Recent investigations have controversially but convincingly interpreted the pathogenesis of atherosclerosis (arteriosclerosis). Atherosclerosis can apparently be the result of ultrachronic, persistent infection by Chlamydia pneumoniae and not the result of heterogenous risk factors. The main arguments for chlamydial genesis are: (1) Correlation of coronary heart disease and other atherosclerotic diseases and antibodies against Chlamydia pneumoniae. (2) Chlamydia pneumoniae could be detected with different techniques (PCR, ICC, immunhistology, electromicroscopy, culture) in a high percentage of atheromas from different sites. (3) According to three successful international studies with macrolides in coronary heart disease. (4) Target cells of atherosclerosis (endothelia, macrophages, muscle cells) can be infected by Chlamydia pneumoniae in vitro. (5) Provocation of arteriitis in animal experiments. (6) The reduction of incidence of atherosclerotic diseases since the 1960s, probably due to advances in antibiotic treatment. (7) Elevated levels of acute-phase proteins and other inflammatory signs (CRP, WBC count, fibrinogin) briefly before cardiac infarction occurs. There are good arguments for intervention studies in coronary heart disease and other manifestations of atherosclerosis. The relevant antibiotics are available for chlamydial infections and are inexpensive and safe. Meticulous protocols and long-term monitoring of patients should be developed.