This Article Extract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Blum, A. Search for Related Content PubMed PubMed Citation Articles by Blum, A. Related Collections Restenosis Catheter-based coronary interventions: stents

(Circulation. 1999;100:e97.)
© 1999 American Heart Association, Inc.

Circulation Electronic Pages

Inflammatory Response in Unstable Angina

Arnon Blum, MD

From Cardiology Branch, NHLBI National Institutes of Health, Bethesda, Md

	To the Editor:

Top To the Editor: References

 
I have read with interest the articleby Liuzzo et al¹ and their interesting conclusion that "These findings ... suggest that the magnitude of the acute-phase response is determined to a greater extent by the individual responsiveness than by the type of provocative stimuli."

I would like to support this theory and to add our experience in this field. Recently, we² published a study in which 55 patients with coronary artery disease were enrolled. We found that a high level (>100 µg/mL) of an inflammatory protein (serum amyloid type A; SAA) could identify patients with severe unstable angina with a high sensitivity and specificity (r=0.85 and 0.86, respectively). Of the patients studied, 75% experienced an increase in their SAA level 24 hours after angioplasty. An increase of SAA by >100% was associated with an increased risk of restenosis, with a relative risk of 6.4 (P<0.05). We found that there was no correlation between the inflammatory state before angioplasty (or the clinical severity) and the restenosis rate; rather, it was the SAA increase 24 hours after angioplasty that was associated with restenosis. Specifically, the SAA level increased dramatically after angioplasty, unrelated to preangioplasty SAA levels or the clinical state of the patient before the procedure.

I believe that "host traits" (genes? immuno-inflammatory mechanisms?) have an important role in the clinical outcome of every disease process, including coronary artery disease.

	References

Top To the Editor: References

 
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.[Abstract/Free Full Text]

2. Blum A, Kaplan G, Vardinon N, Yust I, Burke M, Laniado S, Miller H. Serum amyloid type A may be a predictor of restenosis. Clin Cardiol. 1998;21:655–658.[Medline] [Order article via Infotrieve]

This Article Extract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Blum, A. Search for Related Content PubMed PubMed Citation Articles by Blum, A. Related Collections Restenosis Catheter-based coronary interventions: stents