Loading…

Assessment of systemic inflammation and infective pathogen burden in patients with cardiac syndrome X

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 pneu...

Full description

Saved in:
Bibliographic Details
Published in:The American journal of cardiology 2004-07, Vol.94 (1), p.40-44
Main Authors: Lanza, Gaetano Antonio, Sestito, Alfonso, Cammarota, Giovanni, Grillo, Rita Luciana, Vecile, Elena, Cianci, Rossella, Speziale, Domenico, Dobrina, Aldo, Maseri, Attilio, Crea, Filippo
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:0002-9149
1879-1913
DOI:10.1016/j.amjcard.2004.03.027