Role of inflammation and infection in vascular disease

Relationship of infection, inflammation, and atherosclerosis has been a subject of intensive investigation in recent years. Potential mechanisms whereby chronic infections may play a role in atherogenesis are myriad. Chlamydia pneumoniae (Cp) infection in early life may accelerate atherosclerosis, leading to cardiovascular complications. Other infections, simultaneously occurring with Cp, may result in a synergistic effect to promote atherosclerosis. Chronic Helicobacter pylori infection is known to increase the pH level of the gastric juice and to decrease ascorbic acid levels, both of which will lead to a reduced folate absorption. Low folate hampers the methionine synthase reaction. This leads to an increased concentration of homocysteine in the blood, resulting in damage of endothelial cells. Cytomegalovirus (CMV) infection is associated with accelerated atherosclerosis following cardiac transplantation; several studies have found that patients with a previous CMV infection had a high independent risk of restenosis after coronary angiography. Inflammatory markers are independent predictors of cardiovascular and cerebrovascular events. Large population-based studies such as the study from the MONICA (MONItoring trends and determinants in Cardiovascular disease) Augsberg Center in Germany, the Atherosclerosis Risk in Communities Study, the Women's Health Study, the Honolulu Heart Study, have also suggested the relation between the levels of CRP and risk of coronary disease. Over the past decade also another marker of inflammation has been studied; fibrinogen has been identified as an independent risk factor for CAD in several large prospective studies. All these studies suggested a new, possible role of markers of infection and inflammation beyond traditional cardiovascular risk factors, in the development and progression of atherosclerosis. However, the clinical and therapeutic implications of these results remain to be evaluated. Although antibiotic treatment of infections in CAD patients had no impact on mortality in large prospective trials, promising data is coming from smaller studies and further studies are needed to investigate the possibility to submit this category of high-risk patients to therapeutical approaches of primary prevention.