Infection and inflammation have been suggested to play roles in coronary ar
tery disease (CAD). We hypothesized that: (1) CAD risk is associated with t
he aggregate number of pathogens (pathogen burden), and (2) increased patho
gen burden is associated with elevated levels of C-reactive protein (CRP),
a marker of inflammation, We evaluated 233 patients for CAD. Blood samples
from each patient were tested for immunoglobulin-G (IgG) antibodies to cyto
megalovirus (CMV), Chlamydia pneumoniae, hepatitis A virus (HAV), herpes si
mplex virus type 1 (HSV-IJ and HSV type 2 (HSV-2), and for the CRP levels.
Of the 233 study subjects, 68% had evidence of CAD by coronary angiography.
Although the prevalence of seropositivity for each pathogen tended to be h
igher in the patients with CAD than those without, only the association bet
ween CAD and seropositivity to HAV was significant in multivariate analysis
. Over 75% of study subjects had been exposed to greater than or equal to 3
of the 5 pathogens tested, and analysis determined that increasing pathoge
n burden was significantly associated with increasing CAD risk, even after
adjustment for traditional CAD risk factors. The prevalence of CAD was 48%,
69%, and 85% in individuals with antibodies to less than or equal to 2 pat
hogens, to 3 or 4 pathogens, and to 5 pathogens, respectively. A similar as
sociation between increasing pathogen burden and CRP levels was also found.
The pathogen burden remained a significant predictor of CRP levels after m
ultivariate analysis. Our data suggest that infection does play a role in t
he genesis of atherosclerosis. However, the risk posed by infection is rela
ted to the pathogen burden that may contribute to CAD through inflammatory
responses. (C) 2000 by Excerpta Medica, Inc.