Chronic infection and coronary artery disease.

On a variety of fronts, chronic infection has been found to be significantly associated with the development of atherosclerosis and the clinical complications of unstable angina, myocardial infarction, and stroke. For the most part, these are still just associations. Specific causative relationships on par with that determined between H. pylori and peptic ulcer disease have not yet been established. Potential mechanisms whereby chronic infections may play a role in atherogenesis are myriad. In the case of C. pneumoniae, the effect may result from direct vessel wall colonization, which may damage the vessel directly or indirectly by initiating immunologic responses. In other cases, the effect may simply be that of enhancing the preexisting chronic inflammatory response of the body to standard risk factors, such as hyperlipidemia. Even though the infectious agent may not directly infect the vessel wall, it may perform its critical role from afar. Chronic infection might also influence preexisting plaque by enhancing T cell activation or other inflammatory responses that may participate in the destabilization of the intimal cap. Chronic infection may play a role in the initiation, progression, or destabilization of atherosclerotic plaques. The infectious agents with the most evidence to support a causative role in atherosclerosis include C. pneumoniae and cytomegalovirus. Evidence is mounting for a variety of other potential agents, including H. pylori, various periodontal agents, and even hepatitis A. Future studies are expected to elucidate further the pathophysiologic relationship between chronic infection and atherosclerosis and to evaluate the potential of a variety of treatment approaches, including antibiotics.