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Updated: Jul 25, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Role of infection as a risk factor for atherosclerosis, myocardial infarction, and stroke
K J Mattila1, V V Valtonen, M S Nieminen
1Bayer Finland, Espoo, Finland.
Insights
Infections, including herpesviruses and Chlamydia pneumoniae, are increasingly linked to atherosclerosis and thrombosis. These infections may promote cardiovascular disease by altering inflammatory and clotting factors.
Area of Science:
- Cardiovascular Science
- Infectious Disease Epidemiology
Background:
- Growing evidence links microbial infections to atherosclerosis and thrombosis.
- Herpesviruses are implicated in experimental atherosclerosis and found in human lesions.
- Other infections like Chlamydia pneumoniae and dental infections are associated with coronary heart disease and stroke.
Purpose of the Study:
- To review the evidence linking various infections to atherosclerosis and thrombosis.
- To explore the potential mechanisms by which infections contribute to cardiovascular disease.
- To highlight the role of specific pathogens and inflammatory markers.
Main Methods:
- Review of existing scientific literature and observational studies.
- Analysis of data linking specific infections (e.g., herpesviruses, Chlamydia pneumoniae) to cardiovascular conditions.
- Examination of proposed pathophysiological mechanisms involving inflammatory and hemostatic pathways.
Main Results:
- Herpesviruses experimentally induce atherosclerosis and are detected in human atherosclerotic lesions.
- Cytomegalovirus is found in restenosis lesions post-angioplasty, alongside p53.
- Chlamydia pneumoniae, dental, and respiratory infections correlate with coronary heart disease and ischemic stroke.
- Infections may increase fibrinogen, leukocytes, clotting factors, and cytokines, and alter endothelial cell and macrophage function.
- Low-grade infections may contribute to the inflammation seen in atherosclerotic lesions and acute ischemic events, indicated by elevated C-reactive protein.
Conclusions:
- Infections represent a significant contributing factor to the development of atherosclerosis and thrombosis.
- Further research is warranted to fully elucidate the complex interplay between infections and cardiovascular disease.
- Understanding these links may offer new avenues for prevention and treatment strategies.
Abstract:
An increasing body of evidence has linked infections to atherosclerosis and thrombosis. Herpesviruses cause atherosclerosis in experimental animals. Herpesviruses can also be detected in atherosclerotic lesions in humans. Cytomegalovirus may play a role in arteriosclerosis in transplanted hearts, and this virus, together with tumor suppressor protein p53, can be found in restenosis lesions following angioplasty. Chlamydia pneumoniae and dental infections are associated with coronary heart disease in cross-sectional and longitudinal studies, and preceding respiratory infections are associated with ischemic stroke. Infections may favor formation of atherosclerosis and thrombosis by elevation of blood levels of fibrinogen, leukocytes, clotting factor, and cytokines and by alteration of the metabolism and functions of endothelial cells and monocyte macrophages. Low-grade infections may also be one of the causes of the inflammatory reaction observed in atherosclerotic lesions and acute ischemic symptoms, reflected in elevated levels of C-reactive protein. These observations warrant further studies in this field.
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