Insights into the role of infection in atherogenesis and in plaque rupture

Abstract

In summary, compelling data indicate that infection does contribute to atherogenesis and to the acute complications of atherosclerosis caused by plaque rupture. What has clearly emerged over the past decade, however, is that there are profound complexities inherent in the interactions that occur between different pathogens and a variety of genetically determined host factors, each of which profoundly alters the host's response to infection (Figure 2); these include the host's susceptibility to infection, the magnitude of the host's inflammatory response to a given infection, and whether the host is predisposed to develop an autoimmune response. Therefore, whether a specific pathogen (or combination of pathogens) will initiate, cause progression of, or precipitate one of the acute complications of atherosclerosis will be determined by these complex factors and their complex interactions. It would thus appear that we need considerably more information about an individual's genetically based susceptibility to infection, to inflammation, and to immune responses before we can adequately predict how pathogens influence atherogenesis and its complications in the individual patient. © 2009 American Heart Association, Inc.