(Circulation. 2008;118:672-677.)
© 2008 American Heart Association, Inc.
Contemporary Reviews in Cardiovascular Medicine |
From the Department of Medicine, University of California San Diego, La Jolla.
Correspondence to Dr Daniel Steinberg, Department of Medicine, BSB 1080, University of California San Diego, 9500 Gilman Dr, La Jolla, CA 92093–0682. E-mail dsteinberg@ucsd.edu
Key Words: atherosclerosis hypercholesterolemia inflammation myocardial infarction prevention
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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30%, and the magnitude of the protective effect mirrored the magnitude of the low-density lipoprotein (LDL) lowering.4 However, as has been quite correctly pointed out,5,6 some 70% of those expected to have an event (based on the number of events in the control group) went on to have one during the 5 years of the trial despite statin therapy. For example, in the Scandinavian Simvastatin Survival Study, 502 events occurred in the untreated group and 353 in the statin-treated group. The number of events prevented (n=149), as a percentage of the number expected, was 29.7% (149/502x100); the number of events in the statin group that were not prevented (353) amounts to 70.3% (353/502x100). Looked at this way, the results are admittedly not quite so impressive. In fact, some investigators are now taking the position that we can expect to achieve higher salvage rates only if we supplement LDL-lowering therapies with alternative interventions such as the use of antiinflammatory agents or immunotherapy. This may turn out to be true. However, it is much too early to reach that conclusion for reasons we discuss here. The search for alternative or supplementary therapies is already in full swing and should continue.6–8 We are confident that one day these additional therapies will take their place alongside cholesterol-lowering agents in This article has been cited by other articles:
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