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THE JOURNAL OF CARDIOVASCULAR SURGERY
A Journal on Cardiac, Vascular and Thoracic Surgery
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,632
ORIGINAL ARTICLES CARDIAC PAPERS
The Journal of Cardiovascular Surgery 2000 December;41(6):829-33
Ischemic cardiovascular disease and Helicobacter pylori. Where is the link?
Pellicano R., Oliaro E. *, Gandolfo N. **, Aruta E. ***, Mangiardi L. *, Orzan F. *, Bergerone S. *, Rizzetto M., Ponzetto A.
From the Department of Gastro-Hepatology *Department of Cardiology Hospital Molinette, Turin (Italy)
**Cardiology Unit Hospital Mauriziano, Turin (Italy)
***Cardiology Unit Hospital Giovanni Bosco, Turin (Italy)
Coronary heart disease (CHD) is the leading cause of death in western countries. Although several major risk factors have been identified, they fail to account for all the epidemiological variants of the disease, thus warranting research into novel causal agents. Cardiovascular diseases have long been associated with chronic infections acting through the activation of inflammatory pathways, and antibiotic therapy has been shown to produce a dramatic decrease in the rate of disease recurrence in patients with a history of myocardial infarction or unstable angina. The link between Helicobacter pylori (H. pylori) infection and CHD, first described by Mendall et al. in 1994, has been the subject of a multitude of epidemiological and clinical studies; however, these have been so heterogeneous that not two of them are based 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 extremely important role in the acute phase of myocardial infarction: the bacterium causes platelet aggregation and induces pro-coagulant activity in experimentally infected mice. H. pylori may also contribute to atherosclerosis through an auto-immune process against endothelial cells or an increased concentration of homocysteine in the blood due to decreased levels of folic acid and cobalamin. The exact role of H. pylori cannot yet be fully assessed: there is a clear and present need for further studies with appropriate epidemiological and clinical approaches to investigate through prospective and interventional trial the possible causal relationship between H. pylori and CHD.