title: Effect of prior exposure to Chlamydia pneumoniae, Helicobacter pylori, or cytomegalovirus on the degree of inflammation and one-year prognosis of patients with unstable angina pectoris or non-Q-wave acute myocardial infarction.
abstract: Inflammation and chronic infections may be important features in the pathogenesis of acute coronary syndromes. We describe 6 systemic markers of inflammation in patients with unstable angina or non-Q-wave myocardial infarction and the relations between these markers, seropositivity to chronic infections, and prognosis. C-reactive protein (CRP), serum amyloid A protein (SAA), fibrinogen, interleukin-6 (IL-6), neopterin, procalcitonin, and serum antibody levels to Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus were measured on admission and 48 hours later. One-year clinical follow-up was performed. Plasma levels of acute phase reactants were all elevated on admission and increased further at 48 hours: CRP from 10.1 +/- 2.1 mg/L at baseline to 26.6 +/- 5.1 mg/L at 48 hours (p <0.001); SAA from 27.3 +/- 8.5 to 93.1 +/- 23.2 mg/dl (p <0.005); fibrinogen from 3.2 +/- 0.1 to 3.8 +/- 0.1 g/L (p <0.0001); whereas initial high levels of IL-6 tended also to increase from 9.8 +/- 2 to 15.3 +/- 3.1 pg/ml (p = NS). In contrast, neopterin and procalcitonin remained unchanged. We found no association between levels of each inflammatory marker and the serologic status. Furthermore, levels of inflammatory proteins in patients seronegative to all 3 agents were comparable to those of patients seropositive to 2 or 3 infectious agents. The composite end points of death, myocardial infarction, recurrent angina, or revascularization at 1-year follow-up did not differ according to the serologic status. Thus, in patients with acute coronary syndromes, the acute phase proteins increased over the first 2 days of hospitalization. This initial inflammatory reaction as well as the 1-year clinical outcome did not differ according to the initial serologic status of Chlamydia pneumoniae, Helicobacter pylori, or cytomegalovirus.
authors.affiliation: Department of Cardiology, Pitié-Salpétrière Hospital, Paris, France.
authors.forename: R
authors.initials: R
authors.lastname: Choussat
authors.forename: G
authors.initials: G
authors.lastname: Montalescot
authors.forename: J
authors.initials: J
authors.lastname: Collet
authors.forename: C
authors.initials: C
authors.lastname: Jardel
authors.forename: A
authors.initials: A
authors.lastname: Ankri
authors.forename: A
authors.initials: A
authors.lastname: Fillet
authors.forename: D
authors.initials: D
authors.lastname: Thomas
authors.forename: J
authors.initials: J
authors.lastname: Raymond
authors.forename: J
authors.initials: J
authors.lastname: Bastard
authors.forename: G
authors.initials: G
authors.lastname: Drobinski
authors.forename: J
authors.initials: J
authors.lastname: Orfila
authors.forename: H
authors.initials: H
authors.lastname: Agut
authors.forename: D
authors.initials: D
authors.lastname: Thomas
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism*; D000368:Aged; D000789:Angina, Unstable / Q000097:blood / Q000209:etiology*; D015415:Biomarkers / Q000097:blood; D002690:Chlamydia Infections / Q000097:blood / Q000150:complications; D016993:Chlamydophila pneumoniae; D003587:Cytomegalovirus; D003586:Cytomegalovirus Infections / Q000097:blood / Q000150:complications; D005260:Female; D016481:Helicobacter Infections / Q000097:blood / Q000150:complications; D016480:Helicobacter pylori; D006439:Hemodynamics; D006801:Humans; D007239:Infections / Q000150:complications*; D007249:Inflammation / Q000097:blood*; D016014:Linear Models; D008297:Male; D009203:Myocardial Infarction / Q000097:blood / Q000209:etiology*; D011379:Prognosis; D011446:Prospective Studies
chemical_list: D000209:Acute-Phase Proteins; D015415:Biomarkers