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Infection, antibiotics, and atherothrombosis--end of the road or new beginnings?

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 . . .