While early observations on the possible connection between chlamydia and arteriosclerosis remain unnoticed, it was found recently that in acute myocardial infarction (AMI) a sero response to an epitope of chlamydial lipopolysaccharide (LPS) could be demonstrated in about 70% of cases. Moreover, steadily elevated titres against Chlamydia pneumoniae in patient sera pointed to a possibility that chronic infection due to the agent was exacerbated in AMI. This assumption has been further supported by the finding of (a) elevated C. pneumoniae antibody titres in coronary heart disease patients in several studies, (b) the presence of immune complexes containing chlamydial LPS in acute AMI cases and their formation of antigen excess followed a month later by antibody excess, (c) the presence of antibodies to C. pneumoniae proteins in immune complexes in chronic coronary heart disease. The presence of elevated antibody titres and/or immune complexes containing chlamydial LPS was a significant independent risk factor (up to 2.6, CL, 1.3 to 5.2) for AMI 3-6 months before cardiac incidents in the Helsinki Heart Study. The odds ratio was especially significant (up to 7.2, CL, 1.4 to 35) if the cohort on cholesterol-lowering drug was followed.