On a variety of fronts, chronic bacterial infection is being found to be significantly associated with the development of atherosclerosis and the clinical complications of unstable angina, myocardial infarction, and stroke. Although for the most part, these are still just associations, and specific causative relationships on the par with that determined for Helicobacter pylori and peptic ulcer disease have not been determined. Further studies may well lead to a similar conclusion about these potential mechanisms whereby chronic infections may play a role in atherosclerosis on myocardial infarction. As in the case of Chlamydia pneumoniae, the affect may result from direct vessel wall colonization and infection. This local infection may either react directly on the vessel wall or indirectly through its initiation of a number of immunologic responses. In other cases, the influence of chronic infection on the progression of atherosclerosis may be related to an indirect affect of enhancing the chronic inflammatory response of the body. Even though the infectious agent may not directly infect the vessel wall it may have a critical affect acting from afar. There is a potential that chronic bacterial infection may aggravate pre-existing plaque by enhancing T cell activation as well as other inflammatory responses that may participate in the destabilization of the intimal cap resulting in plaque rupture, progression to acute ischemic syndromes, and ultimate enlargement of the atherosclerotic plaque. Consequently, chronic bacterial infection may play a role in the initiation, the progression, or the destabilization of atherosclerotic plaques. Further studies that are presently ongoing and planned for the near future are expected to not only further elucidate the pathophysiology related with the association between chronic bacterial infection and atherosclerosis but also evaluate whether antibiotic treatment may result in clinical benefit to the patient.