*3.3.4 Infections and atherosclerosis*

The traditional risk factors merely are not adequate to explain the development of atherosclerosis in all patients. Additional risk factors that predispose to atherosclerosis development are yet undetected. The triggers of the arterial injury, which result as an atherosclerotic plaque, have not been clearly identified. The oxidized LDL and heat shock proteins are identified factors, which elicit an inflammatory response through a complex autoimmune response [67–69].

The demonstration of the infectious agents in the atherosclerotic lesions by polymerase chain reaction (PCR) and immunohistochemistry (IHC), and the seroepidemiological studies suggests a presence of an inflammatory trigger pathway initiating with an infection, which results in atherosclerosis and even possibly with its complications [21, 70–72].

Infectious agents can promote atherosclerosis through direct effect of the agents on cellular components of the vessel. The Chlamydia pneumonia and cytomegalovirus infections are the mostly concerned infectious agents demonstrated to have these effects. These mechanisms include smooth muscle cell proliferation and inhibition of their apoptosis, enhancement of smooth muscle cell migration, enhanced foamy cell formation, and increased expression of cytokines and cellular adhesion molecules, which lead to endothelial cell dysfunction. Autoimmune reaction through molecular mimicry of the heat shock proteins could be other possible mechanism [69].
