SYSTEMIC INFLAMMATORY RESPONSES IN ACUTE CORONARY SYNDROME - INCREASED ACTIVITY OBSERVED IN POLYMORPHONUCLEAR LEUKOCYTES BUT NOT T-LYMPHOCYTES

Citation
S. Takeshita et al., SYSTEMIC INFLAMMATORY RESPONSES IN ACUTE CORONARY SYNDROME - INCREASED ACTIVITY OBSERVED IN POLYMORPHONUCLEAR LEUKOCYTES BUT NOT T-LYMPHOCYTES, Atherosclerosis, 135(2), 1997, pp. 187-192
Citations number
21
Journal title
ISSN journal
00219150
Volume
135
Issue
2
Year of publication
1997
Pages
187 - 192
Database
ISI
SICI code
0021-9150(1997)135:2<187:SIRIAC>2.0.ZU;2-Z
Abstract
Background: Local inflammation within the coronary arteries is involve d in the pathogenesis of acute coronary syndrome. However. the contrib ution of a systemic inflammatory response to the pathogenesis of this syndrome has not been well characterized. Accordingly, we investigated systemic inflammatory responses in patients with acute coronary syndr ome. Methods: A total of 83 patients with ischemic heart disease (15 w ith stable exertional angina and 68 with acute coronary syndrome) were studied. The luminol-dependent chemiluminescence (CL) response of pol ymorphonuclear leukocytes (PMNs), which reflects their ability to gene rate oxygen species, was used as a marker for PMN activation. Soluble interleukin-2 receptor (sIL-2R) levels were measured to assess T-lymph ocyte activation. Results : CL counts of whole blood from patients wit h acute coronary syndrome were twice those of patients with stable ang ina (2.38 +/- 0.22 vs 1.10 +/- 0.17 x 10(6) counts, P < 0.05). A compa rison of CL counts between patients with unstable angina and those wit h acute myocardial infarction revealed no significant differences. T-l ymphocyte activity, measured by serum sIL-2R, was significantly lower in patients with acute coronary syndrome than those with stable angina (214.3 +/- 11.5 vs. 358.3 +/- 115.7 U/ml, P < 0.05). Conclusions: Thi s investigation shows that there is a systemic increase in PMN activit y and a decrease in T-lymphocyte activity in patients with acute coron ary syndrome. This contrasts with the pattern of cellular activation s een at sites of local inflammation within atherosclerotic plaques, sug gesting that two independent inflammatory processes (local and systemi c) may be involved in the pathogenesis of this syndrome. (C) 1997 Else vier Science Ireland Ltd.