Editorial
Copyright ©The Author(s) 2015.
World J Cardiol. Apr 26, 2015; 7(4): 187-203
Published online Apr 26, 2015. doi: 10.4330/wjc.v7.i4.187
Table 1 Major results of the clinical and basic research studies on the relationship between coronary heart disease and Helicobacter pylori infection
Study characteristicRef.
Serological parameters
Higher prevalence and concentrations of anti-H. pylori antibodies in CHD vs non-CHD individuals[84-88]
Association between H. pylori CagA positive infections and CHD; exposure of endothelial and smooth muscle components within atherosclerotic plaques to the anti-CagA antibodies[88-92]
Autoimmunity hypothesis: the presence of the immune complexes LeX/Y-anti-LeX/Y IgG in CHD patients infected with H. pylori[47,127,134]
Bacteriological parameters
Detection of H. pylori genomic material (16S rRNA) in the coronary arteries and atheromatous plaques from patients with cardiologic disorders[43,91,103-105]
Presence of viable H. pylori bacteria in atherogenic plaques[106]
Biochemical parameters
Association of H. pylori infection with the increased biochemical and inflammatory parameters of CHD as well as coronary lumen reduction[85,92,107-109]
Higher prevalence of LDL-hiperchlesterolemia, HDL-hypocholesterolemia and elevated levels of CRP in H. pylori infected than uninfected individuals[110,127-129]
Lower activity of serum paraxonase-1 (a major anti-atherogenous component of HDL) and higher carotid-intima media thickness (one of the surrogate marker of atherosclerosis) in H. pylori positive in comparison to negative subjects[108]
Positive correlation between raised LBP levels and the severity of CHD with co-existing H. pylori infection. The escalation of inflammatory process occurring via Toll-like receptors and LPS-LDL complexes[127]
Increased levels of homocysteine in H. pylori infected individuals caused by malabsorption of vitamine B12 and foliate from diet, leading to obesity-related resistance to insulin[48,130,131]
Inflammation and inflammation-related parameters
Increased concentrations of IL-6, IL-8, TNF-α, plasminogen, activator inhibitor type-1, and von Willebrand factor in CHD patients infected with H. pylori[3,38,69,83]
High levels of fibrinogen, a marker of systemic inflammation – putative link between H. pylori infections and pathophysiology of CHD[133]
Recruitment of immune cells to the infectious foci and survival of H. pylori within the endothelium due to interaction of H. pylori LPS Le determinants with E- and L-selectins[38,136]
Stimulation of Th1 lymphocytes to produce cytokines by H. pylori HspB[47, 127,134]
Epidemiological studies
Higher risk of CHD in ethnic groups of Central Africans and Mexican Americans with increased prevalence of H. pylori infections[100-102]
Genetic susceptibility to infections and predisposition to strong inflammatory response[140,145-146]