1174 Edit/bz

vascular diseases. Interest of many authors has been to isolate laboratory values associated with a high risk of the onset or worsening of clinical coronary artery disease. Afterwards, a possible link of these values with chronic infection carrier status was sought. Many conditions related with vascular pathology, such as hypercoagulability, presence of circulating immune complexes and oxidative metabolites, an increase in leukocytes blood count, altered serum lipid profile, resulted associated with H. pylori. This agent may also induce a persistent increased production of interleukin (IL)-6, which possesses proinflammatory and procoagulative properties. IL-6 is also able to increase C reactive protein plasma levels4. This acute phase reactant, widely popular in general practice as an aspecific diagnostic marker, represents a well known potential risk factor for future myocardial ischaemic events5-8. Il-1 and Tumor necrosis factor alfa (TNFa) are, in turn, higly likely to be produced after H.pylori infection. Their action on the endothelium causes various degrees of disfunction. It also has been postulated an autoimmune mechanism based on the expression by H. pylori of a protein similar to human Heat Shock Protein 60 (HSP 60) commonly detectable at the site of plaque 8. First clinico-epidemiological evidences for a correlation between H. pylori and ischemic heart disease came out in a 1994 retrospective study. Since then, many authors reported a correlation time to time strong or spurious. However, data resulted often confused because of a lack of adjustment for other carClassical risk factors for atherosclerosis fail to completely explain the incidence of cardiovascular disease. Increasing evidences, dating from nineteen century observations to current studies, have shown that atherosclerosis is mostly an inflammatory disease and that coronary heart disease status and prognosis have strong relationships with inflammation1,2. On their way to find possible triggers for chronic inflammation, many authors noticed that various types of chronic infection, as those given by Helicobacter pylori and Chlamydia pneumoniae, are associated with an increase in risk factors and prognostic markers of ischemic heart disease (IHD). These chronic persistent infections in a variable number of cases run a symptomless course in infected subjects. Also for this reason, the impact of such a chronic infection on the immune system is hidden and long-term. In particular, the role hypothesized for Helicobacter pylori in the pathogenesis of cardiovascular diseases oversteps the well known pathological models of “acute infection-illness” and could bring new insights for the comprehension of conditions previously labelled as “idiopathic” or “functional”. Helicobacter pylori (H. pylori) is one of the most frequent gastrointestinal infections worldwide. The immunological response this bacterium elicits is a mainstay determinant of gastric mucosal damage. In particular, the production of large amounts of various proinflammatory substances, such as cytokines, eicosanoids and proteins of the acute phase follows the gastric colonization3. Upon the basis of these observations, much interest has grown about its role in most exEuropean Review for Medical and Pharmacological Sciences