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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.Undergraduate students (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.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.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.

Tobacco smoking has been associated with lower cardiovascular reactivity to psychological stress in middle-aged samples, but its impact on cardiovascular reactivity to stress in young adults remains unclear. The present study examined whether young healthy adults showed differing cardiovascular stress reaction profiles depending on their smoking status. Across two laboratory studies (N = 64 and N = 114), we asked participants to complete cognitive stress-tasks while undergoing continuous hemodynamic monitoring. In both studies, there was not a statistically signification association between systolic blood pressure, diastolic blood pressure, or heart rate reactivity to stress (all ps>.05). However, examination of the underlying hemodynamic profile of the stress response suggested differences between non-smokers and smokers in both studies. In Study 1, non-smokers exhibited the expected myocardial response to the active stress-task; however, smokers exhibited a mixed hemodynamic profile. In Study 2, smokers evidenced a weaker myocardial profile to the active stress-tasks compared to non-smokers. However, the examination of the continuous hemodynamic profile score (HP) did not identify statistical differences. These results highlight that any level of the smoking habit is associated with an altered hemodynamic profile in response to stress in smokers, which may have important implications for long-term cardiovascular health. The findings also suggest that controlling for smoking behavior in reactivity research examining blood pressure and heart rate responses to stress in young adults is not necessary.

Objectives: Blunted cardiovascular reactivity is associated with a distinct behavioural profile of greater exposure to early life adversity, coupled with higher levels of behavioural disengagement and symptoms of depression. The present study sought to extend on this work by investigating if behavioural clusters with distinct patterns of reactivity were related to health and behavioural outcomes at baseline and at a 4-year follow-up. Methods: Hierarchical cluster analyses were conducted using longitudinal data drawn from the Midlife Development in the United States (MIDUS 2) Biomarker Project and the MIDUS 3 follow-up 4 years later. During MIDUS, 2 participants (N = 513) underwent a standardized stress testing protocol and had their blood pressure and heart rate monitored throughout. In addition, hierarchical cluster analyses were conducted on responses from measures of early life adversity, behavioural disengagement and depression. Binary logistic regressions were conducted to determine whether cluster membership was related to health and behavioural outcomes which were taken at both time points. Results: Three behavioural clusters emerged with statistically different blood pressure reactivity patterns. The cluster characterized by greater exposure to early life adversity, higher levels of behavioural disengagement and depressive symptoms, had relatively lower blood pressure reactivity patterns compared with both the exaggerated reactivity cluster and the cluster similar to the sample mean. In fully adjusted models, this cluster was associated with hypertension (p = .050) and depressed affect (p = .033), while Cluster 1 characteristic of an exaggerated blood pressure reactivity profile was associated with depressed affect (p

OBJECTIVE The 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. METHODS Mediation analyses were conducted using data from 639 participants drawn from the Midlife Development in the United States (MIDUS II) Biomarker Project. Responses were derived from the Childhood Trauma Questionnaire [CTQ] and Center for Epidemiologic Studies Depression Scale [CES-D]). Participants had their systolic and diastolic blood pressure (SBP, DBP) and heart rate (HR) monitored throughout a standardized stress testing protocol. RESULTS The 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 = -.06, 95% CI [-.13,-.01]; and DBP: β = - .04, [-.07,-.01]), physical abuse (SBP: β = -.05, [-.11,-.01]; DBP: β = -.03, [-.06,-.01]), sexual abuse (SBP: β = -.04, [-.09,-.01]; DBP: β = -.02, [-.05,-.01]), emotional neglect (SBP: β = -.04, [-.09,-.01]; DBP: β = -.02, [-.05,-.01]), physical neglect (SBP: β = -.09, [-.17,-.02]; DBP: β = -.05, [-.09,-.02]) and total CTQ (SBP: β = -.02, [-.03,-.00]; DBP: β = -.01, [-.02,-.00]). CONCLUSIONS The 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.

The psychological pathways linking depression to blunted cardiovascular reactivity (CVR) are still being elucidated. The purpose of the present study was to test whether the association between eveningness, a diurnal/sleep-wake preference and CVR would be mediated by depressive symptoms. One hundred and eighty-two healthy young adults completed measures of morningness/eveningness (the Morningness-Eveningness Questionnaire; MEQ-SA), depressive symptoms (Hospital Anxiety and Depression Scale; HADS) and had their blood pressure and heart rate monitored throughout a standardised stress testing protocol. Results indicated that depressive symptoms were negatively associated with systolic blood pressure (SBP) but not diastolic blood pressure (DBP) or heart rate (HR) reactions to the stress task. Eveningness was also negatively associated with both SBP and DBP, but not HR. As such, those who reported increased depressive symptomology, and higher scores on eveningness displayed a more blunted cardiovascular response. Furthermore, the latter relationship was mediated by depressive symptoms such that those reporting higher scores on eveningness also reported increased depressive symptomology and this resulted in blunted CVR for SBP. These findings withstood adjustment for several confounding factors including time of testing. In conclusion, the present findings highlight the importance of considering eveningness when looking at the depression-blunted CVR relationship.

peer-reviewed The full text of this article will not be available in ULIR until the embargo expires on the 30/11/2021 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.