Evidence relating H. pylori to non-gastrointestinal disease is sparse and inconclusive. Suggested mechanisms whereby infection might increase cardiovascular risk include release of acute-phase reactants including fibrinogen, reduction of HDL cholesterol, elevation of homocysteine levels and immunological cross-reactivity between bacterial and human heat shock proteins. Six published studies relating H. pylori seropositivity to various measures of ischaemic heart disease (IHD)-angiography, acute myocardial infarction, angina symptoms, or electro-cardiographic abnormalities-are all consistent with a modest (up to 2-fold) elevation in risk of IHD among infected subjects after adjustment for age, socioeconomic status and conventional cardiovascular risk factors. The pooled odds ratio from 1 longitudinal, 3 case-control and 2 cross-sectional studies is 1.4 (95% confidence interval 1.1-1.8). Further large-scale longitudinal studies are required to quantify the predictive value of seropositivity, to clarify the causal interpretation and to assess the underlying mechanisms for any link between H. pylori infection and ischaemic heart disease.