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(Circulation. 2001;103:5.)
© 2001 American Heart Association, Inc.

Editorial

Link Between Infection and Atherosclerosis: Who Are The Culprits: Viruses, Bacteria, Both, or Neither?

Prediman K. Shah, MD

From the Division of Cardiology and Atherosclerosis Research Center, Burns and Allen Research Institute and Department of Medicine, Cedars Sinai Medical Center and UCLA School of Medicine, Los Angeles, Calif.

Correspondence to P.K. Shah, MD, Division of Cardiology, Room 5347, Cedars Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048. E-mail shahp@cshs.org

Key Words: Editorials • atherosclerosis • infection

On the basis of an examination of 400 000 sections from 40 autopsy cases in 1935, Leary¹ used the term "abscess" to describe atheromatous plaques, because leukocyte infiltration suggested an inflammatory process. A substantial body of evidence has since implicated inflammation and immune activation in the pathogenesis of atherosclerosis, thrombosis, and neointimal thickening after arterial injury.^{2 3} A number of potential triggers capable of inducing proinflammatory cellular responses have been identified; these include modified lipoproteins, cytokines, chemokines, angiotensin II, hypertension, hyperglycemia, smoking, oxidative stress, and others.^{2 3} However, one of the most interesting developments in recent years has been the hypothesis that one or more infectious agents may play a role in atherothrombosis, either through a direct proinflammatory effect on the vessel wall or through a less specific, long-distance proinflammatory effect.^{2 3 4 5 6}

The possibility of infections contributing to atherosclerosis was suggested in the late 1800s and early 1900s by several authors^{7 8} and, in fact, in 1911, Frothingham suggested that "The sclerosis of old age may simply be a summation of lesions arising from infectious or metabolic toxins."⁹ Specific organisms that have been implicated include viruses such as herpes simplex virus (HSV-1), cytomegalovirus (CMV), hepatitis virus, and bacteria such as Chlamydia pneumoniae, Helicobacter pylori, and porphromonus gingivalis.^{2 3 4 5 6} The evidence implicating infection in atherothrombosis includes the following: (1) seroepidemiological data, (2) the identification of viruses and bacteria in atherosclerotic plaques, (3) a strong association between specific infections such as CMV with transplant atherosclerosis, (4) experimental models showing an induction or acceleration of atherosclerosis . . . [Full Text of this Article]

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