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As early as 1978, evidence in experimental infection of germ-free chickens by herpesvirus was noted to result in arterial disease like human atherosclerosis. Since that time, further associations between human coronary heart disease (CHD) and infection continue to be corroborated; for instance, Helicobacter pylori, Chlamydia pneumoniae, and cytomegalovirus have been associated with human CHD, specifically coronary disease.
It is postulated that infections may effect vascular disease by 1) direct infection of the arterial wall, leading to smooth muscle proliferation and local inflammation; 2) systemic infection leading to endothelial injury or dysfunction due to circulating endotoxin; 3) autoimmune responses in which bacterial antigens cross-react with vessel antigens; 4) systemic inflammation leading to increases in C-reactive protein, leukocyte counts, and cytokines which affect the vascular wall; and 5) altering classical risk factors such as lowering HDL, raising fibrinogen, and raising triglycerides.
Based upon their literature review, assessing odds ratios of seropositivity among cases vs. controls, the authors conclude that the evidence about chronic infections and CHD is of insufficient magnitude to draw strong conclusions, and information is limited by potential biases. Of the three primary candidates for CHD causation, the association evidence is strongest for C. pneumoniae; these associations may eventually require randomized intervention studies to resolve their clinical role.
Danesh J, et al. Lancet 1997;350:430-436.