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Previous Volume 357:2180-2183 November 22, 2007 Number 21 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Raising plasma levels of high-density lipoprotein (HDL) cholesterol has been a therapeutic goal ever since the strong inverse association between HDL levels and the risk of coronary heart disease was first observed.¹ Nearly two decades ago, the discovery that persons in Japan had extremely high levels of HDL cholesterol because of a genetic deficiency involving the cholesteryl ester transfer protein (CETP) led to the concept that pharmacologic inhibition of CETP could raise HDL cholesterol levels. When this theory proved to be true in humans, it led to great anticipation that CETP inhibition would permit the ultimate test of the "HDL . . . [Full Text of this Article]

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From the University of Pennsylvania School of Medicine, Philadelphia.

This article (10.1056/NEJMe0707210) was published at www.nejm.org on November 5, 2007.

Related Letters:

Torcetrapib and Coronary Events
Lackner K. J., Cohn L. J., Dullaart R. P., Kobold A. C. M., van Tol A., Barter P., Shear C. L., Revkin J. H., Rader D. J.
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N Engl J Med 2008; 358:1862-1864, Apr 24, 2008. Correspondence

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