(Circulation. 1999;100:e95.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Enhanced Inflammatory Response to Coronary Angioplasty in Patients With Severe Unstable Angina
From St. George’s Hospital, II Department of Internal Medicine, Seregélyesi, Hungary
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To the Editor: |
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 Top To the Editor: References |
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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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TopTo the Editor:References |
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1. 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.
2.
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.
3.
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.
4. 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]
5.
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.
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