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Cardiovascular disease is the leading cause of death in the western world. Frequent or chronic reductions in heart rate variability (HRV) are a powerful predictor of cardiovascular disease. Psychological stress has been suggested to be an important factor in the development of reduced HRV. Recently, Verkuil et al. (2016) introduced a laboratory-based method to measure additional HRV reduction in everyday life, and reductions in HRV related to psychological stress. In the current paper, we discuss alternative methods to detect additional HRV reductions, in real life data sets without the necessity of laboratory-based calibration, and even in existing data sets. All of these methods use a subset of 24h' worth of HRV and movement data to do so: either the first 10min of every hour, the full 24h, a combination of 10min from three consecutive hours, or a classification of level of movement. We also present a method to visualize HRV and movement data to be able to detect episodes of reduced additional HRV optically. The method that used the full 24h' worth of data detected the largest percentage of episodes of reduced additional HRV that actually match with self-reported stress levels, making this method the most promising., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Ruminative thinking about negative feelings has been prospectively associated with increases in depressive symptoms and heightened risk for new onsets of major depression. One putative pathophysiological mechanism underlying this link might be represented by autonomic nervous system dysfunction. The objective of this longitudinal study was to evaluate the interplay between rumination, autonomic function (as revealed by heart rate variability (HRV) analysis), and depressive symptoms in healthy young subjects, over a three-year period. Rumination and depressive symptoms were evaluated in twenty-two women and twenty men at three assessment points (Time 0, 1 and 2) by the score on the Ruminative Response Scale, and the Center for Epidemiological Studies Depression Scale, respectively. Vagally-mediated HRV was assessed in a laboratory session (Time 0) and in two ambulatory sessions at Time 1 and Time 2 (~13 and 34months after Time 0, respectively). Ruminative thinking was found to be (i) a stable trait characteristic, (ii) more prevalent in women than men, and (iii) positively correlated with depressive symptoms. Moreover, resting HRV was negatively correlated with both rumination and depressive symptoms. Finally, HRV at Time 1 mediated the relationship between rumination at Time 0 and depressive symptoms at Time 2. We conclude that autonomic dysfunction, specifically low vagal tone, may be prospectively implicated in the generation of depressive symptoms in a non-clinical setting., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Excessive cardiac responses to stressful events are a risk factor for morbidity and mortality. Adverse cardiac responses are usually attributed to conscious negative stress and emotions. Yet, cardiac responses might also be affected by emotions that are not consciously reported. Here we tested this hypothesis. Sixty participants were randomly allocated to an evaluated speaking stressor or control condition. Trait, state and implicit anxiety were assessed with the State Trait Anxiety Inventory, visual analog scales and the Implicit Association Test for assessing anxiety, with the latter two assessed before and after the stressor. Results showed that the stressor did not significantly affect implicit anxiety. Yet, participants with high implicit anxiety after the stressor had an overall enhanced heart rate and larger stressor-induced decreases in heart rate variability. These associations were independent of conscious anxiety. The implications of the results for a better understanding of excessive cardiac activity are discussed., (Copyright © 2014 Elsevier B.V. All rights reserved.)

This study examined the psychological processes that may impede or facilitate cardiovascular recovery. It was hypothesized that cardiovascular recovery would be hampered by negative affect and rumination, and facilitated by positive affect. In an experimental study, stress was elicited by exposing participants (N=110) to a mental arithmetic task with harassment. After the stress task, affective levels were manipulated via a movie scene with negative, neutral, or positive emotional valence, or without an affect manipulation (control condition). During the entire experiment, heart rate and systolic and diastolic blood pressure levels were measured continuously. Results indicated that blood pressure recovery was hampered by the negative affect manipulation and by rumination. However, the positive affect manipulation did not facilitate blood pressure recovery. No effects were found on heart rate recovery. In sum, the findings emphasize the importance of negative affect and rumination in stress recovery., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Slow cardiovascular (CV) recovery after stress is a predictor of adverse CV outcomes. Perseverative cognition (PC) about stress has been hypothesized to co-determine slow recovery. In the present study, it was investigated whether two types of trait PC, i.e. trait worry and trait rumination, predicted delayed cardiac recovery after a cognitive stressor. Furthermore, it was examined whether explicit state PC (i.e. negative intrusive thoughts) or implicit state PC (i.e. automatic vigilance) additionally predicted delayed cardiac recovery. Fifty-nine participants performed a stressful task, which consisted of an unsolvable synonym task. After a 6-minute recovery period, participants reported on their level of negative intrusive thoughts (i.e. explicit state PC), and performed a lexical decision task (LDT) to measure automatic vigilance for task-related information (i.e. implicit state PC). Cardiac activity was continuously measured using heart rate (HR) and heart rate variability (HRV). Trait worry and rumination were measured by the Penn State Worry Questionnaire (PSWQ) and the Ruminative Response Scale (RRS), respectively. The results showed that high trait worriers had a slower HR recovery from the cognitive stressor compared to low trait worriers. They also showed delayed HRV recovery, but only when the tendency to dwell upon one's negative mood (the 'brooding' subscale of the RRS) was low. Slow HR recovery was associated with high levels of negative intrusive thoughts and with automatic vigilance, but in the unexpected direction for the latter. These results provide evidence that delayed cardiac recovery is associated with trait as well as state PC, and suggest that brooding attenuates the HRV suppressing effect of high trait worry.

Appropriate regulation of emotions is an important component of health. The physiological effects of coping with anger are a topic of particular interest. In a pioneering series of studies Hokanson found that the mode of anger expression following anger instigation had differential effects on vascular recovery. These differential effects were thought to be a result of social learning of avoidance responses. The present study examined this hypothesis in the context of ethnic differences in cardiovascular recovery responses to anger instigation. Twenty-four African American (AA) and 26 European American (EA) males engaged in two debates, one racially themed and one non-racially themed, with an EA confederate. Cardiovascular measures were recorded at baseline, during the debates and during 10-minute recovery periods following each debate. Anger expression preceding the recovery period was manipulated such that half the participants could express their anger toward the confederate and half had to inhibit their anger toward the confederate. Results showed that both AA and EA participants that inhibited their anger had delayed total peripheral resistance recovery. Importantly, for the other dependent variables differential recovery responses were observed such that EA participants that expressed their anger recovered more quickly whereas AA participants that expressed their anger recovered more slowly. These results are consistent with Hokanson's social learning theory of recovery from anger instigation and have important implications for research on emotion regulation and health.

Stress and anxiety are risk factors for cardiovascular (CV) disease. Worry might be a mediator of their risks by prolonging their cognitive representation and concomitant CV activity. We hypothesized that daily stressors and worry, and trait anxiety and trait worry would be associated with high heart rate (HR) and low heart rate variability (HRV) during waking and the subsequent nocturnal sleep period, and that worry would mediate the effects of daily stressors. Low HRV and high HR are physiological risk factors for CV disease. Using an hourly diary, stressors, worry frequency and duration, and biobehavioral variables were measured during one day in 52 healthy subjects. During this time and the subsequent nocturnal sleep period, ambulatory ECG was measured. Stressors, worry and traits were related to higher HR and lower HRV during waking, and the effects of stressors and worry were extended into the sleeping period. Worry duration mediated the effects of stressors. The results were largely independent of biobehavioral variables including sleep quality. The results support the notion that worry, by prolonging CV activity, is a mediator of the CV risks of stress. They also imply a role for unconscious cognitive representation of stress.

Summary. Recent ambulatory findings showing comparable cardiovascular effects of positive and negative emotions are not consistent with the assumed etiological role of negative affect in stress-related diseases. We tested the hypothesis that regardless of initial reactivity, responses associated with negative emotions would be prolonged compared to responses associated with positive emotions. During 8 h, 33 healthy subjects from a general population reported their emotional arousal, emotional valence and physical activity and recorded their heart rates (HR) after a beep at each 60th min ('initial HR'; T0), followed by two 'prolonged activation' recordings, respectively 5 min later (T1) and 10 min later (T2). While emotional arousal and activity predicted initial HR, prolonged activation at T1 was solely predicted by emotional valence (negative affect) at T0, independent of emotional recovery. The results lend support to the hypothesis that cardiovascular activation after negative emotions last longer than after positive emotions. This finding is consistent with the view that prolonged activation, and not so much reactivity, might be a mechanism underlying the etiological role of negative emotions ('stress') in somatic disease. Perseverative cognition (worry, rumination) might be responsible for this prolonged activation.