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Association of CagA+ Helicobacter pylori infection with aortic atheroma
Haim Shmuely1, Douglas J Passaro, Mordehai Vaturi
1Helicobacter pylori Research Institute, Department of Gastroenterology, Rabin Medical Center, Beilinson Campus Petach Tikvah and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Insights
Infection with CagA-positive Helicobacter pylori strains is linked to aortic atheroma, independent of other risk factors. This suggests CagA-positive H. pylori may play a role in the inflammatory process of atherosclerosis.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Gastroenterology
Background:
- Atherosclerosis is a significant cardiovascular risk.
- Helicobacter pylori infection is common and linked to various health issues.
- The role of specific H. pylori virulence factors, like CagA, in atherosclerosis is not fully understood.
Purpose of the Study:
- To investigate the association between CagA-positive H. pylori infection and aortic atheroma.
- To determine if CagA status independently predicts aortic atherosclerosis.
- To explore the potential role of H. pylori in the inflammatory process of atherosclerosis.
Main Methods:
- Prospective study of 188 subjects diagnosed with aortic atheroma via transesophageal echocardiography.
- Serum IgG antibodies against H. pylori and CagA protein were measured using ELISA and Western blot.
- Multivariate analysis adjusted for coronary artery disease risk factors.
Main Results:
- A linear trend for atheroma presence was observed with CagA-positive H. pylori infection (63%) compared to CagA-negative (46.7%) and uninfected subjects (29%) (p=0.003).
- CagA-positive H. pylori seropositivity was independently associated with aortic atheroma (OR 4.4; p=0.01) after adjusting for risk factors.
- Other significant risk factors included older age, smoking, and elevated triglycerides.
Conclusions:
- Infection with CagA-positive H. pylori strains is independently associated with aortic atherosclerosis.
- A gradient of atherosclerosis exists between uninfected individuals and those with CagA-positive H. pylori infection.
- Further research is warranted to elucidate the role of CagA-positive H. pylori in the inflammatory atherosclerotic process.
Background:
To investigate possible association between infection with CagA(+) strains of Helicobacter pylori and aortic atheroma diagnosed by transesophageal echocardiography.
Methods And Results:
One hundred and eighty-eight consecutive subjects prospectively examined for presence of aortic atheroma (localized intimal thickening of >/=3mm) by transesophageal echocardiography were tested for serum IgG antibodies against H. pylori (enzyme-linked immunosorbent assay) and CagA protein (Western blot assay). The association between infection with H. pylori, CagA status of the infecting H. pylori strains, and aortic atherosclerosis was evaluated after adjusting for coronary artery disease risk factors. There was a linear trend for presence of atheroma in subjects with CagA-positive H. pylori infection (51/81, 63%) compared to subjects with CagA-negative H. pylori infection (21/45, 46.7%) and uninfected subjects (18/62, 29%) (p=0.003). H. pylori seropositivity was not associated with aortic atheroma (OR 2.9; 95% CI, 0.8-10.3; p=0.11) when CagA status is not taken into account. On multivariate analysis, parameters associated with risk of aortic atheroma were CagA-positive H. pylori seropositivity (OR 4.4; 95% CI, 1.4-14.7; p=0.01), older age (OR 1.2; 95% CI, 0.9-14.7; p=0.01), having ever smoked cigarettes (OR 3.6; 95% CI, 1.3-10.0; p<0.001), and elevated serum triglyceride level (OR 3.4; 95% CI, 1.3-9.4; p=0.02).
Conclusions:
After controlling for H. pylori infection and coronary artery disease risk factors, infection with a CagA-positive strain of H. pylori was independently associated with aortic atherosclerosis. This study suggests a gradient of atherosclerosis between uninfected individuals and patients with CagA-positive H. pylori infection and should prompt research into the role of CagA-positive H. pylori infection in the inflammatory atherosclerotic process.
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