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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