Chlamydia pneumoniae in Different Coronary Artery Segments in the Young

Hortoványi, Eszter; Illyés, G.; Glasz, Tibor; Kádár, Anna

doi:10.1078/0344-0338-00179

Cited by 7 publications

(4 citation statements)

References 14 publications

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“…The tropism of various types of pathogens, such as herpes simplex virus, cytomegalovirus, C. pneumoniae and H. pylori , for endothelial and other vascular cells in patients with advanced atherosclerotic CHD has been documented 27, although the precise implications of their localization in the atheromatous plaque remain debatable. A recent study even found the presence of C. pneumoniae DNA in incipient coronary lesions from older children and adolescents 28.…”

Section: Mechanisms By Which Infections Could Trigger Arterial Damagementioning

confidence: 96%

Infection and early atherosclerosis: Does the evidence support causation?

Liuba

Pesonen

2005

Acta Paediatrica

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Although clinical manifestations of atherosclerotic coronary heart disease occur in adult life, the initial stages of its development commence in childhood. Therefore, elucidating the pathogenesis of early atherosclerosis and identifying the network of risk factors have become fundamental priorities for both cardiovascular healthcare providers and scientists. There is mounting evidence from both human studies and animal experiments that infectious pathogens could be implicated in atherosclerosis development. The vulnerability of the arterial wall to the adverse effects of infection is probably augmented when additional risk factors and/or certain proatherogenic genetic profiles are also present. The precise mechanisms whereby infection, alone or in synergy with conventional cardiovascular risk factors, could contribute to atherosclerosis are not fully understood. Conclusion: Injury to the vascular endothelium, which could be elicited by infection through inflammatory, metabolic, autoimmune, and pathogen‐related mechanisms, might be a central link between infection and early atherosclerosis.

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Section: Mechanisms By Which Infections Could Trigger Arterial Damagementioning

confidence: 96%

Infection and early atherosclerosis: Does the evidence support causation?

Liuba

Pesonen

2005

Acta Paediatrica

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“…Sampling, and most of the histology procedures were published elsewhere. 6,7 Intimal lesions were classified in keeping with the suggestion of the American Heart Association. 12 The following coronary changes were analysed: Type I structural pattern showing different grades of intimal thickening.…”

Section: Methodsmentioning

confidence: 99%

Early atherosclerosis and Chlamydia pneumoniae infection in the coronary arteries

Hortoványi

Illyés

Kádár

2003

Pathol. Oncol. Res.

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“…This group was able to demonstrate the presence of the organisms in all the post-mortem atheromas but in none of the control cases. Since then a number of other studies provided positive and negative results about the presence of the bacterium in atherosclerotic lesions [26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44]. There have been a large number of studies in experimental models showing that atherosclerotic lesions can be accelerated following respiratory infection with Chlamydia pneumonia.…”

Section: A) Chlamydia Pneumoniaementioning

confidence: 97%

Infections and Atheromatous Plaque: Current Therapeutic Implications

Charakida¹,

Tousoulis²

2013

Current Pharmaceutical Design

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Infections are the most common inflammatory triggers and acute and chronic infections have been associated with the development and progression of atherosclerotic disease raising interest in the infectious hypothesis of atherosclerosis. Pathogens have been identified in atherosclerotic plaques and large epidemiological studies have documented conflicting associations between serological evidence of infection and cardiovascular events. Influenza A was mostly studied as a trigger for cardiovascular events during winter months, whilst cytomegalovirus, Chlamydia pneumoniae, helicobacter pylori and porphyromonas ginigivalis were the most studied chronic pathogens which had been associated with the development and progression of cardiovascular disease. Infectious agents can contribute to atherosclerosis by having a direct effect on the vascular wall or via indirect effects including inflammatory responses and molecular mimicry. Efforts to prevent infection with vaccination or treat specific infectious agents with antibiotics have provided mostly negative results, thereby challenging the validity of the infectious hypothesis of atherosclerosis.

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Chlamydia pneumoniae in Different Coronary Artery Segments in the Young

Cited by 7 publications

References 14 publications

Infection and early atherosclerosis: Does the evidence support causation?

Infection and early atherosclerosis: Does the evidence support causation?

Early atherosclerosis and Chlamydia pneumoniae infection in the coronary arteries

Infections and Atheromatous Plaque: Current Therapeutic Implications

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