Cytomegalovirus in the pathogenesis of atherosclerosis - The role of inflammation as reflected by elevated C-reactive protein levels

Citation
Jh. Zhu et al., Cytomegalovirus in the pathogenesis of atherosclerosis - The role of inflammation as reflected by elevated C-reactive protein levels, J AM COL C, 34(6), 1999, pp. 1738-1743
Citations number
20
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
07351097 → ACNP
Volume
34
Issue
6
Year of publication
1999
Pages
1738 - 1743
Database
ISI
SICI code
0735-1097(19991115)34:6<1738:CITPOA>2.0.ZU;2-0
Abstract
OBJECTIVES We hypothesized that cytomegalovirus ( infection: 1) stimulates an inflammatory response, reflected by elevated C-reactive protein (CRP) le vels, and 2) predisposes to coronary artery disease (CAD), in part, through CMV-induced inflammation. BACKGROUND Although some studies show an association between CMV and athero sclerosis, others do not. We believed that CMV exerted an atherogenic effec t by inducing inflammation, and the disparate results may derive partly fro m individual variability in the capacity to control CMV inflammatory activi ty. METHODS Blood samples were tested for CMV seropositivity and CRP levels fro m 238 individuals being evaluated for CAD by coronary angiography. RESULTS An elevated CRP level (>0.5 mg/dl) was a significant CAD determinan t even after adjustment for traditional CAD risk factors (odds ratio [OR] = 2.4; p = 0.02). Moreover, CMV seropositivity was significantly associated with increased CRP levels ip = 0.04 after adjustment for CAD risk factors), suggesting that CMV could evoke subclinical inflammatory response. However , considerable host variation existed in this response to CMV. When adjuste d for CAD risk factors, the OR for CAD were 1.3 in the subgroup with CMV se ropositivity alone (p = 0.7), 2.3 in the subgroup with elevated CRP levels alone (p = 0.2), and 4.3 in the subgroup with combined CMV seropositivity a nd elevated CRP levels (p = 0.01). CONCLUSIONS Our results suggest that 1) CMV elicits a subclinical inflammat ory response, but only in certain individuals, and 2) individuals with an i nflammatory response appear susceptible to the atherogenic effects of CMV w hereas those without appear resistant. These results may partly explain the disparate results of studies attempting to relate CMV to atherogenesis. (C ) 1999 by the American College of Cardiology.