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Age related inflammatory characteristics of coronary artery disease
Elias Najib1, Rajesh Puranik, Johan Duflou
1Discipline of Pathology, School of Medical Science and Bosch Institute, University of Sydney, Sydney, Australia.
Insights
Older individuals exhibit heightened coronary plaque inflammation and reduced regulatory T cells (Tregs). Younger individuals, despite less inflammation, also experienced fatal outcomes, suggesting other factors influence plaque stability.
Area of Science:
- Cardiovascular Immunology
- Atherosclerosis Research
- Immunogerontology
Background:
- Coronary heart disease (CHD) is a leading cause of mortality, with immune dysregulation playing a key role in its development.
- Age-related immune system changes in atherogenesis, particularly in premature disease, are not well understood.
- This study investigates age-specific immunological differences in coronary artery plaques.
Purpose of the Study:
- To identify differential immunological mediators in coronary plaques of younger versus older deceased individuals.
- To characterize age-dependent inflammatory profiles within atherosclerotic plaques.
- To explore potential age-related factors influencing plaque stability and CHD outcomes.
Main Methods:
- Coronary artery plaques were obtained from younger (<50 years) and older (>60 years) male decedents, along with controls.
- Demographic and forensic pathological data were collected for all subjects.
- Immunohistochemistry was employed to analyze plaque composition and immune cell infiltration.
Main Results:
- Older subjects showed increased heart-to-body weight ratio, plaque necrosis, and calcification compared to younger subjects.
- Plaques from older individuals had significantly higher levels of CD3(+) T cells and myeloperoxidase.
- Conversely, older subjects exhibited lower numbers of macrophages and Foxp3(+) regulatory T cells (Tregs) in their plaques.
- No significant age-dependent differences were observed in IL-17 or IL-10 levels.
Conclusions:
- Coronary plaque inflammation displays distinct age-dependent characteristics.
- Older individuals present with a plaque phenotype characterized by elevated inflammation and reduced Treg cell infiltration.
- The fatal outcomes in younger individuals, despite lower plaque inflammation, suggest alternative factors are critical for plaque stability and warrant further investigation for therapeutic implications.
Background:
Coronary heart disease, often associated with fatal outcomes, is increasingly common. Immune dysregulation is a key process in atherogenesis, yet age and other immune related factors are poorly characterised, especially in premature disease. The current study is to investigate the differential immunological mediators in the plaque specific to older and younger decedents.
Methods:
Coronary artery plaques were collected from male decedents as follows: Younger (< 50 years; n=30), older (> 60 years; n=30) and control (n=10). Demographic and forensic pathological data were collected. Plaques were investigated, using detailed immunohistochemistry.
Results:
Older subjects had 20% elevated heart to body weight ratio compared to younger subjects (p<0.05), as well as 40% higher levels of plaque necrosis (p<0.05) and 90% more calcification (p<0.05). There was a three-fold higher amount of infiltrating CD3(+) T cells (p<0.05) and myeloperoxidase production (p<0.05) within plaque from older subjects than younger. Interestingly, older subjects had 50% and 70% lower numbers of infiltrating macrophage (p<0.05) and Foxp3(+) Treg cells (p<0.05), respectively, in the plaque compared to younger subjects. There were no significant age-dependent differences in IL-17 or IL-10 secretion.
Conclusion:
Our data suggests that there are indeed age-dependent characteristics of culprit coronary plaque inflammation. In particular, older subjects demonstrate a plaque phenotype with higher amounts of inflammation and lower levels of Treg cells. Despite lower levels of inflammation, younger subjects also had fatal outcomes, indicating that alternative factors may be more important in plaque stability. These observations may have therapeutic consequences and hence warrant further investigation.
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