Infection and early atherosclerosis: Does the evidence support causation?

Abstract

Although clinical manifestations of atherosclerotic coronary heart disease occur in adult life, the initial stages of its development commence in childhood. Therefore, elucidating the pathogenesis of early atherosclerosis and identifying the network of risk factors have become fundamental priorities for both cardiovascular healthcare providers and scientists. There is mounting evidence from both human studies and animal experiments that infectious pathogens could be implicated in atherosclerosis development. The vulnerability of the arterial wall to the adverse effects of infection is probably augmented when additional risk factors and/or certain proatherogenic genetic profiles are also present. The precise mechanisms whereby infection, alone or in synergy with conventional cardiovascular risk factors, could contribute to atherosclerosis are not fully understood.Injury to the vascular endothelium, which could be elicited by infection through inflammatory, metabolic, autoimmune, and pathogen-related mechanisms, might be a central link between infection and early atherosclerosis.