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(Circulation. 2003;107:220.)
© 2003 American Heart Association, Inc.

Infectious Serology and Atherosclerosis

How Burdensome Is the Risk?

Joseph B. Muhlestein, MD; Jeffrey L. Anderson, MD

From the Cardiovascular Department, LDS Hospital, Intermountain Health Care, and the Department of Internal Medicine, University of Utah, Salt Lake City, Utah.

Correspondence to Dr Muhlestein or Dr Anderson, LDS Hospital, Cardiology Division, 8th Ave and C St, Salt Lake City, UT 84143. E-mail ldbmuhle@ihc.com

Key Words: Editorials • atherosclerosis • risk factors

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In recent years, atherosclerosis has come to be recognized as active and inflammatory, rather than simply a passive process of lipid infiltration.¹ Inflammation occurs in response to vascular oxidative stress and injury through known and unknown stimuli. Inflammatory triggers undoubtedly include oxidized and glycosylated products (eg, modified lipoproteins). Given their association with inflammation, infectious agents also are being explored as potential inciters of vascular inflammation and promoters of atherosclerosis.^2,3

See p 251

The role of infection in human atherosclerosis remains elusive. However, the ability of infectious agents to induce several (if not all) of the inflammatory mechanisms active in atherothrombosis has been demonstrated experimentally. Several direct and indirect cellular and molecular mechanisms by which vascular and selected extra-vascular infections may promote atherosclerosis are listed in Table 1⁴ and are discussed elsewhere.² In response to pathogens, pathogen-induced products (eg, reactive oxygen species, oxidized low-density lipoprotein) or cross-reacting, autologous molecules, local and systemic (circulating) inflammatory mediators are induced (including chemokines, cytokines, and adhesion molecules), inflammatory cells are recruited and proliferate (monocyte/macrophages, T lymphocytes, smooth muscle cells), and proinflammatory, prothrombotic, and matrix-degrading molecules are expressed. Endothelial dysfunction ensues, lipid accumulation is promoted, and plaque growth and, subsequently, destabilization and thrombosis occur.

View this table: [in this window] [in a new window]   TABLE 1. Cellular and Molecular Mechanisms by Which Infections May Promote Atherosclerosis

Potential atherogenic mechanisms have been most extensively explored for Chlamydia pneumoniae (Cpn) and cytomegalovirus (CMV) (and other Herpesviridae). Cpn and CMV infect vascular wall cells (and selected nonvascular cells) and may provoke or accelerate atherosclerosis by a variety of these . . . [Full Text of this Article]

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Circulation 2003 107: 251-257. [Abstract] [Full Text]

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