Biomedical subjects
William Gerin
Publications and source records attributed to William Gerin.
Psychological and physical stress-induced cardiovascular reactivity and diurnal blood pressure variation in women with different work shifts.
There is increasing evidence that diurnal blood pressure (BP) variation, in addition to high BP per se, is related to target organ damage and the incidence of cardiovascular events. However, the determinants of diurnal BP variation are not adequately understood. This paper tests the hypothesis that cardiovascular reactivity to acute stress and/or delayed recovery predicts greater diurnal BP variation (i.e., a lower sleep/awake BP ratio). We studied the relationship of diurnal BP variation (assessed by ambulatory BP monitoring) to mental stress (mental arithmetic and anger recall tasks) and physical stress (treadmill)-induced cardiovascular reactivity and recovery in 87 female nurses who worked different shifts. The sleep/awake systolic BP (SBP) ratio was negatively correlated with relative SBP reactivity (maximum SBP increase/baseline SBP: r = -0.21, p = 0.06) and relative stress response (average of SBP during stress/baseline SBP:r = -0.23, p = 0.04) induced by anger recall, while the correlations of the sleep/awake SBP ratio with other parameters of reactivity or recovery in the anger recall or mental arithmetic task were not significant. When subjects were divided into day-shift workers (n=54) and night-shift workers (n = 33), the sleep/awake SBP ratio was negatively correlated with relative SBP reactivity (r = -0.41, p = 0.02) and relative stress response of SBP (r = -0.48, p = 0.006) induced by anger recall, and positively correlated with recovery rate (r = 0.34, p = 0.06) in the latter group, while these correlations were not significant in the former group. The sleep/awake SBP ratio was inversely correlated with the exercise-induced SBP increase in the day-shift workers (r = -0.30, p = 0.03), while this association was not found in the night-shift workers. In conclusion, cardiovascular reactivity triggered by psychological and physical stress in the laboratory may be a weak, but significant, determinant of diurnal BP variation; in addition, work shift (day or night) appears to moderate the relationship between these two pressor mechanisms.
The role of rumination in recovery from reactivity: cardiovascular consequences of emotional states.
OBJECTIVE: While most investigations of the link between blood pressure responses and later disease have focused on acute reactivity during stressful tasks, there is some theoretical and empirical reason to believe that examining recovery and later re-creations of BP responses may also be useful. Two experiments explored situational determinants of sustained BP elevations, examining whether the extent of recovery and the ability to later mentally recreate the response are influenced by the magnitude or emotionality of the initial task and also whether preventing rumination after a stressor has ended speeds recovery. METHOD: Experiment 1, with 72 normotensive male and female undergraduates, examined BP and heart rate before, during, and after a task and also before, during, and after the mental re-creation of that task. Four tasks were used, designed to produce high initial reactivity with an emotional component (mental arithmetic with harassment), low reactivity with emotion (shock avoidance), high reactivity without emotion (physical exercise), or low reactivity without emotion (cold pressor). Experiment 2, with 20 normotensive male and female undergraduates, compared the cardiovascular recovery of persons who were either given a distractor task or just sat quietly immediately after a mental arithmetic task. RESULTS: Study 1 revealed that only the emotional tasks were associated with delayed BP recovery and elevations during later rumination. Blood pressure during recovery and later rumination was independent of the original reactivity. Experiment 2 found that participants with the distractor, who presumably could not ruminate, showed better BP recovery. CONCLUSIONS: Situations that put people at risk may include not just those that cause large BP elevations, but also emotion-producing situations that lead to sustained and recurring elevations.
Psychophysiological reactivity: mechanisms and pathways to cardiovascular disease.
OBJECTIVE: This article examines possible sources of heightened psychophysiological reactivity in relation to risk for hypertension and coronary artery disease. The idea that exaggerated reactions to psychological stress may predict greater risk for future disease has some support in the psychosomatic and behavioral medicine literature. However, the pathways by which exaggerated reactivity could arise in a given person and the implications of different sources of reactivity for potential disease relationships have received little attention. METHODS: This topic is approached through a selective literature review and by means of a neurophysiologically based model of individual differences in physiological reactivity. Temperament characteristics, cognitive processes, neurophysiology, and peripheral physiology are used to indicate three levels that could contribute to exaggerated physiological reactivity. RESULTS: At the top level in the model, activity of the frontal cortex and limbic system establish cognitive-emotional sources of activation that may underlie exaggerated physiological reactivity. In the absence of these influences, large responses may be more likely when exaggerated subcortical response tendencies are present via the hypothalamus or brain stem. Finally, peripheral alterations may account for larger reactions in persons who have otherwise normal emotional and hypothalamic and brainstem response tendencies. Cognitive-emotional and hypothalamic-brainstem sources of altered reactivity may cause or aggravate disease. In contrast, altered peripheral reactivity suggests that a pathophysiologic process may be present, serving as a marker for disease. CONCLUSIONS: These three levels of analysis allow for organization of existing data in the area of cardiovascular reactivity and for planning future studies in a hypothesis-building framework.
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.
Cardiovascular reactivity: status quo and a research agenda for the new millennium.
This article introduces a series of articles that assess the present status of the cardiovascular reactivity construct as well as the progress that has been made since a critical review of the reactivity literature by Pickering and Gerin was published in 1990.
The role of angry rumination and distraction in blood pressure recovery from emotional arousal.
OBJECTIVE: Cardiovascular recovery of prestress baseline blood pressure has been implicated as a possible additional determinant of sustained blood pressure elevation. We hypothesize that angry ruminations may slow the recovery process. METHOD: A within-subjects design was used in which resting baseline blood pressure and heart rate measurements were assessed on 60 subjects, who then took part in two anger-recall tasks. After each task, subjects sat quietly and alone during a 12-minute recovery period randomized to with or without distractions. During baseline, task, and recovery, blood pressure was continuously monitored; during recovery, subjects reported their thoughts at five fixed intervals. RESULTS: Fewer angry thoughts were reported in the distraction condition (17%) compared with no distraction (31%; p = .002); an interaction showed that this effect was largely the result of the two intervals immediately after the anger-recall task. Trait rumination interacted with distraction condition such that high ruminators in the no-distraction condition evidenced the poorest blood pressure recovery, assessed as area under the curve (p = .044 [systolic blood pressure] and p = .046 [diastolic pressure]). CONCLUSIONS: People who have a tendency to ruminate about past anger-provoking events may be at greater risk for target organ damage as a result of sustained blood pressure elevations; the effect is exacerbated when distractions are not available to interrupt the ruminative process.