(Circulation. 2001;103:2915.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Department of Medicine II (S.B., H.J.R., C.B., C.E.-K., J.M.), Department of Medical Statistics and Documentation (G.R.), and Department of Clinical Chemistry (G.H., M.O.), Johannes Gutenberg University, Mainz, and EUROIMMUN, Lübeck (K.S.), Germany.
Correspondence to Dr Stefan Blankenberg, Johannes Gutenberg University Mainz, Department of Medicine II, Langenbeckstraße 1, 55131 Mainz, Germany. E-mail stefan.blankenberg{at}uni-mainz.de
BackgroundProspective data relating previous exposure to cytomegalovirus (CMV) to the risk of cardiac mortality are controversial. We investigated the effect of previous exposure to CMV infection on the risk of future cardiac diseaserelated death in relation to an underlying inflammatory response.
Methods and
ResultsCoronary angiography was
performed in 1134 subjects, and 989 patients with documented
coronary artery disease were studied prospectively. CMV-IgG
titers and interleukin (IL)-6 levels were measured before angiography.
Increasing titers of CMV correlated with the elevation of IL-6 levels
(P<0.001) after adjustment for
possible confounders. All patients were followed up for a median of 3.1
years (maximum 4.3 years). During follow-up, 96 patients died, 70 of
cardiac disease. Overall, CMV seropositivity was not related to cardiac
mortality after adjustment for confounding variables
(P=0.19). In contrast, in
patients with elevated IL-6 levels (
11.9 pg/mL, median level), CMV
seropositivity was independently associated with a 3.2-fold (95% CI
1.4 to 7.3, P=0.007) increase
in risk of future cardiac death, whereas in individuals without IL-6
elevation, previous CMV infection had no effect on cardiac
mortality.
ConclusionsCMV seropositivity in patients with an inflammatory response is independently associated with future cardiac mortality, whereas this association is lost in patients who do not demonstrate an inflammatory response. These data support the hypothesis that the atherosclerotic effects of CMV are mediated through an underlying inflammatory response.
Key Words: viruses risk factors ischemia thrombosis survival
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