Association of Virulent
            <i>Helicobacter pylori</i>
            Strains With Ischemic Heart Disease

Pasceri, Vincenzo; Cammarota, Giovanni; Patti, Giuseppe; Cuoco, L.; Gasbarrini, Antonio; Grillo, R; Fedeli, G.; Gasbarrini, Giovanni; Maseri, Attilio

doi:10.1161/01.cir.97.17.1675

Cited by 280 publications

(184 citation statements)

References 27 publications

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“…25,26 In most but not all seroepidemiological evaluations, subjects with a prominent immune response to C pneumoniae or (virulent strains of) H pylori, as indicative of chronic infection status, faced an excess risk of coronary heart disease, stroke, and vascular death. 7,[13][14][15][27][28][29] Finally, chronic bronchitis, as defined by self-reported clinical symptoms, and periodontal disease have LR denotes likelihood ratio. ORs were derived from multiple stepwise logistic regression analysis.…”

Section: Discussionmentioning

confidence: 99%

“…4 -8,31 Among subjects with chronic infections, risk of atherosclerosis tended to be higher in those with a prominent inflammatory response (Figure 3), which may indicate high virulence of the underlying pathogen or atherogenic host-pathogen interactions. 13,14,27,31 Induction of systemic inflammation has been proposed to be of pathogenetic relevance in the association of infection and atherosclerosis and may rely in part on the endothelial toxicity of bacterial endotoxin and the action of proinflammatory cytokines. 7,19 Recently, we demonstrated that in smokers and subjects with chronic infections, high concentrations of circulating endotoxin predict a substantially increased risk of atherosclerosis (Figure 4).…”

Section: Discussionmentioning

confidence: 99%

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Chronic Infections and the Risk of Carotid Atherosclerosis

et al. 2001

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Background-Chronic infections have been implicated in the pathogenesis of atherosclerosis, yet from an epidemiological perspective, this concept remains controversial. Methods and Results-The Bruneck Study is a prospective population-based survey on the pathogenesis of atherosclerosis.In 826 men and women 40 to 79 years old (1990 baseline), 5-year changes in carotid atherosclerosis were thoroughly assessed by high-resolution duplex scanning. The presence of chronic respiratory, urinary tract, dental, and other infections was ascertained by standard diagnostic criteria. Chronic infections amplified the risk of atherosclerosis development in the carotid arteries. The association was most pronounced in subjects free of carotid atherosclerosis at baseline (age-/sex-adjusted odds ratio [95% CI] for any chronic infection versus none, 4.08 [2.42 to 6.85]; PϽ0.0001) and applied to all types of chronic (bacterial) infections. It remained independently significant after adjustment for classic vascular risk attributes and extended to low-risk individuals free of conventional risk factors. Among subjects with chronic infections, atherosclerosis risk was highest in those with a prominent inflammatory response. Markers of systemic inflammation, such as soluble adhesion molecules and circulating bacterial endotoxin, and levels of soluble human heat-shock protein 60 and antibodies to mycobacterial heat-shock protein 65 were elevated in subjects with chronic infections and predictive of an increased risk of atherosclerosis. Conclusions-The present study provides solid evidence for a role of common chronic infections in human atherogenesis.Induction of systemic inflammation and autoimmunity may be potential pathophysiological links.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chronic Infections and the Risk of Carotid Atherosclerosis

et al. 2001

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“…Second, H pylori strains bearing the cytotoxin-associated gene A seem to be more decisive for their pathogenic contribution in atherosclerosis, although the mechanisms are unknown. 21,25 Moreover, smoking is a stress factor for endothelial cells. Evidence has indicated that both active and passive cigarette smoking is associated with endothelial dysfunction, and endothelial abnormalities may predispose to the atherogenic and thrombotic problems associated with cigarette smoking.…”

Section: Zhu Et Almentioning

confidence: 99%

Association of serum antibodies to Heat-Shock protein 65 with coronary calcification levels. suggestion of Pathogen-Triggered autoimmunity in early atherosclerosis

Zhu¹,

Katz²,

Quyyumi³

2004

ACC Current Journal Review

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Background-Previous studies demonstrated an association between antibodies to mycobacterial heat-shock protein 65 (mHSP65) and carotid artery thickening. We examined whether mHSP65 antibodies are associated with levels of coronary calcification that appear to reflect preclinical coronary artery disease (CAD). Methods and Results-Serum specimens from 201 healthy asymptomatic subjects (52% male; mean age, 56.6 years) undergoing electron-beam computed tomographic imaging were used to measure levels of mHSP65 and human HSP60 antibodies and antibodies to several infectious pathogens. We found that 84% of the study subjects had anti-mHSP65 IgG antibodies. Mean titers of mHSP65 antibodies were higher (1:394 versus 1:267, Pϭ0.012) in individuals with than in those without elevated levels of coronary calcium (calcium score Ն150). Increasing titers of mHSP65 antibodies were significantly associated, in a dose-response manner, with elevated levels of coronary calcification. Individuals with the highest titers of mHSP65 antibodies (Ն1:800) had an adjusted odds ratio (OR) of 14.3 for having elevated coronary calcium (Pϭ0.004). Association of mHSP65 antibodies with elevated coronary calcification levels was independent of CAD risk factors after multivariate adjustment (Pϭ0.037). Interestingly, mHSP65 antibody titers were correlated with Helicobacter pylori infection (Pϭ0.004), which maintained significance after adjustment for CAD risk factors and seropositivities to other pathogens (adjusted OR, 3.1; 95% CI, 1.4 to 6.6). No association was found between antibodies to human HSP60 and levels of coronary calcification. Conclusions-Antibodies to mHSP65 are associated with elevated levels of coronary calcification and correlated with H pylori infection, suggesting that pathogen-triggered autoimmunity plays a role in early atherosclerosis.

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“…Thus, there is a possibility that the pharmacokinetics of pitavastatin might be modified by H. pyloriinduced severe chronic gastritis. Some infectious diseases, such as Chlamydia pneumoniae infection, have been considered as risk factors for coronary heart disease (18), and several studies have pointed to an association between H. pylori infection and vascular changes due to the alteration of the serum lipid profile (19,38). Previous studies reported that the serum T-Chol, TG, or LDL concentrations in H. pylori-infected persons are significantly elevated over those in noninfected individuals (39,40).…”

Section: Discussionmentioning

confidence: 99%

Pitavastatin Fails to Lower Serum Lipid Levels or Inhibit Gastric Carcinogenesis in Helicobacter pylori–Infected Rodent Models

Toyoda

Tsukamoto²,

Takasu

et al. 2009

Cancer Prevention Research

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Statins are commonly used lipid-lowering drugs that reduce the risk of cardiovascular morbidity and mortality. Although recent studies have pointed to chemopreventive effects of statins against various cancers, their efficacy for gastric cancer is unclear. Here, we examined the effects of pitavastatin, a lipophilic statin, on Helicobacter pylori (H. pylori)-associated stomach carcinogenesis and gastritis using Mongolian gerbil and mouse models. The animals were allocated to H. pylori + N-methyl-N-nitrosourea administration (gerbils, 52 weeks) or H. pylori infection alone groups (gerbils and mice, 12 weeks). After H. pylori infection, they were fed basal diets containing 0 to 10 ppm of pitavastatin. The incidences of H. pylori-associated gastric adenocarcinomas and degrees of chronic gastritis were not decreased by pitavastatin compared with those of control values. Expression of interleukin-1β and tumor necrosis factor-α mRNAs in the pyloric mucosa was markedly up-regulated in pitavastatin-treated animals. Furthermore, in the H. pyloriinfected groups, serum total cholesterol, triglyceride, and low-density lipoprotein levels were significantly increased by pitavastatin treatment, contrary to expectation. In the short-term study, H. pylori-infected gerbils and mice also showed significant up-regulation of serum triglyceride levels by pitavastatin, whereas total cholesterol was markedly reduced and low-density lipoprotein exhibited a tendency for decrease in noninfected animals. These findings indicate pitavastatin to be ineffective for suppressing gastritis and chemoprevention of gastric carcinogenesis in H. pylori-infected gerbils. Our serologic results also suggest that the H. pylori infection and consequent severe chronic gastritis interfere with the cholesterol-lowering effects of pitavastatin.

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Association of Virulent Helicobacter pylori Strains With Ischemic Heart Disease

Cited by 280 publications

References 27 publications

Chronic Infections and the Risk of Carotid Atherosclerosis

Chronic Infections and the Risk of Carotid Atherosclerosis

Association of serum antibodies to Heat-Shock protein 65 with coronary calcification levels. suggestion of Pathogen-Triggered autoimmunity in early atherosclerosis

Pitavastatin Fails to Lower Serum Lipid Levels or Inhibit Gastric Carcinogenesis in Helicobacter pylori–Infected Rodent Models

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