Enhanced inflammatory response in patients with preinfarction unstable angina

Citation
G. Liuzzo et al., Enhanced inflammatory response in patients with preinfarction unstable angina, J AM COL C, 34(6), 1999, pp. 1696-1703
Citations number
54
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
07351097 → ACNP
Volume
34
Issue
6
Year of publication
1999
Pages
1696 - 1703
Database
ISI
SICI code
0735-1097(19991115)34:6<1696:EIRIPW>2.0.ZU;2-D
Abstract
OBJECTIVES We assessed the extent and the time course of the acute phase re sponse following myocardial cell necrosis and its relationship with the pre sence of preinfarction unstable angina (UA). BACKGROUND Elevated levels of acute phase proteins have been reported in pa tients with UA and in patients with acute myocardial infarction (MI). METHODS C-Reactive Protein (CRP), serum amyloid A protein (SAA) and interle ukin-6 (IL-6) were measured in 36 patients with MI admitted within 3 h from symptoms onset. All patients had normal levels of creatine kinase and of t roponin T on admission, rising above diagnostic levels within 6 to 12 h. Bl ood samples for CRP, SAA and IL-6 measurements were taken on admission, at 6, 24, 48, 72 h and at discharge. RESULTS Twenty of the 36 patients studied presented an unheralded MI (Group 1); the remaining 16 patients had symptoms of unstable angina in the prece ding 7 days (Group 2). Group 2 patients have much higher levels of CRP and SAA on admission (median values 8.8 vs. 3 mg/L and 28 vs. 3.4 mg/L, respect ively, all p < 0.001). Following the necrotic insult, despite similar infar ct size and clinical signs of reperfusion, Group 2 patients had strikingly higher peaks of IL-6 (median values 85.2 vs. 19 pg/ml, p < 0.05), CRP (50 v s. 31.4 mg/L, p < 0.05) and SAA (228 vs. 45 m/L, p < 0.001). CONCLUSIONS Our data demonstrated that the acute phase response is greatly enhanced in patients with preinfarction UA compared with those presenting w ith an unheralded MI. The significant differences in acute phase response o bserved in these two clinical presentations of MI indicate a major differen ce in their underlying pathogenetic components. (C) 1999 by the American Co llege of Cardiology.