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Helicobacter pylori infection is identified as a cardiovascular risk factor in Central Africans

Authors Longo-Mbenza B, Nkondi, Mokondjimobe, Gombet, Ngaporo Assori I, Ibara, Ellenga-Mbolla, Vangu, Mbungu

Received 29 November 2011

Accepted for publication 25 January 2012

Published 15 August 2012 Volume 2012:8 Pages 455—461

DOI https://doi.org/10.2147/VHRM.S28680

Review by Single-blind

Peer reviewer comments 4

Benjamin Longo-Mbenza,1 Jacqueline Nkondi Nsenga,2 Etienne Mokondjimobe,3 Thierry Gombet,3 Itoua Ngaporo Assori,3 Jean Rosaire Ibara,3 Bertrand Ellenga-Mbolla,3 Dieudonné Ngoma Vangu,4 Simon Mbungu Fuele4

1Faculty of Health Sciences, Walter Sisulu University, Mthatha, South Africa; 2Division of Gastroenterology, University of Kinshasa, Kinshasa, Democratic Republic of the Congo; 3Faculty of Health Sciences, University of Marien Ngouabi, Brazzaville, Democratic Republic of the Congo; 4Biostatistics Unit, Lomo Medical Center, Limete, Kinshasa, Democratic Republic of the Congo

Background: Helicobacter pylori is now incriminated in the pathogenesis of atherosclerosis.
Objective: To examine the importance of H. pylori infection as a cardiovascular disease (CVD) risk factor.
Methods: Two hundred five patients (128 with H. pylori infection [HP-seropositive] and 77 without) had a baseline assessment for other potential CVD risk factors and were followed prospectively for 10 years (1999–2008). They were assessed on a monthly basis for the outcomes of carotid plaque, angina pectoris, myocardial infarction, and stroke. In the HP-seropositive group, male sex and quartile 4 for IgG anti-H. pylori antibodies (anti-HP Ab) were correlated with traditional CVD risk factors, stroke, myocardial infarction, and angina pectoris.
Results: At the baseline assessment, the levels of carotid intima-media thickness, blood fibrinogen, total cholesterol, fasting plasma glucose, and uric acid were higher in H. pylori-infected patients than in the uninfected group. Serum HDL-cholesterol was significantly lower in the HP-seropositive group. Men had higher levels of IgG anti-HP Ab, waist circumference, blood pressure, uric acid, and total cholesterol than women. Within the HP-seropositive group, individuals in quartile 4 for IgG anti-HP Ab had higher rates of elevated fibrinogen, diabetes mellitus, low high-density lipoprotein cholesterol, arterial hypertension, and high total cholesterol than those in quartile 1. After adjusting for traditional CVD risk factors, H. pylori infection was the only independent predictor of incident carotid plaque (multivariate odds ratio [OR] = 2.3, 95% confidence interval [CI]: 1.2–7.2; P < 0.0001) and incident acute stroke (multivariate OR = 3.6, 95% CI: 1.4–8.2; P < 0.0001). Within the HP-seropositive group and after adjusting for traditional CVD risk factors, male sex was the only independent predictor of incident angina pectoris (multivariate OR = 3.5, 95% CI: 1.6–16; P < 0.0001), incident acute stroke (multivariate OR = 3.2, 95% CI: 1.4–28; P < 0.0001), and acute myocardial infarction (multivariate OR = 7.2, 95% CI: 3.1–18; P < 0.0001).
Conclusion: Our study provides evidence for an association among known CVD risk factors, carotid plaque, stroke, and H. pylori infection. Among infected individuals, there is a significant association among severity of HP-seropositivity, male sex, and CVD. The eradication of H. pylori infection may therefore reduce the emerging burden of CVD in Africa.

Keywords: Helicobacter pylori, stroke, myocardial infarction, cardiovascular disease, carotid plaque, Africans

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