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Allan Shor, MMed; James I. Phillips, PhD

JAMA. 1999;282:2071-2073.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Atherosclerosis is a major cause of stroke, coronary heart disease, peripheral vascular disease, and aortic aneurysm. Because of the prevalence and importance of these diseases, atherosclerotic lesions within arteries have been extensively studied.^1-2 While many risk factors have been identified,^1-2 the mechanism by which the lesions are formed remains unknown. The most popular concept is that the endothelium lining the lumen of the artery becomes damaged. This damage alters the properties of the endothelium and leads to a cascade of events culminating in fibrosis, necrosis, lipid accumulation, and eventually calcification. There have been several candidates forwarded as putative initiators of endothelial injury including microorganisms.¹ Recent studies have shown an association between an obligate intracellular bacterium, Chlamydia pneumoniae, and atherosclerosis.^3-4

Chlamydia pneumoniae was first described by Grayston et al⁵ in 1986. Seroepidemiological studies have concluded that the majority of the population has been . . . [Full Text of this Article]

Author Affiliations: National Centre for Occupational Health (Drs Shor and Phillips) and South African Institute for Medical Research, School of Pathology, University of the Witwatersrand, (Dr Shor) Johannesburg, South Africa.

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