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Updated: Jul 16, 2026

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
Impact of infectious burden on extent and long-term prognosis of atherosclerosis
Christine Espinola-Klein1, Hans J Rupprecht, Stefan Blankenberg
1Department of Medicine II, Johannes Gutenberg University Mainz, Germany. espinola@mail.uni-mainz.de
Background:
Recent findings suggest a causative role of infections in the pathogenesis of atherosclerosis. In hypothesizing an association between infectious agents and the development of atherosclerosis, we would expect a correlation to the extent of atherosclerosis. Moreover, this effect could be multiplied by the number of pathogens to which an individual had been exposed.
Methods And Results:
In 572 patients, IgG or IgA antibodies to herpes simplex virus 1 and 2, cytomegalovirus, Epstein-Barr virus, Hemophilus influenzae, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Helicobacter pylori were measured. The extent of atherosclerosis was determined by coronary angiography, carotid duplex sonography, and evaluation of the ankle-arm index. Elevated IgA antibodies against C pneumoniae (P<0.04) and IgG antibodies against H pylori (P<0.02), cytomegalovirus (P<0.05), and herpes simplex virus 2 (P<0.01) were associated with advanced atherosclerosis (> or =2 vascular regions), adjusted for age, sex, cardiovascular risk factors, and highly sensitive C-reactive protein. Infectious burden divided into 0 to 3, 4 to 5, and 6 to 8 seropositivities was significantly associated with advanced atherosclerosis, with an odds ratio (95% CI) of 1.8 (1.2 to 2.6) for 4 to 5 (P<0.01) and 2.5 (1.2 to 5.1) for 6 to 8 seropositivities (P<0.02) (adjusted). After a mean follow-up of 3.2 years, cardiovascular mortality rate was 7.0% in patients with advanced atherosclerosis and seropositive for 0 to 3 pathogens compared with 20.0% in those seropositive for 6 to 8 pathogens.
Conclusions:
Our results support the hypothesis that infectious agents are involved in the development of atherosclerosis. We showed a significant association between infectious burden and the extent of atherosclerosis. Moreover, the risk for future death was increased by the number of infectious pathogens, especially in patients with advanced atherosclerosis.
Insights
Infectious agents like Chlamydia pneumoniae and Helicobacter pylori are linked to atherosclerosis. Higher infectious burden correlates with more severe atherosclerosis and increased cardiovascular mortality risk.
Area of Science:
- Cardiovascular disease research
- Infectious disease pathology
- Immunology
Background:
- Emerging evidence suggests infections play a role in atherosclerosis development.
- A higher number of pathogen exposures may exacerbate atherosclerosis extent.
Purpose of the Study:
- To investigate the association between specific infectious agents and the extent of atherosclerosis.
- To determine if infectious burden correlates with cardiovascular mortality.
Main Methods:
- Antibody levels (IgG, IgA) for 8 pathogens were measured in 572 patients.
- Atherosclerosis extent was assessed using coronary angiography, carotid duplex sonography, and ankle-arm index.
- Cardiovascular mortality was tracked over a mean of 3.2 years.
Main Results:
- Elevated antibodies to Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpes simplex virus 2 were associated with advanced atherosclerosis.
- A higher infectious burden (6-8 seropositivities) significantly correlated with advanced atherosclerosis (OR 2.5).
- Cardiovascular mortality was substantially higher in patients with advanced atherosclerosis and high infectious burden (20.0% vs 7.0%).
Conclusions:
- Findings support the role of infectious agents in atherosclerosis pathogenesis.
- A significant association exists between infectious burden and atherosclerosis severity.
- Increased infectious pathogen exposure elevates future mortality risk, particularly in advanced atherosclerosis patients.
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