Circulation. 1999;100:e95
(Circulation. 1999;100:e95.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Enhanced Inflammatory Response to Coronary Angioplasty in Patients With Severe Unstable Angina
Kornél Simon, MD;
Éva Öry, MD;
Tamás Böhm, MD
From St. George’s Hospital, II Department of Internal Medicine,
Seregélyesi, Hungary
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To the Editor:
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We congratulate Liuzzo et al on the recent publication of their
study,
1 which suggests that disruption of culprit
coronary stenoses
by PTCA does not necessarily lead to
an increase in the level
of systemic inflammatory markers (C-reactive
protein [CRP],
serum amyloid A protein [SAA], and interleukin-6
[IL-6]) in
patients with unstable angina. The authors found that
serum
levels of CRP, SAA, and IL-6 did not change after PTCA in
unstable
angina patients with normal pre-PTCA (basal) levels but that
they
significantly increased in those with raised pre-PTCA values.
Surprisingly,
the authors demonstrated that coronary
arteriography also evoked
a detectable transient elevation of CRP, SAA,
and IL-6 serum
levels in unstable angina patients with high basal
values. Pre-PTCA
and pre–coronary arteriography serum levels
of CRP and
SAA closely correlated with the corresponding
postintervention
peak values of both PTCA and coronary
arteriography.
As the authors emphasize, it is well documented that elevated
levels of acute-phase proteins are associated with an unfavorable
short- and long-term prognosis in patients with coronary artery
disease2 3 4 ; conversely, patients with CRP levels within
the normal range tend to have a better prognosis.5 In
light of these data, it would be interesting to know whether the 2
well-matched subgroups of study patients with unstable angina, ie,
those with versus those without acute-phase protein response, show the
same or different clinical stability and/or therapeutic responsiveness
in the pre- and post-PTCA periods. Furthermore, because
coronary arteriography could also trigger additional
acute-phase protein elevation in a significant proportion of patients
with unstable angina, should this transient moderate increase of
systemic inflammatory response after coronary arteriography
(like PTCA) also be considered a marker for instability of culprit
coronary lesions in unstable angina patients with raised basal
levels of acute-phase protein?
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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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Liuzzo G, Biasucci LM, Gallimore JR, Grillo RL,
Rebuzzi AG, Pepys MB, Maseri A. Prognostic value of C-reactive protein
and plasma amyloid A protein in severe unstable angina. N
Engl J Med. 1994;331:417–424.[Abstract/Free Full Text]
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Thompson SG, Kienast J, Pyke SDM, Haverkate F, van de
Loo JCW. Hemostatic factors and the risk of myocardial infarction or
sudden death in patients with angina pectoris. N Engl J
Med. 1995;332:635–641.[Abstract/Free Full Text]
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Haverkate F, Thompson SG, Pyke SDM, Gallimore JR,
Pepys MB, for the European Concerted Action on Thrombosis and
Disabilities Angina Pectoris Study Group. Production of
C-reactive protein and risk of coronary events in stable and
unstable angina. Lancet. 1997;349:462–466.[Medline]
[Order article via Infotrieve]
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Ridker PM, Cushman M, Stamper MJ, Tracy RP, Hennekens
CH. Inflammation, aspirin, and the risk of
cardiovascular disease in apparently healthy men.
N Engl J Med. 1997;336:973–979.[Abstract/Free Full Text]
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To the Editor:
References