(Circulation. 1996;94:872-873.)
© 1996 American Heart Association, Inc.
Articles |
Does Atherosclerosis Have an Infectious Etiology?
the University of Texas–Houston Medical School.
Correspondence to L. Maximilian Buja, MD, Dean, The University of Texas–Houston Medical School, 6431 Fannin–MSB G.010, Houston, TX 77030. E-mail buja@dean.med.uth.tmc.edu.
Key Words: Editorials • atherosclerosis • viruses • follow-up studies
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Introduction |
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Atherosclerosis develops as a response of the vessel wall to injury.1 Careful review of epidemiological studies indicates that the classic risk factors, eg, hypercholesterolemia, cigarette smoking, and hypertension, account for the majority but not the entirety of the etiology and pathogenesis of the clinical complications of atherosclerosis, including ischemic heart disease and acute myocardial infarction.2 3 Furthermore, exact knowledge regarding the mechanisms by which the various established risk factors contribute to the development and progression of lesions is incomplete. These facts have led investigators to pursue other possible etiologies and factors that may be involved in the etiology and pathogenesis of atherosclerosis and its complications.
An alternate explanation that recently has received considerable attention is the infectious theory of atherosclerosis. The hypothesis that infectious agents are causal agents in atherosclerosis originally was formulated in the first two decades of this century.4 5 However, this concept received little attention until the late 1970s, when Fabricant et al6 showed that chickens experimentally infected with an avian herpes virus developed florid vascular lesions similar to those of human atherosclerosis. Subsequently, many investigators have reported observations implicating certain infectious agents in human atherosclerotic disease. Specifically, observations have been presented implicating Chlamydia pneumoniae, Helicobacter pylori, HSV, and CMV as possible primary etiologic factors or cofactors in the pathogenesis of atherosclerosis, including ischemic heart disease and cerebrovascular disease.7 8 9 10 11 12 13 14 15 Two basic lines of evidence have been presented: (1) detection of the agent in atherosclerotic lesions by immunocytochemistry and molecular biology and (2) epidemiological evidence based on serological
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