ISSN:0033-3174    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:0033-3174    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

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.

ISSN:0033-3174    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Objective and MethodsThis article is a selective review of recent findings bearing on the conceptualization and measurement of cardiovascular reactivity to psychological challenge, with a focus on several issues relevant to the reliability, content validity, construct validity, and criterion validity of these measures.Results and ConclusionsWith respect to reliability, use of standardized task demands and aggregated scores are associated with enhanced short-term reliability, but the long-term reliability of cardiovascular reactivity has not been sufficiently documented. With respect to content validity, existing evidence suggests that “vascular” or “cardiac” tasks may evoke responses that reflect similar distributions of individual difference, whereas associations between responses to “physical” and “psychological” tasks are modest. The evidence is not clear at present with respect to the importance of including affective or interpersonal stimuli as part of trait reactivity assessments. With respect to construct validity, existing data show that cardiovascular reactivity to psychological challenge is largely independent of standard measures of autonomic function. With respect to criterion validity, recent studies point to a number of methodological limitations that may have restricted our ability to detect lab-to-life generalizability of reactivity measures in the past. Continued progress in understanding and measuring reactivity as an individual difference dimension is essential in helping us to evaluate emerging evidence examining the relationship between reactivity and disease risk.

ISSN:0033-3174    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveCardiovascular 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.MethodsWe illustrate current understanding of stress–cardiovascular disease relationships with examples from the human and animal psychophysiology, epidemiology, and genetics literature.ResultsIn 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.ConclusionsA 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.

ISSN:0033-3174    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveThis 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.MethodsThis 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.ResultsAt 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.ConclusionsThese 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.

ISSN:0033-3174    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveThe objective of this review is to evaluate the evidence for the hypothesis that cardiovascular reactivity can predict the development of preclinical (elevated blood pressure, ventricular remodeling, carotid atherosclerosis) and/or clinical cardiovascular disease states.MethodsA review of the literature was conducted examining prospective studies.ResultsThree large epidemiological studies with long-term follow-up periods (20 years or more) have found blood pressure responses to the cold pressor task to be predictive of subsequent essential hypertension in initially normotensive samples. Studies showing less consistent results have tended to use shorter-term follow-up periods. A larger body of literature demonstrates consistent associations between stress-related cardiovascular reactivity and blood pressure elevations in youth over the course of 1 to 6 years; such relationships have not been consistently shown among adult samples. Moderately consistent evidence points to a positive relationship between reactivity and other measures of subclinical disease (increased left ventricular mass and carotid atherosclerosis) among the few prospective studies that have examined these issues to date. A number of additional factors, however, such as baseline levels of disease risk and exposure to psychosocial stress, seem to moderate these relationships. Health status at baseline also seems to moderate the association between reactivity and clinical coronary heart disease in recent reports: two of three existing studies in initially healthy samples show no evidence of a relationship between reactivity and clinical outcomes, whereas three of four studies in samples with preexisting coronary heart disease or essential hypertension show a positive relationship between reactivity and subsequent disease states.ConclusionsThere is reasonable evidence to suggest that cardiovascular reactivity can predict the development of some preclinical states (eg, increased left ventricular mass and blood pressure) states and perhaps even new clinical events in some patients with essential hypertension or coronary heart disease. However, much more information is needed concerning moderating and potentially confounding variables before the robustness of the positive relationships can become clinically useful.

ISSN:0033-3174    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveEvidence concerning whether sleep disturbances in older adults predict mortality is mixed. However, data are limited to self-reported sleep problems and may be confounded with other comorbidities. We examined whether electroencephalographic (EEG) sleep parameters predicted survival time independently of known predictors of all-cause mortality.MethodsA total of 185 healthy older adults, primarily in their 60s through 80s, with no history of mental illness, sleep complaints, or current cognitive impairment, were enrolled in one of eight research protocols between October 1981 and February 1997 that included EEG sleep assessments. At follow-up (mean [SD] = 12.8 [3.7] years after baseline, range = 4.1–19.5), 66 individuals were positively ascertained as deceased and 118 remained alive (totalN= 184).ResultsControlling for age, gender, and baseline medical burden, individuals with baseline sleep latencies greater than 30 minutes were at 2.14 times greater risk of death (p= .005, 95% CI = 1.25–3.66). Those with sleep efficiency less than 80% were at 1.93 times greater risk (p= .014, CI = 1.14–3.25). Individuals with rapid eye movement (REM) sleep percentages in the lowest 15% or highest 15% of the total sample’s distribution (percentage of REM <16.1 or >25.7) were at 1.71 times greater risk (p= .045, CI = 1.01–2.91). Percentage of slow-wave sleep was associated with time to death at the bivariate level, but not after controlling for potential confounders.ConclusionsOlder adults with specific EEG sleep characteristics have an excess risk of dying beyond that associated with age, gender, or medical burden. The findings suggest that interventions to optimize and protect older adults’ sleep initiation, continuity, and quality may be warranted.

ISSN:0033-3174    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:0033-3174    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

ObjectiveAlcoholics who are at risk for infectious disease show profound disturbances of sleep along with decrements of cellular immunity. This study examined the relationships between sleep, nocturnal expression of immunoregulatory cytokines, and natural killer (NK) cell activity in alcoholic patients as compared with control subjects.MethodsAlcoholic patients (N= 24) and comparison control subjects (N= 23) underwent all-night polysomnography and serial blood sampling at 23:00, 03:00, and 06:30 hours. Stimulated expression of TH1 (interferon gamma, IFN-&ggr;), anti-inflammatory/TH2 (interleukin 10, IL-10), and proinflammatory cytokines (IL-6) was measured along with NK cell activity across the night.ResultsAlcoholic patients showed lower levels of IL-6 production, suppression of the IL-6/IL-10 ratio, and a reduction of NK cell activity, coupled with losses of delta sleep and increases of rapid eye movement sleep, as compared with control subjects. In addition, alcoholics showed a persistent low ratio of IFN-&ggr;/IL-10 and reduced levels of NK cell activity, whereas controls had increases of these two immune measures across the night. IL-6 also differentially changed in the two groups; alcoholics showed increases and controls had decreases of IL-6 from 03:00 hours to 06:30 hours. At 06:30 hours, rapid eye movement sleep predicted increases of IL-6 and decreases of NK cell activity independent of the relative contribution of age and chronic alcohol consumption. At 23:00 hours before sleep onset, levels of IL-10 predicted subsequent amounts of delta sleep.ConclusionsThese data further implicate sleep in the regulation of immune function and suggest that disordered sleep contributes to immune alterations in patients with chronic alcoholism. Moreover, the association between awake levels of the anti-inflammatory/TH2 cytokine IL-10 and subsequent amounts of delta sleep support the notion of a bidirectional interplay between cytokines and sleep in humans.

ISSN:0033-3174    

出版商:OVID    

年代:2003

数据来源: OVID