Coronary heart disease (CHD) is the leading cause of death in western count
ries. Although several major risk factors have been identified, they fail t
o account for all the epidemiological variants of the disease, thus warrant
ing research into novel causal agents. Cardiovascular diseases have long be
en associated with chronic infections acting through the activation of infl
ammatory pathways, and antibiotic therapy has been shown to produce a drama
tic decrease in the rate of disease recurrence in patients with a history o
f myocardial infarction or unstable angina. The link between Helicobacter p
ylori (H. pylori) infection and CHD, first described by Mendall et al. in 1
994, has been the subject of a multitude of epidemiological and clinical st
udies; however, these have been so heterogeneous that not two of them are b
ased on a comparable selection of patients and focused on the same kind of
disease, e.g. stable coronary heart disease or acute myocardial infarction.
Evidence from animal studies supports the thesis that H. pylori plays an e
xtremely important role in the acute phase of myocardial infarction: the ba
cterium causes platelet aggregation and induces pro-coagulant activity in e
xperimentally Infected mice. H. pylori may also contribute to athero-sclero
sis through an auto-immune process against endothelial cells or an increase
d concentration of homocysteine in the blood due to decreased levels of fol
ic acid and cobalamin. The exact role of H. pylori cannot yet be fully asse
ssed: there is a clear and present need for further studies with appropriat
e epidemiological and clinical approaches to investigate through prospectiv
e and interventional trial the possible causal relationship between H. pylo
ri and CHD.