Inflammation and infection in stable coronary disease and the acute coronary syndrome

Citation
Jb. Garcia et al., Inflammation and infection in stable coronary disease and the acute coronary syndrome, REV ESP CAR, 54(4), 2001, pp. 453-459
Citations number
51
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
REVISTA ESPANOLA DE CARDIOLOGIA
ISSN journal
03008932 → ACNP
Volume
54
Issue
4
Year of publication
2001
Pages
453 - 459
Database
ISI
SICI code
0300-8932(200104)54:4<453:IAIISC>2.0.ZU;2-P
Abstract
Objective. To study whether inflammation and infection are related to coron ary artery disease. Design. Sixty patients (44 males, mean age 62 +/- 13 years) with acute coro nary syndrome and 40 with stable coronary artery disease (31 males, age 64 +/- 10 years) and a control group of 40 individuals (34 males, 53 +/- 5 yea rs) were analyzed. IgG against Chlamydia pneumoniae, Cytomegalovirus and He licobacter pylori plus C-reactive protein were assessed in all serum sample s. In addition, IgM against C. pneumoniae and Cytomegalovirus on admission and C-reactive protein one month later were measured in acute patients. Results. No IgM seropositivity was observed. A high prevalence of IgG serop ositivity with no significant differences among the groups was found: C. pn eumoniae: acute group 44 (73%), stable group 29 (73%) and control group 25 (63%); Cytomegalovirus: 55 (92%), 37 (92%) and 38 (95%), respectively; and H. pylori, 43 (72%), 32 (80%) and 34 (85%) respectively. There was a high r ate of positive C-reactive protein in the acute group: 48 (80%) vs 10 (25%) the stable group and 0% the control group (p < 0.001). C-reactive protein levels were higher in Q-wave infarction than in unstable angina/ non-Q-wave infarction (median 22.65 vs 7.69, p < 0.001). One month later, C-reactive protein levels decreased (median 22.65 vs 3.38, p < 0.001), but were still positive in 40%. Conclusions. These data suggest that inflammation is detected by the common ly used methods in clinic practice in acute coronary syndromes and to a les ser extent in stable coronary artery disease. It seems that different mecha nisms other than infection account for this inflammatory response, at least this being so when infection is assessed by serology. Serology does not ap pear to be an adequate method to determine the possible relationship among coronary syndromes, infection and inflammation.