Investigating the Effects of Markers of Biological Stress on the Association between Adverse Childhood Experiences and Central Artery Stiffness

Adverse childhood experiences (ACEs) have been shown to be associated with an increased risk of cardiovascular disease (CVD). One mechanism by which ACEs may increase CVD risk is through their association with central artery stiffness. Pathways linking ACEs to arterial stiffness have not yet been fully elucidated; however, increased biological stress has been postulated to play a critical role. Recently, two markers have emerged as being potentially useful measures of biological stress—telomere length (TL) and mitochondrial DNA copy number (mtDNAcn). Here, the potential effects of TL and mtDNAcn on the association between ACEs and central artery stiffness were examined. It was hypothesized that TL and/or mtDNAcn would be associated with both ACEs and central artery stiffness, and that these markers would influence the association between ACEs and arterial stiffness. 185 individuals (n = 102 females) aged 19-25 years (mean age 22.5 ± 1.5 years) were included in the current analyses. ACEs were assessed using the CTES 2.0. Central artery stiffness was assessed non-invasively as carotid-femoral pulse wave velocity (cfPWV). TL and mtDNAcn were assessed using qPCR techniques. Multiple linear regression analyses were used to examine the associations between ACEs, TL, mtDNAcn, and cfPWV after adjustment for several covariates. ACEs were independently associated with cfPWV (β = 0.147, p = 0.035). Both TL and mtDNAcn were independently associated with cfPWV (β = -0.169, p = 0.012 and β = -0.525, p = 0.017, respectively). There was no significant association between ACEs and either TL or mtDNAcn (both p > 0.05); and neither marker influenced the association between ACEs and cfPWV. Increasing ACEs were associated with a faster cfPWV. This association was not influenced by either TL or mtDNAcn, suggesting that these markers do not provide a link between ACEs and arterial stiffness. Reduced TL and mtDNAcn were also associated with a faster cfPWV. Future studies are required to better understand the association between ACEs, markers of biological stress, and arterial stiffness

Serum MMP‐3 and its association with central arterial stiffness among young adults is moderated by smoking and BMI

Central arterial stiffness is an independent predictor of cardiovascular disease. It is characterized by a marked reduction in the elastin-collagen ratio of the arterial wall extracellular matrix (ECM), and is largely the result of degradation of various ECM components. Matrix metalloproteinase-3 (MMP-3) may contribute to central arterial stiffness via its involvement in ECM homeostasis and remodeling. This study examined the association between serum MMP-3 concentrations and central arterial stiffness and potential interactions of MMP-3 and traditional cardiovascular risk factors in a population of healthy young adults. A total of 206 participants (n = 109 females) aged 19–25 years were included in the current study. Central arterial stiffness was measured non-invasively as carotid-femoral pulse wave velocity (cfPWV) (m/s). MMP-3 concentrations (ng/ml) were measured using ELISA techniques. Regression analyses were used to examine the association between cfPWV and MMP-3, adjusting for age, sex, smoking status, body mass index (BMI), instantaneous mean arterial pressure (MAP) and heart rate, and serum C-reactive protein. Interactions between MMP-3 with smoking, BMI, sex, and MAP were analyzed in subsequent regression models. MMP-3 was an independent predictor of cfPWV (β = 0.187, p = 0.007), and significant interactions between MMP-3 and regular smoking (β = 0.291, p = 0.022), and MMP-3 and BMI (β = 0.210, p = 0.013) were observed. Higher serum MMP-3 concentrations were associated with a faster cfPWV and thus, greater central arterial stiffness. Interactions between MMP-3 and smoking, and MMP-3 and BMI may, in part, drive the association between MMP-3 and central arterial stiffness.Canadian Institutes of Health Researc