ObjectiveThe pathways underlying the early life adversity and cardiovascular reactivity association remain unclear. The current study examined the role of current depressive symptoms on this relationship.MethodsMediation analyses were conducted using data from 639 participants drawn from the Midlife Development in the United States 2 Biomarker Project. Responses were derived from the Childhood Trauma Questionnaire and Center for Epidemiologic Studies Depression Scale. Participants had their systolic and diastolic blood pressure (SBP, DBP) and heart rate monitored throughout a standardized stress testing protocol.ResultsThe association between early life adversity and reactivity was mediated by current depressive symptoms; all adversity factors were linked to higher levels of current depressive symptoms, which, in turn, were associated with lower cardiovascular reactivity. For emotional abuse, this was noted for SBP (β = −0.06 [95% confidence interval {CI}, −0.13 to −0.01]) and DBP (β = −0.04 [−0.07 to −0.01]), physical abuse (SBP: β = −0.05 [−0.11 to −0.01]; DBP: β = −0.03 [−0.06 to −0.01]), sexual abuse (SBP: β = −0.04 [−0.09 to −0.01]; DBP: β = −0.02 [−0.05 to −0.01]), emotional neglect (SBP: β = −0.04 [−0.09 to −0.01]; DBP: β = −0.02 [−0.05 to −0.01]), physical neglect (SBP: β = −0.09 [−0.17 to −0.02]; DBP: β = −0.05 [−0.09 to −0.02]), and total Childhood Trauma Questionnaire score (SBP: β = −0.02 [−0.03 to −0.00]; DBP: β = −0.01 [−0.02 to −0.00]).ConclusionsThe present findings extend research and demonstrate that depression is an underlying mechanism linking early life adversity and blunted cardiovascular reactivity.

Background There is considerable evidence documenting associations between early life adversity, behavioral disengagement, and depression with blunted cardiovascular reactivity to acute psychological stress. However, while often examined as independent predictors, it is also likely that a combination of these factors uniquely relate to cardiovascular reactivity. Purpose The present study employed multivariate cluster analysis to examine if distinct combinations of these outcomes relate to cardiovascular stress reactivity. Methods Participants (N = 467) were predominantly female (60.6%) with a mean age of 19.30 years (SD = 0.82). Measures of early life adversity, behavioral disengagement, and depression were completed; in addition, participants had their blood pressure and heart rate monitored throughout a standardized stress testing session. Cardiovascular reactivity was calculated as the difference between mean stress and mean baseline cardiovascular values. Results Analyses revealed two clusters with distinct patterns of exposure to early life adversity, levels of behavioral disengagement and depression, uniquely related to cardiovascular reactivity. In unadjusted models, Cluster 1 that was characterized by greater exposure to early life adversity, higher levels of behavioral disengagement and depression, was associated with lower systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) reactivity. Cluster 2 was characterized by reactivity values similar to the sample means. In fully adjusted models, Cluster 1 predicted heart rate reactivity to stress. Conclusions The present study identifies a behavioral cluster that is characteristic of a blunted heart rate reactivity profile, significantly extending the research in this area.

Recent theoretical developments in cardiovascular reactivity research suggest the association between depression and blunted reactions to stress is linked to motivational factors. Thus, the present study aimed to test whether the association between depressive symptoms and cardiovascular reactivity to acute stress was mediated by motivation; be it intrinsic or extrinsic motivation. One hundred and eighty‐two healthy young adults completed measures of motivation (Global Motivation Scale; GMS), and depression (Hospital Anxiety and Depression Scale; HADS) and had their blood pressure and heart rate monitored throughout a standardised stress testing protocol. Results indicated that depression was negatively associated with both systolic blood pressure (SBP) and heart rate (HR) reactions to the stress task (all ps < .05), such that those who reported higher depressive symptomology displayed a blunted response. Furthermore this relationship was mediated by intrinsic, but not extrinsic motivation; the blunted responses were less pronounced through intrinsic motivation. The present findings add extensively to existing research and confirm that motivation is an underlying mechanism linking depression and cardiovascular reactivity.

Objective: This study examines if Type D personality is (1) associated with cardiovascular reactivity to acute stress in a healthy sample, and (2) has predictive utility for cardiovascular reactivity above its individual subcomponents (negative affect; NA, social inhibition; SI), as well as anxiety and depression.Design: Undergraduate students (n = 173) competed a standardised cardiovascular reactivity experimental protocol consisting of resting baseline and stressor phase (mental arithmetic), with systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) monitored throughout. Main Outcome Measures:The main outcome measures were cardiovascular reactivity to the stressor, which was operationalised as the difference between resting baseline and the stressor phase for SBP, DBP and HR. Results:The continuous Type D interaction term (NA × SI) significantly predicted lower SBP reactivity to the mental arithmetic stressor amongst women, independent of NA, SI and confounding variables. Moreover, this remained significant after adjustment for anxiety and depressive symptoms. Depression, NA and SI were also significant independent predictors of SBP reactivity amongst women. Conclusion:Type D personality is associated with lower SBP reactivity to acute stress in women, which may be indicative of blunted cardiovascular reactivity. This association was independent of NA, SI, Anxiety and Depression.

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