(Circulation. 2000;101:1758.)
© 2000 American Heart Association, Inc.
Editorial |
Circulating Markers of Inflammation for Vascular Risk Prediction
Are they Ready for Prime Time
Key Words: Editorials • atherosclerosis • inflammation
Over the last several years, the idea that inflammation plays a key role in atherosclerosis and its complications has received considerable attention.1 Inflammatory cell infiltration is observed in atherosclerotic plaques at virtually all stages, from the fatty streak to the advanced atheromatous lesions with plaque disruption and thrombosis.1 2 Atherosclerosis is substantially prevented when the biological effects of genes critical for the initiation or maintenance of inflammatory cell recruitment, survival, proliferation, and activation, such as monocyte chemotactic protein-1, interleukin-8, and macrophage colony stimulating factor, are eliminated by gene knockout in atherosclerosis-prone dyslipidemic mice.3 4 5 Similarly, the inhibition of inflammatory signaling pathways mediated by the ligation of CD-40 also results in reduced atherosclerosis in mice.6
Inflammatory cells may also play a key role in promoting plaque
disruption by stimulating matrix degradation, inhibiting smooth muscle
cell function or survival, and promoting thrombosis by producing tissue
factor.2 Similarly, the atheroprotective effects of a
variety of interventions such as statins, apolipoprotein A-1/HDL,
aspirin, and fibrates are often associated with the evidence of reduced
inflammation, further bolstering the notion that inflammation and
atherosclerosis are causally related.2 7 8
Although all of the potential triggers of inflammation are not fully
known, cytokines, oxidized lipoproteins, and local
(arterial) and distant infections (gingivitis, bronchitis)
have been implicated.2 9 Early reports from small,
randomized trials have shown a reduced clinical event rate with the use
of macrolide antichlamydial antibiotics.2 These
preliminary observations support the notion that Chlamydia
pneumoniae infection may be causally related to atherothrombosis,
although a direct anti-inflammatory effect of macrolides, independent
of
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