While it is clear that high blood cholesterol leads to development of coronary heart disease, some people with that disorder have average or low cholesterol levels, a situation that has long puzzled researchers. A number of studies have investigated whether various infectious agents may play a role in the development of atherosclerosis. An NIH special panel reported on preliminary evidence linking the bacterial agent Chlamydia pneumoniae and one of the herpes viruses, cytomegalovirus, to the development of artery disease in 1997. Now a report from Europe seems to have found another connection.

Tracking 826 patients with atherosclerosis over a 5-year period, researchers found that the presence of chronic respiratory, urinary tract, dental, and other infections amplified the risk of hardening of the carotid arteries. The association was strongest in those people with no carotid atherosclerosis at the baseline measurement. In those people with chronic infections, the risk was highest in those who had a prominent inflammatory response. The researchers call their data "solid evidence" for a role of common chronic infections in development of arterial disease, perhaps through systemic inflammation and autoimmunity.

Findings such as these open new avenues for prevention and treatment. That is what happened to ulcer disease in the 1990s: long thought to have been the result of excess production of gastric acid, it turns out that peptic ulcers are caused by bacteria. Treatment of the bacteria has eliminated many long-term treatment regimens and special diets for people with ulcers.

Sources:

• Kiechl S, Egger G, Mayr M, et al. Chronic infections and the risk of carotid atherosclerosis. Circulation 2001;103:1064. (Abs.)
• Libby P, Egan D, Skarlatos S. Roles of infectious agents in atherosclerosis and restenosis. Circulation 1997;96:4094-4103.