Atherosclerosis is the most common cause of cardiovascular diseases, especially the ischemic heart disease and stroke, and is among the top four causes of death worldwide . Atherosclerosis is a compound Greek word for athero meaning gruel or paste and sclerosis meaning hardness; it is a disorder of large and medium arteries that begins with damage to the vascular endothelial cells and changes in the blood circulation and subsequent to the formation of the atherosclerosis plaques including the necrotic cores, calcified region, lipid particles, smooth muscle cells (SMCs), endothelial cells (ECs), polymorphonuclear cells (PMNs) and foamy cells (alternative macrophages) [60–61]. According to the available evidence, the most prominent stimulants for the formation and development of the atherosclerotic plaques are processes of vascular endothelium damage (especially the intima) and the chronic inflammation [60–62]. Infectious agents, especially Chlamydia pneumoniae, Mycobacterium tuberculosis and Helicobacter pylori, are among the most important infections that can cause chronic inflammation to escape the immune system and appear to be involved in the formation of the atherosclerotic plaques . The hypothesis of the role of Helicobacter pylori infection and atherosclerosis was first reported by Menall et al. and the track of Helicobacter pylori infection has been observed in atherosclerotic plaques of coronary, carotid and aortic arteries [38, 63]. In particular, the eradication of H. pylori infection decreased the CRP and proinflammatory response and improved the endothelial dysfunction and protective effect on early stages of the atherosclerosis formation [64–66]. In the present study, we collected and analyzed all the published articles about Helicobacter pylori infection in the Iranian cardiovascular patients, since the prevalence of atherosclerosis is high in Iran and a significant population in Iran is infected with H. pylori. Thus, the studies about the Iranian patients can provide very valuable results regarding the impact of H. pylori infection and the susceptibility to cardiovascular disorders. According to the present comprehensive meta-analysis, the rate of colonization with Helicobacter pylori and the formation of atherosclerotic plaques in the Iranian CAD patients are significantly related and may make the individuals susceptible to the cardiovascular disorders. According to the literature review, Helicobacter pylori contributes to the formation of the atherosclerotic plaques and CAD through the chronic inflammation, injuries and endothelial dysfunction, as well as the impaired body metabolism (Fig. 4). Studies have shown that chronic inflammation during atherosclerosis stimulates Th1 activity and causes the production of pro-inflammatory responses that result in calling and recruiting the inflammatory cells especially PMNs subsequent to the IL-1, IL-6, IFN-ϒ and TNF-α production, and macrophages also enter into the location in response to MCP1 / 2, inducing the inflammatory reactions that result in the destruction and dysfunction of the endothelial cells [61–63, 67–68]. Since H. pylori is capable of inducing the chronic inflammatory and Th1 response, it seems that it may be involved in the pathogenesis of atherosclerosis [67–68]. Furthermore, H. pylori can in some cases of chronic gastritis lead to atrophy and malabsorption of vitamin B12 and folic acid by stopping the gastric acid production, resulting in high levels of homocysteine, which increases the damage to the vessel wall through the stimulation of nitric oxide (NO) production and inflammation, and its serum level is elevated in a large number of patients affected by atherosclerosis and CAD [69–72]. According to existing studies, the people infected with H. pylori develop dyslipidemia . Hoffmeister et al. demonstrated that the CAD patients infected with Helicobacter pylori had higher levels of cholesterol, LDL, triglyceride, and apolipoprotein-B as compared to the CAD patients infected with chlamydia pneumonia or cytomegalovirus, and the HDL levels of these patients were also lower . However, similar studies have shown that after eradication of the infection with H. pylori, the serum levels of HDL and apolipoprotein-AI / AII increase and cholesterol, triglyceride, while that of the LDL levels decrease. It seems that helicobacter pylori increase the fatty acid by disrupting the fatty acid metabolism and causes it to be deposited on the vessel wall [73–75]. Metabolic disorders can also provide the of incidence of atherosclerosis . Gillum et al. showed that there was a significant relationship between H. pylori seropositivity and CAD in the diabetic patients . Moreover, de Luis showed that the rate of CAD and cerebrovascular disorders between the diabetic patients infected with H. pylori is high . In his studies, Polyzos et al. proved that infection with H. pylori is associated with resistance to insulin, and perhaps the infection with H. pylori via the impact on the metabolism (particularly glucose) of the body might lead to atherosclerosis, especially since the glucose resistance is improved subsequent to the eradication of infection with H. pylori and the level of the adiponectin (a factor for preventing metabolic disorders) is increased [79–80]. Processes such as hypertension and arterial stiffness have been implicated in the process of atherosclerosis, and studies have shown that there is a significant relationship between infection with helicobacter pylori and these factors [81–82]. Recently, the effect of Helicobacter pylori virulence factors has also been studied on atherosclerosis, and a previous report has shown a significant relationship between the infection with cytotoxin-associated gene A (CagA) positive strains and carotid plaque . Also, Bastiani et al. showed that H. pylori CagA seropositivity was very high in the patients who encountered stroke . It has been found in this respect that CagA strains induce atherosclerosis by the destruction of the vascular endothelial cells, modification of the oxidized LDL and stimulating the inflammation, and eradicating H. pylori CagA infection has stopped the above processes having a protective effect in the patients [85–87]. In addition, it has nowadays been suggested that CagA and HSPs stimulate the production of autoantibodies and endothelial dysfunction that ultimately lead to atherosclerosis [88–89]. There have been numerous reports about the relationship between Helicobacter pylori infection and the cardiovascular disease (CAD) [63, 89]. According to the literature review, Longo-Mbenza et al. evaluated the cardiovascular risk factors, in a longitudinal (provident) study, in 205 patients for a ten-year follow-up and showed that H. pylori IgG titers were high in a substantial population of CAD patients . In their studies on a population of 2029 in South Korea, Park et al. demonstrated that there was a significant relationship between H. pylori seropositivity and the CAD patients (ORs: 1.23; p = 0.049) . Other case-control studies conducted in India, Turkey, and Japan confirmed the results of previous studies [91–94]. Our study also confirmed the relationship between Helicobacter pylori infection and atherosclerosis in the CAD patients. Isolation of H. pylori from the atherosclerotic plaques is one of the most important evidence for approval of the role of this microorganism in the atherosclerosis and CAD [63, 89]. Extensive studies are so far fulfilled in this regard. For instance, the rate of isolation of H. pylori from atherosclerosis was 27.2–33.5% in the study by Jha et al. . In another study in Argentina, the carotid plaque isolation was about 83% . In a cross-sectional study in Turkey, Kilic et al. found that the rates of H. pylori isolation from the atherosclerotic plaques and non-atherosclerotic vascular wall specimens were 48.2% and 19.2%, respectively . However, H. pylori was not isolated from any atherosclerotic plaques in the studies in Italy and Poland [97–98]. Rahmani et al. demonstrated in their meta-analysis study that there was a significant relationship between the infection with H. pylori and Myocardial infraction in the Iranian patients (ORs = 2.53) . In a meta-analysis of 18 epidemiological studies Danesh et al. found no significant relationship between H. pylori infection and the coronary heart disease (CHD) . In a meta-analysis that Zhong et al. did on a 4041 population of stroke patients, it was shown that there was a significant relationship between H. pylori infection and ischemic stroke . In another study by Zhong et al., it was found that there was a significant relationship between H. pylori infection and the coronary artery disease in the European (ORs: 2.11) and US (ORs: 1.43) patient populations . However, in another meta-analysis, 13 studies were reviewed and no significant relationship was found between H. pylori and the stroke . Recent studies have suggested that infection with strains lacking CagA and vacuolating cytotoxin A (VacA) may lead to controversial results. Thus, the role of virulence helicobacter pylori factors and the cardiovascular disorders have been considered in the recent studies [63, 89]. In a study on 684 CAD patients, Mayr et al. showed that infection with CagA strains has a significant relationship with the atherosclerosis (P = 0.08) . In a cross-sectional study on seven case-control studies, Cremonini et al. found a significant relationship between the stroke and CagA seropositivity (ORs: 1.65) . In their studies, Sun et al. showed that there was no relationship between H. pylori CagA + strains infection and the coronary heart disease (CHD) (ORs: 0.8) .