Although Helicobacter pylori (Hp) primarily colonizes gastric mucosa, it can occasionally inhabit in atherosclerotic plaques. Both forms of Hp infection may be involved in the pathogenesis of atherosclerosis via activation of a systemic or local inflammatory host reaction and induction of plaque progression and/or instability, possibly leading to coronary syndromes. The association between Hp infection and cardiovascular endpoint prevalence remains uncertain; however, it has been reported in many epidemiological investigations and may be reasonably explained by pathophysiological mechanisms. Besides the inflammatory pathway, Hp infection may trigger acute coronary syndromes by enhanced platelet reactivity and increased risk of gastrointestinal bleeding (type 2 myocardial infarction). The former seems to be predominantly related to the stimulatory effect of Hp infection on von Willebrand factor-binding and P-selectin activation, and the latter results from cytotoxic bacteria properties and aggravation of digestive tract injury related to aspirin or dual antiplatelet therapy. Despite these premises, the role of Hp infection in cardiovascular syndromes should still be recognized as controversial and requiring randomized, controlled trials to evaluate the outcome of Hp eradication in both cardiac and gastroenterological endpoints. Such need is also justified by potential bias of previous studies resulting from (1) using different diagnostic methods for identification of Hp infection, since only a small number of studies required confirmation of active Hp infection; and from (2) common lack of adjustment for important confounders such as socioeconomic status, smoking and effectiveness of eradication therapy, as well as the genetic characteristics of both the host and the bacterium.Copyright © 2014, Springer-Verlag Berlin Heidelberg.
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