Table 1.

Major results of the clinical and basic research studies on the relationship between coronary heart disease and Helicobacter pylori infection

Study characteristic	Ref.
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]

CagA: Cytotoxin-associated gene A; CHD: Coronary heart disease; CRP: C-reactive protein; Ig: Immunoglobulines; HDL: High density lipoprotein; Hsp: Heat shock protein; LBP: Lipopolysaccharide binding protein; IL: Interleukin; LDL: Low density lipoprotein; Le: Lewis; TNF: Tumor necrosis factor.