More than a century ago, inflammation and infection were considered to have atherogenic effects. During last century, however, this hypothesis was completely abandoned, and the old idea that coronary heart disease (CHD) possibly has an infectious etiology has only re-emerged in recent years. Both viral and bacterial pathogens have been proposed to be associated with the inflammatory changes found in atherosclerosis. Herpes group viruses, especially cytomegalovirus (CMV) and herpes simplex virus type 1 (HSV1), have been associated with both atherosclerosis and restenosis. Helicobacter pylori and dental infections have also been linked to CHD, but the evidence is strongest for a respiratory tract bacterium, Chlamydia pneumoniae. The association was originally found in seroepidemiological studies, but the presence of organisms in atherosclerotic lesions, the first animal studies and preliminary successful intervention trials with antibiotics suggest that C. pneumoniae may have a pathogenetic role in the disease. The causal relationship has not yet been proven, but ongoing large intervention trials and research on pathogenetic mechanisms may lead to the use of antimicrobial agents in the treatment of CHD in the future.