Chlamydia pneumoniae is frequently found in atherosclerotic lesions, and hi
gh titers of specific antibodies are associated with increased risk for acu
te myocardial infarction, However, a causative relation has not been establ
ished yet. We performed a prospective study of 93 patients undergoing percu
taneous transluminal coronary angioplasty (PTCA) to investigate whether ang
ioplasty influences Chlamydia-specific antibody titers and whether there is
an association with restenosis, Blood samples were obtained before and 1 a
nd 6 months after angioplasty, Antibodies against chlamydial lipopolysaccha
ride and against purified C. pneumoniae elementary bodies were measured by
enzyme-linked immunosorbent assay (ELISA). After angioplasty, the prevalenc
e of antibodies to lipopolysaccharide rose from 20 to 26% for immunoglobuli
n A (IgA), from 53 to 64% for IgG, and from 2 to 7% for IgM (P = 0.021, 0.0
04, and 0.046, respectively). There was a rapid increase of mean antibody t
iters of all antibody classes within 1 month of PTCA, During the following
5 months, antibody titers decreased slightly but were still higher than bas
eline values. Results of the C. pneumoniae-specific ELISA were essentially
the same. The rise of anti-Chlamydia antibodies was not caused by unspecifi
c reactivation of the immune system, as levels of antibodies against cytome
galovirus did not change. Neither seropositivity nor antibody titers were r
elated to restenosis. However, increases in mean IgA and IgM titers were re
stricted to patients who had suffered from myocardial infarction earlier in
their lives. In conclusion, we show that PTCA induces a stimulation of the
humoral immune response against C. pneumoniae. These data support the idea
that plaque disruption during angioplasty might make hidden chlamydial ant
igens accessible to the immune system.