Abstract
Inflammation plays a key role in coronary artery disease (CAD), but whether it is
involved in the pathogenesis of syndrome X (SX) is not known. Thus, we assessed the
presence of systemic inflammation in patients with SX and its possible relation to
infections from Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and Epstein-Barr virus. We studied 55 patients with SX (57 ± 8
years old; 27 women), 49 with stable angina and obstructive CAD (56 ± 8 years old;
24 women), and 60 healthy controls (57 ± 11 years old; 24 women). Plasma levels of
high-sensitivity C-reactive protein and interleukin-1 receptor antagonist were measured
in all patients. Infection from Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and Epstein-Barr virus was assessed in 43 patients with SX, 40
patients with CAD, and in 39 controls. Patients with SX had lower serum levels of
C-reactive protein than did patients with CAD (4.06 ± 6.8 vs 5.99 ± 7.8 mg/L, p =
0.013) but higher levels of C-reactive protein than did controls (1.75 ± 1.98 mg/L;
p = 0.008). Plasma levels of interleukin-1 receptor antagonist were higher in patients
with CAD (570 ± 738 pg/ml) and patients with SX (494 ± 677 pg/ml) than in controls
(254 ± 174, pg/ml; p = 0.0003 vs CAD and p = 0.013 vs SX) but did not differ significantly
between patients with CAD or SX (p = 0.20). There were no differences across groups
in the prevalence of infection from Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus, and Epstein-Barr virus and in the prevalence of 1, 2, 3, and 4
infections (p = 0.99). Among patients with SX, no correlation was found between markers
of inflammation and indexes of disease activity (angina episodes, exercise test results).
Our data show evidence of increased low-grade systemic inflammation in patients with
cardiac SX, which was unrelated to an increased infectious pathogen burden.
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Article info
Publication history
Accepted:
March 4,
2004
Received in revised form:
March 4,
2004
Received:
January 22,
2004
Identification
Copyright
© 2004 Excerpta Medica Inc. Published by Elsevier Inc. All rights reserved.
