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This is the first study to investigate the influence of adverse childhood experiences (ACEs) on left ventricular mass (LVM) and function. We identified experiencing any childhood household dysfunction was associated with lower LVM in young adults independent of sex, recent life stress, BMI and height, smoking, physical activity, and inflammation. We speculate an inflection point in LVM occurs in midlife predisposing these individuals toward a hypertrophic profile and elevated risk of heart disease in later life, although this requires longitudinal investigation.

Adverse childhood experiences (ACEs) are associated with greater prevalence of cardiovascular disease and altered acute stress reactivity. The current study investigated the effect of ACEs on hemodynamic and autonomic responses to orthostatic stress imposed by 60° head-up tilt (HUT) in young adults. Two-hundred twenty-six healthy young adults (age = 22.6 ± 1.5 yr; n = 116 females) without cardiovascular disease participated and had complete data. Participants underwent supine blood pressure (BP), R-R interval (RRI), cardiac output (CO), total peripheral resistance (TPR), and cardiovagal baroreflex sensitivity (cvBRS) testing followed by a transition to 60° HUT where measures were reassessed. Childhood adversity exposures were assessed based on categorical exposure and nonexposure to childhood household dysfunction and maltreatment, and

Adverse childhood experiences (ACEs), such as maltreatment and severe household dysfunction, represent a significant threat to public health as ACEs are associated with increased prevalence of several chronic diseases. Biological embedding, believed to be rooted in dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, is the prevailing theory by which chronic diseases become imprinted in individuals following childhood adversity. A shift towards HPA axis hypoactivity occurs in response to ACEs exposure and is proposed to contribute towards altered cortisol secretion, chronic low-grade inflammation, and dysregulated hemodynamic and autonomic function. This shift in HPA axis activity may be a long-term effect of glucocorticoid receptor methylation with downstream effects on hemodynamic and autonomic function. Emerging evidence suggests syncopal tendencies are increased among those with ACEs and coincides with altered neuroimmune function. Similarly, chronic low-grade inflammation may contribute towards arterial baroreceptor desensitization through increased arterial stiffness, negatively impacting autonomic regulation following posture change and increasing rates of syncope in later life, as has been previously highlighted in the literature. Although speculative, baroreceptor desensitization may be secondary to increased arterial stiffness and changes in expression of glucocorticoid receptors and arginine vasopressin, which are chronically altered by ACEs. Several research gaps and opportunities exist in this field and represent prospective areas for future investigation. Here, we synthesize current findings in the areas of acute psychosocial stress reactivity pertaining to HPA axis function, inflammation, and hemodynamic function while suggesting ideas for future research emphasizing systemic interactions and postural stress assessments among those with ACEs. This review aims to identify specific pathways which may contribute towards orthostatic intolerance in populations with history of childhood adversity.

An association among adults between adverse childhood experiences (ACEs) and arterial stiffness and between arterial stiffness and cardiovascular disease has been established. Recent cross-sectional evidence suggests that ACEs is linked to the development and progression of arterial stiffness, but it remains unclear when these changes begin to manifest. We examine the relationship between ACEs and changes in arterial stiffness from childhood into adulthood using population-based longitudinal data. The Niagara Longitudinal Heart Study (NLHS) pilot data included 76 young adults (females = 44), with an average age of 21 years (SD = 1), and had a follow-up period of 9 years. Mixed effects modeling was used to examine the effect of ACEs on changes in arterial stiffness over time adjusting for sex, changes in heart rate, systolic blood pressure, body mass index, and physical activity. Individuals with four or more ACEs have a greater increase in arterial stiffness over time from childhood into young adulthood. This increase was similar for both males and females and independent of the effects of change in heart rate, systolic blood pressure, body mass index, and physical activity. Exposure to ACEs is associated with greater increase in arterial stiffness, a marker for cardiovascular disease among adults. This suggests that interventions targeted at individuals with high exposure to ACEs early on in life could lower the risk of arterial stiffness and in turn the cascade of events leading to cardiovascular disease. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s40653-020-00311-3) contains supplementary material, which is available to authorized users.

IntroductionRecent reviews have found substantial links between a toxic childhood environment including child abuse and severe household dysfunction and adult cardiovascular disease (CVD). Collectively referred to as adverse childhood experiences (ACEs), this toxic environment is prevalent among children, with recent Canadian estimates of child abuse at 27%–32%, and severe household dysfunction at 49%. Based on these prevalence rates, the potential effect of ACEs on CVD is more significant than previously thought. Yet, how ACEs amplify the risk for later CVD remains unclear. Lifestyle risk factors only partially account for this connection, instead directing attention to the interaction between psychosocial factors and physiological mechanisms such as inflammation. The Niagara Longitudinal Heart Study (NLHS) examines how ACEs influence cardiovascular health (CVH) from childhood to early adulthood. Integrating the stress process and biological embedding models, this study examines how psychosocial and physiological factors in addition to lifestyle factors explain the relationship between ACEs and CVH.MethodsThis follow-up study combines three baseline studies from 2007 to 2012 that collected CVH measures including child blood pressure, heart rate, left ventricular structure and function, arterial stiffness indices and baroreflex sensitivity on 564 children. Baseline data also include anthropometric, biological, lifestyle, behavioural, and psychosocial measures that varied across primary studies. Now over 18 years of age, we will recruit and retest as many participants from the baseline studies as possible collecting data on ACEs, CVH, anthropometric, lifestyle and psychosocial measures as well as blood, saliva and hair for physiological biostress markers.Ethics and disseminationEthics approval has been received for the NLHS follow-up. Written consent to participate in the follow-up study is obtained from each participant. Results testing all proposed hypotheses will be submitted for publication in peer-reviewed journals.

Purpose: The present investigation evaluated the validity and reliability of carotid-toe PWV (ctPWV) as a non-intrusive measure of systemic arterial stiffness in healthy young adults. Methods: The Validity Trial examined the association and agreement between cfPWV and ctPWV in 33 adults (24 ± 2 years; 14 females), while the Reliability Trial assessed the variability in cfPWV and ctPWV in 13 adults (22 ± 2 years; 5 females) over repeat visits. Proximal pulse waves were acquired (applanation tonometry) from the left common carotid (CCA) for both measures, while distal pulse waves were acquired from the left femoral artery (applanation tonometry) and the second left toe (pulse oximeter) for cfPWV and ctPWV, respectively. Results: cfPWV (5.3 ± 0.7, 3.9–6.5 m/s) and ctPWV (5.4 ± 0.5, 4.6–6.3 m/s) demonstrated a moderate-to-strong positive linear correlation (r = 0.79, P < 0.01) and a strong intra-class correlation (ICC; ICC = 0.86, P < 0.01). The Bland–Altman plot demonstrated agreement between cfPWV and ctPWV with no fixed bias (0.1 m/s, ± 2SD: −0.8 to 0.9 m/s, P > 0.05) and all data points falling within ±2 SD of the mean difference between measures. cfPWV and ctPWV demonstrated reliability across visits as evidenced by low coefficients of variation (cfPWV: 3.4 ± 2.6%, ctPWV: 2.6 ± 2.5%) and strong ICCs (cfPWV: ICC = 0.91, ctPWV: ICC = 0.84, both P < 0.01). Conclusions: Through comparison with cfPWV, this study provides evidence to suggest that ctPWV yields a valid and reliable index of arterial stiffness in healthy young adults.

Cardiovagal baroreflex sensitivity (cvBRS) measures the efficiency of the cardiovagal baroreflex to modulate heart rate in response to increases or decreases in systolic blood pressure (SBP). Given that baroreceptors are located in the walls of the carotid sinuses (CS) and aortic arch (AA), the arterial mechanics of these sites are important contributors to cvBRS. However, the relative contribution of CS and AA mechanics to cvBRS remains unclear. This study employed sex differences as a model to test the hypothesis that differences in cvBRS between groups would be explained by the vascular mechanics of the AA but not the CS. Thirty-six young, healthy, normotensive individuals (18 females; 24 ± 2 yr) were recruited. cvBRS was measured using transfer function analysis of the low-frequency region (0.04–0.15 Hz). Ultrasonography was performed at the CS and AA to obtain arterial diameters for the measurement of distensibility. Local pulse pressure (PP) was taken at the CS using a hand-held tonometer, whereas AA PP was estimated using a transfer function of brachial PP. Both cvBRS (25 ± 11 vs. 19 ± 7 ms/mmHg, P = 0.04) and AA distensibility (16.5 ± 6.0 vs. 10.5 ± 3.8 mmHg−1 × 10−3, P = 0.02) were greater in females than males. Sex differences in cvBRS were eliminated after controlling for AA distensibility ( P = 0.19). There were no sex differences in CS distensibility (5.32 ± 2.3 vs. 4.63 ± 1.3 mmHg−1 × 10−3, P = 0.32). The present data demonstrate that AA mechanics are an important contributor to differences in cvBRS.