Do infections and other inflammatory disease cause CVD through increases in inflammatory mediators?
This question could be important in determining the population-level contribution of inflammation to CVD burden; however, the question cannot be answered at this time. Studies of the relationship between infectious burden and CVD have been limited by measures of previous infection rather than long-term, persistent, or active infection. In addition, the role of infection in stimulating inflammation and therefore atherosclerosis is not established.
