A large body of evidence exists that implicates a number of microbial
agents in the pathogenesis of coronary heart disease (CHD), This, if p
roven, may have far-reaching implications for the prevention and treat
ment of CHD and other atherosclerotic disease, The histopathology of a
therosclerosis and its natural history suggest infectious causation at
many points along the progression of disease, particularly with regar
d to CHD, and a number of pathogens have been the focus of study, Vira
l agents implicated include Coxsackie B-4 virus, for which tenuous ser
o-epidemiological associations exist, and the Herpesviridae. The anima
l herpesvirus causing Marek's disease in chickens causes atherosclerot
ic lesions in these animals, Herpes simplex virus I and TI have been f
ound in aortic smooth muscle and produce changes in vitro in smooth mu
scle that are similar to those seen at the beginning of atherosclerosi
s and which may also explain some of the features of atherosclerotic c
omplications, Cytomegalovirus is implicated more strongly sero-epidemi
ologically by in-vivo detection in atherosclerotic lesions and by its
links with post-cardiac transplant vasculopathy - a syndrome similar t
o atherosclerosis. Bacteria have also been shown to have links with CH
D, Chlamydia pneumoniae and Helicobacter pylori have both been associa
ted sero-epidemiologically with CHD, and these findings have been cons
olidated by recent work showing their presence in atherosclerotic lesi
ons in adults, Bacterial infections in general lead to many changes in
lipid, thrombic and other acute-phase protein metabolism, and some of
these changes occur with both C. pneumoniae and H. pylori infections,
The ubiquity and similar epidemiological features to CHD of all these
microbial pathogens make the resolution of the causative issue imposs
ible by retrospective means, All that can be shown at present are a va
riety of weak and strong links, the significance of which can only be
determined by large and perhaps lifetime prospective studies.