In 1908, Sir William Osler was the first to suggest that infection might play a role in the pathogenesis of atherosclerosis . Even though this view was not widely accepted originally, a renewed interest currently abounds regarding the contribution of infection to the pathogenesis and progression of ischemic heart disease. The current concept of atherosclerosis is based on the model “response to injury” proposed by Ross in 1986 . This model suggests that infection may contribute to the formation of atherosclerosis through injury to the vascular endothelium along with inflammatory, metabolic and hemostatic mechanisms . In the ‘70s, formation of atherosclerotic lesions in the arteries of chickens infected with herpes virus was demonstrated experimentally . The recent discovery of Helicobacter pylori, as an etiological agent of another chronic disease, peptic ulcer, suggests that an infectious etiology for atherosclerosis should be considered . Since then, associations between ischemic heart disease and some Gram-negative bacteria, such as Helicobacter pylori and Chlamydia pneumoniae, and certain herpes viruses, especially cytomegalovirus , have been reported. Most of the published material consists of epidemiological studies based on associations between the serology of the respective antibodies and ischemic heart disease or on immunohistochemical evidence of the presence of bacteria or viruses in atherosclerotic lesions. Recently, new evidence originating from controlled clinical trials has emphasized this new paradigm for managing ischemic heart disease . This study aims to provide an updated review of the evidence available relating infection to coronary atherosclerosis.