastatin or pravastatin; secondary prevention: pravastati
n or simvastatin). The highest risk of events in any group was in the smoke
rs on placebo. This information may increase clinician and patient awarenes
s as to the marked harmful effect of smoking relative to effective, evidenc
e-based treatment (ie, the use of statins).