Atherothrombotic vascular disease is the leading cause of death in most of the western nations and predicted to become the leading cause of death in the world over the next decade. A number of risk factors have been identified that increase the risk of atherothrombosis and they include family history of premature vascular disease, dyslipidemia, smoking, hypertension, insulin resistance and diabetes mellitus, obesity, atherogenic diet, hyperhomocystenemia, estrogen deficiency, and lack of physical activity. However, these conventional risk factors do not account for all of the attributable risk of atherothrombotic vascular disease. A search for additional risk factors has led to the idea that chronic infections may be an important risk factor. Chronic infections as potential culprits in the vascular inflammatory response have received renewed interest since the critical role of inflammation in the evolution, progression, and destabilization of atherothrombosis has been recognized (1–3). From a historical perspective, the idea that infections may contribute to atherosclerosis was suggested by several authors around the beginning of the 20th century (4,5). In fact, in 1911, Frothingham stated that “The sclerosis of old age may simply be a summation of lesions arising from infectious or metabolic toxins” (6). Based on examination of 400,000 sections from 40 necropsy cases, Leary coined the term “abscess” to 136describe atheromatous plaques containing leucocyte infiltration (7). Based on recent seroepidemiologic data, human pathology, biological plausibility, experimental models, and pilot clinical trials, a potential causal link between chronic infections and atherothrombotic disease has received much attention in recent years (8–10).