Jos F. Brosschot

The relationship of autonomic imbalance, heart rate variability and cardiovascular disease risk factors

Cardiovascular disease (CVD) is the leading cause of death and disability worldwide. The understanding of the risk factors for CVD may yield important insights into the prevention, etiology, course, and treatment of this major public health concern. Autonomic imbalance, characterized by a hyperactive sympathetic system and a hypoactive parasympathetic system, is associated with various pathological conditions. Over time, excessive energy demands on the system can lead to premature aging and diseases. Therefore, autonomic imbalance may be a final common pathway to increased morbidity and mortality from a host of conditions and diseases, including cardiovascular disease. Heart rate variability (HRV) may be used to assess autonomic imbalances, diseases and mortality. Parasympathetic activity and HRV have been associated with a wide range of conditions including CVD. Here we review the evidence linking HRV to established and emerging modifiable and non-modifiable CVD risk factors such as hypertension, obesity, family history and work stress. Substantial evidence exists to support the notion that decreased HRV precedes the development of a number of risk factors and that lowering risk profiles is associated with increased HRV. We close with a suggestion that a model of autonomic imbalance may provide a unifying framework within which to investigate the impact of risk factors, including psychosocial factors and work stress, on cardiovascular disease.

Toward a causal model of cardiovascular responses to stress and the development of cardiovascular disease

Objective Cardiovascular reactivity is hypothesized to mediate the relationship between stress and cardiovascular disease. We describe three considerations that are crucial for a causal model of cardiovascular responses to stress: the need for laboratory-life generalizability, the role of interactions between environmental exposures and individual response predispositions, and the importance of the duration of both stressor exposure and cardiovascular responding. Methods We illustrate current understanding of stress–cardiovascular disease relationships with examples from the human and animal psychophysiology, epidemiology, and genetics literature. Results In a causal model of reactivity, the usefulness of laboratory assessment rests on the assumption that laboratory-based cardiovascular reactivity predicts responses in the natural environment. We find only limited generalizability and suggest that cardiovascular responses to stress can be better understood when examined in the natural environment. The interaction of individual response predispositions and stressor exposures contributes to the development and progression of cardiovascular disease; stress-disease relationships could therefore be better understood if predispositions and exposures were assessed simultaneously in interactive models. Cardiovascular responses to stress are likely to be most deleterious when responses are prolonged. Responses may vary in their magnitude, frequency, and duration; however, reactivity captures only response magnitude. The assessment of anticipatory and recovery measures, with response magnitude, may therefore lead to a more useful model of the stress-disease relationship. Conclusions A causal model of cardiovascular responses to stress should generalize to the real world, assess interactions between individual predispositions and environmental exposures, and focus on sustained pathogenic exposures and responses.

Expanding stress theory: Prolonged activation and perseverative cognition

Several theories of the stress-disease link have now incorporated prolonged activation. This article argues that these theories still lack an important element, that is, the cognitive nature of the mechanism that causes stress responses to be sustained. The perception of stress and the initial response to it do not automatically lead to prolonged activation. The active cognitive representations of stressors need to be prolonged in order to extend their physiological concomitants. We call this mediating process perseverative cognition, and it is manifested in phenomena such as worry, rumination, and anticipatory stress. We summarize evidence suggesting that these phenomena are indeed associated with physiological activation, including cardiovascular, endocrinological and immunological parameters. This evidence is still far from sufficient, due to the many methodological insufficiencies in the studies involved. Nevertheless, it makes clear that cognitive phenomena characterized by perseverative cognition may be likely candidates to mediate the effects of stress sources on somatic disease. We also argue that there is a dearth of evidence supporting the role of prolonged activation. There are a limited number of studies demonstrating prolonged activity related to stressors and emotional episodes, and their methodologies often do not allow unambiguous conclusions. Even more important, the crucial assumption that prolonged activation actually leads to pathogenic states and disease has received hardly any attention yet and therefore is still largely unsupported. There are only a few studies that showed that anticipatory responses and slow recovery from stress predicted disease states.

Anger inhibition, cardiovascular recovery, and vagal function: a model of the link between hostility and cardiovascular disease.

A model of the association between hostility and cardiovascular disease (CVD) is proposed based upon anger inhibition, slow cardiovascular recovery, and low parasympathetic activity (vagal tone). This model is opposed to the more conventional model that emphasizes anger expression, cardiovascular reactivity, and high sympathetic tone. We argue that in social reality, incidences of anger inhibition outnumber incidences of anger expression to a great extent, irrespective of preferred expression style. Moreover, slow cardiovascular recovery, rather than high reactivity, may be the mechanism underlying the CVD risk associated with anger inhibition. Both anger inhibition and slow cardiovascular recovery are associated with a persistently low vagal tone. Thus, the anger inhibition/vagal inhibition model seems more consistent with the actual nature of anger in daily life and with the known cardiovascular control mechanisms. The model may better account for the chronic pathophysiological state that is believed to lead to CVD. Importantly, an experimental inhibition/recovery paradigm might also allow to test potential behavioral and cognitive accelerators of cardiovascular recovery. As an example of an important socially-mediated health risk that may be elucidated using the anger inhibition/vagal inhibition model, we discuss Black-White differences that have been found in CVD.

Cardiac effects of momentary assessed worry episodes and stressful events.

Objective: To hypothesize that increased heart rate (HR) and decreased heart rate variability (HRV) occurs not only during stressful events but also during episodes in which stress is cognitively represented, but not necessarily present, i.e., during worry. Methods: Ambulatory HR and HRV of 73 female and male teachers were recorded for 4 days, during which they reported, on an hourly basis using computerized diaries, the number and characteristics of worry episodes and stressful events. Multilevel regression models were used, controlling for biobehavioral variables. Results: Compared with neutral periods, worry episodes and stressful events had independent effects on HR (2.00 beats/min and 2.75 beats/min, respectively) and HRV (−1.07ms and −1.05, respectively). Neither psychological traits nor biobehavioral variables influenced these results. Effects were most pronounced for work-related worry on HR (9.16 beats/min) and HRV (−1.19 ms), and for worry about anticipated future stress on HR (4.79 beats/min). Conclusions: Worry in daily life might have substantial cardiac effects in addition to the effects of stressful events, especially in the form of work-related and anticipatory stress, the latter being a type of stress that has been largely neglected in stress research. CV = cardiovascular; HR = heart rate; HRV = heart rate variability; BP = blood pressure; BMI = body mass index; PSWQ = Penn State Worry Questionnaire; WDQ = Worry Domain Questionnaire; BDI = Beck Depression Inventory; STAI = Spielberger Trait Anxiety; CM = Cook-Medley hostility scale; IHAT = Interpersonal Hostility Assessment Technique.

Influence of life stress on immunological reactivity to mild psychological stress

&NA; This study investigated the effects of self‐reported life stress and locus of control on reactivity of several immune parameters to a mild and short‐lasting interpersonal stressor. Subjects were 86 male teachers aged 24 to 55 years. Immune reactivity was defined as changes in numbers of monocytes. T‐lymphocytes and subsets, HLA‐DR+ cells, and NK cells as well as changes in (in vitro) proliferative responses of peripheral blood lymphocytes to the antigens PHA and PWM. Multiple regression analysis was used to study the interaction effects of life stress and locus of control by experimental condition on immune reactivity. Life stress, but not locus of control, influences reactivity of the immunological parameters to the stressor. In particular, high numbers of daily hassles were associated with stressor‐induced decreases in numbers of T cells and NK cells in peripheral blood. On the other hand, numbers of HLA‐DR+ cells in high life stress scorers decreased only slightly during the stressor, whereas they increased in the control condition. The findings suggest that accumulated life stress is related to reactivity of immunological parameters to subsequent experimental stress. Possible physiological explanations and implications of these effects are discussed.

Conscious and unconscious perseverative cognition: Is a large part of prolonged physiological activity due to unconscious stress?

Prolonged physiological activity is believed to be a key factor mediating between stress and later disease outcomes. Few studies, however, have investigated the crucial psychological factors that cause prolonged activity. This article proposes that conscious as well as unconscious perseverative cognition are the critical factors. Perseverative cognition indicates repetitive or sustained activation of cognitive representations of past stressful events or feared events in the future. In daily life, most prolonged physiological activity is not due to stressful events but to perseverative cognition about them. We and others have already found evidence that conscious perseverative cognition, i.e., worry, has physiological effects, in both laboratory and real life settings, and that perseverative cognition mediates prolonged responses to stressful events. Yet, there are convincing reasons to expect that unconscious perseverative cognition has an even larger role in stress-related prolonged activity. Firstly, since the greater part of cognitive processing operates without awareness, a considerable part of perseverative cognition is likely to be unconscious too. People may not be aware of most of their stress-related cognitive processes. Secondly, our recent studies have shown that increased activity of the autonomic nervous system continues after conscious perseverative cognition has stopped: It goes on for several hours and even during sleep. This and several other findings suggest that a considerable part of increased physiological activity may be due to unconscious perseverative cognition. The article closes with suggesting methods to test unconscious perseverative cognition and ways to change it, and concludes with stating that the notion of unconscious perseverative cognition potentially opens an entirely new area within stress research.

Phobia-related cognitive bias for pictorial and linguistic stimuli.

The purpose of this study was to examine whether anxiety-related cognitive bias for threat is stronger for threatening pictures than for threatening words. Spider-phobic participants (n = 31) and control participants (n = 33) performed a pictorial and linguistic spider Stroop task. Spider-phobic participants showed a marked bias for threat. However, this bias was similar for pictures and for words, although the spider-phobic group evaluated the pictures as being more aversive. The results suggest that automatic processing of threatening information in people with phobias is triggered in an on-off fashion, independent of subjective threat of the stimuli. This lack of distinction in automatic processing of weak and strong predictors of danger may be fundamental to the irrational nature of anxiety disorders.

Worry about health in smoking behaviour change

Many smokers and ex-smokers worry about their health. Given that worry keeps attention focused on the threat, it was expected that worrying about health in smokers would motivate them to quit and in ex-smokers may prevent relapse. Furthermore, worry was expected to influence the process of smoking cessation in interaction with self-efficacy, which is a measure of control over smoking, and with disengagement beliefs, which distorts the threatening meaning of potential motivating information. In the present study 380 smokers and 324 ex-smokers were recruited to join a prospective study with a follow-up of eight months. At T1, smoking/quitting behavior, worry and the other psychological constructs were assessed. At T2 quitting activity in smokers and relapse in ex-smokers were assessed. As expected, smokers who worried about the health effects of smoking reported higher quitting activity at T2. The three-way interactions between worry, self-efficacy and disengagement beliefs in the prospective prediction of quitting activity and relapse were significant: Among smokers with high self-efficacy combined with strong disengagement beliefs, worry led to more quitting activity. Among ex-smokers with low self-efficacy combined with strong disengagement beliefs, worry led to more relapse. The present results suggest new ways of approaching the stimulation of quitting and the prevention of relapse.

Prolonged Cardiac Effects of Momentary Assessed Stressful Events and Worry Episodes

Objectives: To test the hypothesize that increased heart rate (HR) and decreased heart rate variability (HRV) are not only due to concurrent stressful events and worries but also to stressors and worries occurring in the preceding hours or stressors anticipated to occur in the next hour. Worry was expected to mediate at least part of the prolonged effects of stressors. Methods: Ambulatory HR and HRV of 73 teachers were recorded for 4 days, during which the participants reported occurrence and duration of worry episodes and stressful events on an hourly basis, using computerized diaries. Multilevel regression models were used, accounting for effects of several biobehavioral variables. Results: Stressful events were not associated with changes in HR or HRV. However, worry episodes had effects on concurrent HR and HRV (2.55 beats/minute; −5.76 milliseconds) and HR and HRV in the succeeding hour (3.05 beats/minute; −5.80 milliseconds) and 2 hours later (1.52 beats/minute; −3.14 milliseconds). These findings were independent of emotions, physical activity, posture, and other biobehavioral factors. Conclusion: Worry has effects on cardiac activity, and these effects were still visible after 2 hours. The latter finding suggests that a considerable part of prolonged activation may be induced by unconscious stress-related cognition. CV = cardiovascular disease; HR = heart rate; HRV = heart rate variability; BP = blood pressure; BMI = body mass index; ECG = electrocardiogram.