Circulation. 1999;100:e98
(Circulation. 1999;100:e98.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Inflammatory Response in Unstable Angina
Horea Rus, MD, PhD;
Florin Niculescu, MD, PhD
From University of Maryland, School of Medicine, Department of Pathology,
Baltimore, Md
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To the Editor:
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We read with great interest the article by Liuzzo et al
1
regarding
the systemic inflammatory markers associated with unstable
angina.
We would like to also emphasize the fact that the increase of
inflammatory
markers is present not only in the circulation, as
shown in
their article, but also in the arterial
atherosclerotic wall
itself. We
2 3 have previously
measured C-reactive protein (CRP)
and interleukin-6 (IL-6) levels
eluted from human aortic wall
with atherosclerosis.
High levels of CRP were present in fatty-streak
lesions and
uncomplicated fibrous plaques.
2 Low levels of CRP
were
found only in a few normal areas. As measured by ELISA,
IL-6 levels
were statistically significantly higher in the fibrous
plaques than in
normal areas. IL-6 was localized by immunohistochemistry
as both
intracellular and extracellular deposits. Compared with
its serum
levels, IL-6 was 200-fold higher in the atherosclerotic
wall than in
serum.
3 The accumulation of CRP and IL-6 in the
atherosclerotic
wall is a marker for a local inflammatory process.
Our data suggest that both local production and the
accumulation of proteins from plasma may contribute to the increased
levels observed in atherosclerotic lesions.2 3 Serum
amyloid A (SAA) is also present in the atherosclerotic
wall.4 Arterial vessel injury is followed by
the release of soluble arterial proteins in circulation.
Such constant release of IL-6 from vulnerable atherosclerotic plaques
in patients with unstable angina may account for the increased serum
basal levels seen by Liuzzo et al in their study.1
At 6 hours after PTCA, IL-6 levels were twice the basal level
(Table 3 in Reference 1 ). This early and rapid increase
suggests that the liberation of IL-6 from the atherosclerotic wall is
responsible for the increased levels seen after PTCA in the patients
with unstable angina. On the other hand, all measured proteins peaked
at 24 hours after PTCA. This also suggests participation of local
release in the increased serum level. The high instability of the
advanced atherosclerotic lesions, including plaque fissures and
ulceration, suggests that this phenomenon is more prominent in patients
with unstable angina. The accumulation of CRP, IL-6, and SAA in
uncomplicated lesions may be followed by their release from ruptured
plaques and may contribute to the increased serum level.
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References
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Liuzzo G, Buffon A, Biasucci LM, Gallimore JR,
Caligiuri G, Vitelli A, Altamura S, Ciliberto G, Rebuzzi AG, Crea F,
Pepys MB, Maseri A. Enhanced inflammatory response to coronary
angioplasty in patients with severe unstable angina.
Circulation. 1998;98:2370–2376.[Abstract/Free Full Text]
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Vlaicu R, Niculescu F, Rus HG, Cristea A.
Immunoglobulins and complement components in human aortic
atherosclerotic wall. Atherosclerosis. 1985;55:35–50.[Medline]
[Order article via Infotrieve]
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Rus HG, Vlaicu R, Niculescu F. Interleukin-6 and
interleukin-8 protein and gene expression in human arterial
atherosclerotic wall. Atherosclerosis. 1996;127:267–271.
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Yamada T, Kakihara T, Kamishima T, Fukuda T, Kawai T.
Both acute and constitutive serum amyloid A are present in
atherosclerotic lesions. Pathol Int. 1996;46:787–800.[Medline]
[Order article via Infotrieve]
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To the Editor:
References