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

医学 新喋呤 降钙素原 内科学 不稳定型心绞痛 胃肠病学 衣原体 心肌梗塞 C反应蛋白 幽门螺杆菌 纤维蛋白原 肺炎 肺炎衣原体 急性期蛋白 心脏病学 炎症 免疫学 败血症 衣原体科
作者
R. Choussat,Gilles Montalescot,Jean‐Philippe Collet,Claude Jardel,Annick Ankri,Anne‐Marie Fillet,D. Thomas,Josette Raymond,Jean‐François Delfraissy,G Drobinski,J Orfila,Henri Agut,Daniel Thomas
出处
期刊:American Journal of Cardiology [Elsevier]
卷期号:86 (4): 379-384 被引量:52
标识
DOI:10.1016/s0002-9149(00)00950-4
摘要

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.
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