84 research outputs found

    Child-mediated health communication: A conceptual framework for increasing stroke literacy in hard to reach populations

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    Effectively engaging economically-disadvantaged ethnic minority communities for promoting health has proved to be challenging for a variety of reasons, including factors related to healthcare access, literacy, inadequate or ineffective cultural appropriateness of materials, and the relatively low priority for health due to competing demands related to economic hardship. We have developed a framework of Child-Mediated Health Communication (CMHC), which focuses on children as channels for carrying out health promotion interventions to parents and other caregivers. CMHC is an innovative, alternative strategy for engaging this underserved population, where traditional methods of health promotion have not been successful. We discuss the theoretical foundation, development, and effectiveness of a CMHC framework in our stroke preparedness communication intervention, Hip Hop Stroke

    Effect of Anger Provocation on Endothelium-Dependent and -Independent Vasodilation

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    Anger is an independent predictor of coronary heart disease events, although the mechanisms for this relation are unclear. The effects of an anger-provoking interview compared with a neutral interview on endothelium-dependent and -independent vasodilation assessed by brachial artery ultrasound were examined in 14 healthy subjects without coronary heart disease risk factors. The anger provocation condition, but not the neutral condition, caused a significant impairment in endothelium-dependent vasodilation at 90 minutes compared with baseline (p = 0.004) and 30 minutes (p = 0.013). Similarly, endothelium-independent vasodilation was significantly impaired at 90 minutes after the angry interview compared with baseline (p = 0.003) and 30 minutes (p = 0.001). The decreases in endothelium-dependent and -independent vasodilation were greater after the anger-provoking interview than after the neutral interview, especially between 30 and 90 minutes. In conclusion, preliminary results suggest that an episode of anger is associated with a dysregulation in endothelium-dependent and -independent pathways, suggesting that these mechanisms might contribute to the link between anger and coronary heart disease events. Although anger is associated with increased short- and long-term risk for coronary heart disease (CHD) events, independent of traditional CHD risk factors,1, 2, 3, 4, 5 and 6 the mechanisms that underlie this relation are unknown. Endothelial dysfunction plays a major role in the development of atherosclerosis.7 Traditional CHD risk factors are associated with endothelial dysfunction8 and may also impair arterial vasodilation in response to exogenous nitric oxide (NO), suggesting concomitant vascular smooth muscle dysfunction.8 and 9 Thus, the higher risk for CHD events associated with anger may be similarly mediated through an impairment in endothelium-dependent vasodilation (EDV) with or without an impairment in endothelium-independent vasodilation (EIV). To our knowledge, the effects of anger on EDV and EIV have never previously been examined. To test this hypothesis, we examined the effects of anger induction in humans on EDV and EIV assessed by brachial artery ultrasonography

    Are there consequences of labeling patients with prehypertension? An experimental study of effects on blood pressure and quality of life

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    Objective The prehypertension classification was introduced to facilitate prevention efforts among patients at increased risk for hypertension. Although patients who have been told that they have hypertension report worse outcomes than unaware hypertensives, little is known about whether or not prehypertension labeling has negative effects. We evaluated the effects of labeling individuals with prehypertension on blood pressure and health-related quality of life three months later. Methods One hundred adults (aged 19 to 82 [mean=40.0] years; 54% women; 64% racial/ethnic minorities) with screening blood pressure in the prehypertensive range (120–139/80–89 mm Hg) and no history of diagnosis or treatment of elevated blood pressure were randomly assigned to either a “Labeled” group in which they were informed of their prehypertension, or an “Unlabeled” group in which they were not informed. Subjects underwent office blood pressure measurement, 24-hour ambulatory blood pressure monitoring and completed self-report questionnaires at baseline and at three months. Results Multilevel mixed effects regression analyses indicated that changes in the white coat effect, office blood pressure, mean daytime ambulatory blood pressure, and physical and mental health did not differ significantly between the two groups. Adjusting for age, sex, race/ethnicity and body mass index did not affect the results. Conclusion These findings suggest that labeling patients with prehypertension does not have negative effects on blood pressure or quality of life. Additional research is needed to develop approaches to communicating with patients about their blood pressure that will maximize the clinical and public health impact of the prehypertension classification

    Rumination as a Mediator of Chronic Stress Effects on Hypertension: A Causal Model

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    Chronic stress has been linked to hypertension, but the underlying mechanisms remain poorly specified. We suggest that chronic stress poses a risk for hypertension through repeated occurrence of acute stressors (often stemming from the chronic stress context) that cause activation of stress-mediating physiological systems. Previous models have often focused on the magnitude of the acute physiological response as a risk factor; we attempt to extend this to address the issue of duration of exposure. Key to our model is the notion that these acute stressors can emerge not only in response to stressors present in the environment, but also to mental representations of those (or other) stressors. Consequently, although the experience of any given stressor may be brief, a stressor often results in a constellation of negative cognitions and emotions that form a mental representation of the stressor. Ruminating about this mental representation of the stressful event can cause autonomic activation similar to that observed in response to the original incident, and may occur and persist long after the event itself has ended. Thus, rumination helps explain how chronic stress causes repeated (acute) activation of one's stress-mediating physiological systems, the effects of which accumulate over time, resulting in hypertension risk
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