C. Kosaka et al., Possible role of chronic infection with Chlamydia pneumoniae in Japanese patients with acute myocardial infarction, JPN CIRC J, 64(11), 2000, pp. 819-824
Citations number
41
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Chlamydia pneumoniae, a common human respiratory pathogen, has been implica
ted in the pathogenesis of coronary heart diseases (CHD) in several seroepi
demiological studies. The present case-control study investigated the relat
ion between serologic evidence of C. pneumoniae infection and CHD in a Japa
nese population. Two groups of cases were enrolled: 26 patients with acute
myocardial infarction (AMI) and 46 patients with effort angina pectoris (e-
AP). Their data were compared with 58 age-matched healthy controls and also
compared with 53 patients with vasospastic angina (VSA) as pathological co
ntrol subjects, Anti-C. pneumoniae specific IgA and IgG antibody titers wer
e measured by enzyme-linked immunosorbent assay (ELISA). The mean indices o
f IgG-type antibody in AMI and e-AP were not significantly different from t
hose in either the normal controls or VSA group. On the other hand, the mea
n indices of IgA-type antibody in AMI were significantly higher than in the
normal controls (1.39+/-0.83 in AMI vs 0.84+/-0.58 in controls, p<0.001) a
nd VSA (1.39+/-0.83 in AMI vs 1.05+/-0.61 in VSA, p<0.05) group. However, t
he differences in the IgA titers in the e-AP group compared with the normal
controls did not reach a significant level. The odds ratio associated with
the seropositivity of IgA for AMI against the normal controls was 3.89 (95
% confidence interval (CI): 1.16-13.10) and that against VSA was 6.90 (95%
CI: 1.73-27.52) after adjustment for risk factors for CHD and/or age, sex a
nd smoking status. In 6 patients the elevated IgA titers were sustained eve
n at 3 months after the episode of AMI. These results suggest that seroposi
tivity for IgA-type antibody against C. pneumoniae may be a significant ris
k factor for the development of AMI. The possible mechanisms include chroni
c inflammation in the coronary artery due to persistent C. pneumoniae infec
tion.