In recent years, the results of some studies have revealed the possible potential role of several infectious agents in the inflammatory mechanism of atherosclerosis. The detection of specific antibodies against microorganisms such as Chlamydia pneumoniae and cytomegalovirus as well as antibodies directed to heat shock proteins in the sera of atherosclerotic patients and the presence of genomic material in atheromatous plaques all provide evidence supporting the presumptive role of infectious agents in atherosclerosis. There are some findings that can be accepted as clues for the possible involvement of Mycobacterium tuberculosis in atherosclerosis. These consist of the presence of high levels of mycobacterial heat shock protein 65 in atherosclerotic patients, and in animal studies, the detection of atherosclerotic changes in the vascular wall of animals vaccinated with recombinant heat shock protein 65, and Mycobacterium tuberculosis containing heat shock protein 65. The probable proatherogenic effect of the specific immune response to BCG-associated heat shock protein was also suggested. The mycobacterium cell wan contains a phospholipid, phosphatidylinositol, which was shown to have a procoagulant effect similar to that of a cytomegalovirus possessing phosphatidylserine, another phospholipid showing a procoagulant effect. These data suggest that Mycobacterium tuberculosis may also be involved in the pathogenesis of atherosclerosis.