Abstract
The immunologic response in atherosclerosis involves not only intrinsic cells of the
artery wall, but also circulating leukocytes, lymphocytes, and macrophages. Interaction
of various arms of the immune response modulates plaque development and stability,
and it is conceivable that immunologic effects of some cardiovascular therapies may
contribute to their mechanism of benefit. The preponderance of data has accrued with
the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins). Statin effects,
such as inhibition of T cell activation, tissue factor expression, or reduction of
platelet hyperreactivity, may elicit beneficial effects in vitro and in vivo in patients
with coronary artery disease. Moreover, aspirin may limit oxidation of lipoproteins
and fibrinogen, and it may inhibit cytokine-induced nitric oxide synthase II expression.
The hypothesis that selective inhibition of cyclooxygenase-2 (COX-2) may increase
risk of myocardial infarction is controversial and may also be of questionable clinical
significance. Finally, angiotensin-converting enzyme (ACE) inhibitors not only reduce
proinflammatory mediators, such as interleukin-6, but also enhance the concentration
of anti-inflammatory cytokines, such as interleukin-10. Because ACE is expressed at
the shoulder region of atherosclerotic plaques, and ACE activity is enhanced in unstable
plaques, ACE inhibition may also contribute to plaque stability. This article reviews
the potential immunomodulatory potencies of aspirin, COX-2 inhibitors, statins, and
ACE inhibitors as established pharmacotherapy in patients with coronary artery disease.
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Article info
Footnotes
☆This work was supported by a Grant from the Leducq Foundation and by Grant No. SFB566/B9 from the Deutsche Forschungsgemeinschaft.
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© 2003 Excerpta Medica Inc. Published by Elsevier Inc. All rights reserved.
