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(Stroke. 2003;34:333.)
© 2003 American Heart Association, Inc.

Advances in Stroke 2002

Infection, Inflammation, and Atherosclerosis

J. David Spence, MD John Norris, MD

From the Stroke Prevention & Atherosclerosis Research Centre, Robarts Research Institute, London, Ontario (J.D.S.), and Stroke Research Unit, Sunnybrook & Women’s College Hospital, University of Toronto, Toronto (J.N.), Canada.

Correspondence to David Spence, MD, Stroke Prevention & Atherosclerosis Research Centre, 1400 Western Rd, London, Ontario N6G 2V2, Canada. E-mail dspence@robarts.ca

Key Words: atherosclerosis • Chlamydia pneumoniae • Helicobacter pylori • inflammation

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

Only half of coronary artery disease,^1,2 and half of carotid plaque measured by ultrasound,³ can be explained by the usual risk factors: age, sex, hypertension, hyperlipidemia, smoking, and diabetes. It is likely that much of unexplained atherosclerosis is genetic: a Swedish twin study showed that myocardial infarction below age 46 is almost entirely heritable.⁴ This suggests that few environmental factors remain to be discovered that would make a major contribution to atherosclerosis. Recently, the notion that infection may be important in atherosclerosis has been of interest.

A recent study has shown that C-reactive protein, a marker of inflammation, was a stronger predictor of cardiovascular events than was low-density lipoprotein cholesterol level.⁵ It has been postulated for more than a century that infection may be responsible for atherosclerosis;⁶ this issue has recently been reviewed by Fong.⁷ Organisms that have been implicated include Chlamydia pneumoniae, cytomegalovirus, Helicobacter pylori, and periodontal infections.

The mechanisms by which the association may be explained include increased coagulation,^8,9 endothelial dysfunction,¹⁰ instability of plaque,^11,12 and increased progression of atherosclerosis because of the influence of inflammation on plaque progression.¹³ In a rabbit model, infection accelerates atherosclerosis, and treatment with azithromycin prevents the effect.¹³

Growing evidence suggests that infection with C pneumoniae may be associated with increased risk of coronary events^14–16 and more rapid restenosis after angioplasty.¹⁷ C pneumoniae has been identified in carotid endarterectomy specimens,¹⁸ and two studies have shown an association of Chlamydia antibody titers with stroke.^19,20 Early studies of antibiotic treatment for C pneumoniae have . . . [Full Text of this Article]

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