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If you are interested in the topic of whether statins should be used
for primary prevention, you may want to look at the March 31, 2007
edition of The Lancet, which prints three letters responding to John
Abramson and James Wright's 1/20/07 comment, Are lipid-lowering
guidelines evidence-based?; Lancet 2007; 369:168-69. Abramson and
Wright argued that there is no evidence that lipid-lowering therapy
reduces mortality in individuals without evident coronary artery
disease.
Ruth McPherson and Nihan Kavaslar of the University of Ottawa Heart
Institute argue that Abramson and Wright "do not take into account the
fact that, owing to the young age of the participants and short
treatment period, none of the primary prevention studies was powered
to detect changes in total mortality." They argue that "moderately
low LDL cholesterol concentrations maintained over the course of a
lifetime greatly reduce long-term risk."
Marcus M. Reidenberg of Weill Cornell Medical College points out that
for people with HDL concentrations above 1.11 mmol/L in the four
placebo-controlled primary prevention trials for which HDL
stratification was presented, the number needed to treat to prevent
one cardiovascular event was much higher than the value of 67 people
treated for 5 years cited by Abramson and Wright. He concludes that
"the lack of benefit of statins for primary prevention, especially for
people with high HDL concentrations, does not imply that these people
do not have a high risk of having a cardiovascular event. It simply
means that statin therapy does not lower the risk."
Luca Mascitelli and Francesca Pezzatta point out that there is reason
to believe that side-effects of statins are much more common in
clinical practice than was found in statin trials. They conclude
that "statin therapy might worsen quality of life" and also might
discourage exercise because of muscle pain caused by the statins.
Author's reply: Abramson and Wright point out that the eight
available trials for primary prevention comprise more than 40,000
individuals, and that "these pooled data are certainly powered to
detect a reduction in mortality and fail to do so." In addition, they
state that although there is an association between LDL cholesterol
and coronary artery disease in some populations, "one can not assume
that predicted benefits from epidemiological data will be achieved in
drug intervention trials." They support subgroup analysis with
respect to people with high HDL concentrations, as suggested by
Reidenberg. They also support testing the hypothesis that statin-
related muscle complaints interfere with the ability of patients to
exercise. They conclude that "the first step in resolving these
issues is for the CTT collaborators to respond to these challenges."