作者: Jacek Budzyński , Marek Koziński , Maria Kłopocka , Julia Maria Kubica , Jacek Kubica
DOI: 10.1007/S00392-014-0720-4
关键词:
摘要: Although Helicobacter pylori (Hp) primarily colonizes gastric mucosa, it can occasionally inhabit in atherosclerotic plaques. Both forms of Hp infection may be involved the pathogenesis atherosclerosis via activation a systemic or local inflammatory host reaction and induction plaque progression and/or instability, possibly leading to coronary syndromes. The association between cardiovascular endpoint prevalence remains uncertain; however, has been reported many epidemiological investigations reasonably explained by pathophysiological mechanisms. Besides pathway, trigger acute syndromes enhanced platelet reactivity increased risk gastrointestinal bleeding (type 2 myocardial infarction). former seems predominantly related stimulatory effect on von Willebrand factor-binding P-selectin activation, latter results from cytotoxic bacteria properties aggravation digestive tract injury aspirin dual antiplatelet therapy. Despite these premises, role should still recognized as controversial requiring randomized, controlled trials evaluate outcome eradication both cardiac gastroenterological endpoints. Such need is also justified potential bias previous studies resulting (1) using different diagnostic methods for identification infection, since only small number required confirmation active infection; (2) common lack adjustment important confounders such socioeconomic status, smoking effectiveness therapy, well genetic characteristics bacterium.