Present findings showed patients with H. pylori infection are about 3 times more at risk of CHD independent to history of DM, DLP, HTN, CRP status and IL-6 level. Our findings were in accordance with few studies which evaluated the H. pylori association with CHD and acute myocardial infarction, but the chance which was suggested for this infection role in present study was higher compared to other studies.10
In the new decade, many study evaluated the role of H. pylori infection in extra-digestive disorders and the results was surprising. For examples, one study showed that H. pylori infection decrease the blood pressure value in patients who suffer from hypertension.17
In addition, a few studies have demonstrated the association of some kinds of DLP and H. pylori infection.18
In a case control study, relationship of H. pylori infection with insulin resistance was suggested.20
On the other hand, it was documented that this gram negative bacterium induces the higher levels of some inflammatory biomarkers like CRP and IL-6.21
Accordingly, H. pylori association with some cardiovascular risk factors has been suggested and also it was shown that this bacterium induces some inflammatory cytokines. In the present study, the role of these risk factors and cytokines were adjusted, therefore, the remained higher chance may be due this adjusting and reveal the independent role of H.pylori infection in atherosclerosis process.
One study in a Korean population by Lee et al.12
suggested that H. pylori infection is not an independent risk factor for CHD. In their study, method of data adjusting were different from our study and prothrombin time, activated partial thrombin time, CRP, and fibrinogen were used for adjusting. Also, an upper gastrointestinal endoscopy for diagnosis of H. pylori infection was used, so these differences in methods of two studies probably justifies these different findings.
Mechanisms which were suggested as responsible for the possible association of H. pylori infection and CHD are as follows:17
Firstly, damaging influence of H. pylori and its products like cytokines, cytotoxins on coronary endothelium; secondly, activation of immune mechanisms by this bacteria which react with the nuclei of monocytes in atherosclerotic vessel wall and cytoplasm of fibroblast-like cell in atherosclerosis plaques; thirdly, H. pylori induces releasing of nitric oxide by vascular endothelium interferes with fibrinogen level which cause the reduction of the normal capacity of muscular relaxation and lead to vasoconstriction and adverse hemodynamic balance; finally, this infection elevates thromboxane which is measured as TXB that results in platelets activation.
Adjusting data for history of DM, DLR, HTN, CRP status and IL-6 level should be considered as a strength of this study while, cross-sectional design of study and absence of the other not measured confounders in adjusting data should be regarded as its limitations. Further studies are needed to evaluate the causal relationship between H. pylori infection eradication and CHD. It would be very important because screening and treatment of this infection by specific antibiotics could be easily done, if we hypothesize H. pylori infection eradication as an adjunctive measure for decreasing CHD.
In conclusion, since atherosclerosis process is multi factorial, H. pylori infection probably is one of the risk factors independent of DM, DLP, HTN, CRP status and IL-6 level.