title: Assessment of systemic inflammation and infective pathogen burden in patients with cardiac syndrome X.
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.
authors.affiliation: Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Rome, Italy. g.a.lanza@inwind.it
authors.forename: Gaetano Antonio
authors.initials: GA
authors.lastname: Lanza
authors.forename: Alfonso
authors.initials: A
authors.lastname: Sestito
authors.forename: Giovanni
authors.initials: G
authors.lastname: Cammarota
authors.forename: Rita Luciana
authors.initials: RL
authors.lastname: Grillo
authors.forename: Elena
authors.initials: E
authors.lastname: Vecile
authors.forename: Rossella
authors.initials: R
authors.lastname: Cianci
authors.forename: Domenico
authors.initials: D
authors.lastname: Speziale
authors.forename: Aldo
authors.initials: A
authors.lastname: Dobrina
authors.forename: Attilio
authors.initials: A
authors.lastname: Maseri
authors.forename: Filippo
authors.initials: F
authors.lastname: Crea
mesh_terms: D002097:C-Reactive Protein; D016022:Case-Control Studies; D002690:Chlamydia Infections / Q000150:complications / Q000453:epidemiology; D016993:Chlamydophila pneumoniae; D003324:Coronary Artery Disease / Q000097:blood* / Q000150:complications; D003586:Cytomegalovirus Infections / Q000150:complications / Q000453:epidemiology; D020031:Epstein-Barr Virus Infections / Q000150:complications / Q000453:epidemiology; D005260:Female; D016481:Helicobacter Infections / Q000150:complications / Q000453:epidemiology; D016480:Helicobacter pylori; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000453:epidemiology* / Q000382:microbiology / Q000821:virology; D007558:Italy / Q000453:epidemiology; D008297:Male; D017566:Microvascular Angina / Q000097:blood* / Q000150:complications; D008875:Middle Aged; D015995:Prevalence
chemical_list: D002097:C-Reactive Protein