Circulation. 1998;97:1671-1674
(Circulation. 1998;97:1671-1674.)
© 1998 American Heart Association, Inc.
Inflammation, Infection, and Cardiovascular Risk
How Good Is the Clinical Evidence?
Paul M. Ridker, MD, MPH
From the Cardiovascular Division and the Division of Preventiv Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.
Correspondence to Dr Paul M Ridker, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115 E-mail pmridker@bics.bwh.harvard.edu
Key Words: Editorials • inflammation • infection • Helicobacter pylori • Chlamydia pneumoniae • C-reactive protein
Despite
substantial gains in the prevention and treatment of acute myocardial
infarction, many atherothrombotic events occur among individuals
without readily apparent risk factors. Several lines of basic research
indicate that inflammation and perhaps chronic infection may play
important roles in the initiation and progression of
atherosclerosis. For example, pathological studies
demonstrate that atherosclerotic lesions are heavily infiltrated with
cellular components associated with inflammation, influx of neutrophils
into the walls of the epicardial vessels has been demonstrated in
response to acute ischemia, and sites of acute plaque rupture
are preferentially associated with inflammatory
components.1 2 3 4 5 6 Further, proinflammatory
cytokines as well as cellular adhesion molecules involved in
the attachment of monocytes to the endothelial wall
appear to be critical in early atherogenesis.7 8
With regard to chronic infection, evidence of prior exposure to
Chlamydia pneumoniae, cytomegalovirus, and
Helicobacter pylori has been detected within human
atherosclerotic tissues,9 10 11 12 13 14 and it has been
hypothesized that these organisms may activate
vessel-associated leukocytes or lead to a transformation of vascular
smooth muscles or endothelial
cells.15 In addition, animal studies suggest that
infection with cytomegalovirus and perhaps other agents can lead to
endothelial lesions similar to that of human
atherosclerosis.16 17
From an epidemiological perspective, however, the role of
inflammation and infection as potential cardiovascular
risk factors is far from certain. Although several studies have
reported associations between exposure to various infectious agents and
prevalent coronary disease,18 19 20 21 22 23 24 25 these
data derive almost exclusively from cross-sectional or retrospective
studies that cannot establish a temporal relation between exposure and
disease. Furthermore, it is . . . [Full Text of this Article]
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