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Previous Volume 352:1706-1709 April 21, 2005 Number 16 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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Two large, high-quality, and convincingly negative clinical trials for the secondary prevention of coronary heart disease,^1,2 published in this issue of the Journal, raise questions as to whether we are at the end of the road or should move on to new beginnings as we explore the hypothesis that infection plays a role in atherosclerosis. Evidence that vascular inflammation is an important mechanism involved in all stages of atherogenesis continues to accumulate. Such evidence has legitimately raised the question of whether infection is one of the inflammatory stimuli that operate in the pathophysiology of atherothrombosis, either locally, within vascular tissue, . . . [Full Text of this Article]

Source Information

From the University of Utah School of Medicine, LDS Hospital, Salt Lake City.

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