ArticleThe American journal of pathology2007
Persistent Chlamydia pneumoniae infection of cardiomyocytes is correlated with fatal myocardial infarction.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 22 citations in OpenAlex.
- Cardiovascular Diseases and Pharmacomicrobiomics: A Perspective on Possible Treatment Relevance.Biomedicines · 2021Review
- Timely approaches to identify probiotic species of the genus Lactobacillus.Gut pathogens · 2013Article
- Pneumonia: an arrhythmogenic disease?The American journal of medicine · 2013Article
- Laboratory diagnosis of persistent human chlamydial infection.Frontiers in cellular and infection microbiology · 2013Review
- Incidence of cardiovascular events after hospital admission for pneumonia.The American journal of medicine · 2011Article
- Chlamydia pneumoniae infection and cardiac risk factors in patients with myocardial infection.ARYA atherosclerosis · 2011Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
Acute myocardial infarction (AMI) associated with unfavorable prognosis is likely to be the consequence of a diffuse active chronic inflammatory process that destabilizes the whole coronary tree and myocardium, suggesting a possible common causal agent underlying both conditions. The main objective of this study was to investigate whether Chlamydia pneumoniae (CP) infection occurred beyond the coronary plaques, namely in the myocardium of individuals who died of AMI. The presence of CP cell wall antigen (OMP-2) and CP-HSP60 was investigated in the myocardium and coronary plaques of 10 AMI and 10 age-matched control patients by immunohistochemistry, electron microscopy, and molecular biology. OMP-2 antigens were found in the unaffected myocardium of 9 of 10 AMI patients. Conversely, only 1 of 10 control patients exhibited a positive staining for CP. Moreover, OMP-2 and CP-HSP60 were detected in the whole coronary tree. CP presence was strongly associated with a T-cell inflammatory infiltrate. Our results suggest that CP may underlie both coronary and myocardial vulnerabilities in patients who died of AMI and corroborate the notion that CP may act by reducing cardiac reserves, thus worsening the ischemic burden of myocardium.
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