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      State Anxiety Is Associated with Cardiovascular Reactivity in Young, Healthy African Americans

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          Abstract

          Although several studies have shown that enhanced cardiovascular reactivity can predict hypertension development in African Americans, these findings have not been consistent among all studies examining reactivity and hypertension susceptibility. This inconsistency may be explained by the influence of anxiety (state and trait) on the blood pressure response to stress. Therefore, this study sought to determine whether anxiety is associated with blood pressure response to cold pressor (CP) and anger recall (AR) stress tests in young healthy African Americans. Modeling using state and trait anxiety revealed that state anxiety predicts systolic (SBP) and diastolic blood pressure DBP response to CP and AR ( P ≤ 0.02). Interestingly, state anxiety predicted heart rate changes only to CP ( P < 0.01; P = 0.3 for AR). Although trait anxiety was associated with SBP response to AR and not CP, it was not a significant predictor of reactivity in our models. We conclude that anxiety levels may contribute to the variable blood pressure response to acute stressors and, therefore, should be assessed when performing cardiovascular reactivity measures.

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          Most cited references67

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          Greater cardiovascular responses to laboratory mental stress are associated with poor subsequent cardiovascular risk status: a meta-analysis of prospective evidence.

          An increasing number of studies has tested whether greater cardiovascular responses to acute mental stress predict future cardiovascular disease, but results have been variable. This review aimed quantitatively to evaluate the association between cardiovascular responses to laboratory mental stress and subsequent cardiovascular risk status in prospective cohort studies. We searched general bibliographic databases, PsycINFO, Web of Science, and PubMed, up to December 2009. Two reviewers independently extracted data on study characteristics, quality, and estimates of associations. There were 169 associations (36 articles) of stress reactivity and 30 associations (5 articles) of poststress recovery in relation to future cardiovascular risk status, including elevated blood pressure, hypertension, left ventricular mass, subclinical atherosclerosis, and clinical cardiac events. The overall meta-analyses showed that greater reactivity to and poor recovery from stress were associated longitudinally with poor cardiovascular status (r=0.091 [95% CI: 0.050 to 0.132], P<0.001, and r=0.096 [95% CI: 0.058 to 0.134], P<0.001, respectively). These findings were supported by more conservative analyses of aggregate effects and by subgroup analyses of the methodologically strong associations. Notably, incident hypertension and increased carotid intima-media thickness were more consistently predicted by greater stress reactivity and poor stress recovery, respectively, whereas both factors were associated with higher future systolic and diastolic blood pressures. In conclusion, the current meta-analysis suggests that greater responsivity to acute mental stress has an adverse effect on future cardiovascular risk status, supporting the use of methods of managing stress responsivity in the prevention and treatment of cardiovascular disease.
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            Chronic psychosocial factors and acute physiological responses to laboratory-induced stress in healthy populations: a quantitative review of 30 years of investigations.

            This meta-analysis included 729 studies from 161 articles investigating how acute stress responsivity (including stress reactivity and recovery of hypothalamic-pituitary-adrenal [HPA] axis, autonomic, and cardiovascular systems) changes with various chronic psychosocial exposures (job stress; general life stress; depression or hopelessness; anxiety, neuroticism, or negative affect; hostility, aggression, or Type-A behavior; fatigue, burnout, or exhaustion; positive psychological states or traits) in healthy populations. In either the overall meta-analysis or the methodologically strong subanalysis, positive psychological states or traits were associated with reduced HPA reactivity. Hostility, aggression, or Type-A behavior was associated with increased cardiovascular (heart rate or blood pressure) reactivity, whereas anxiety, neuroticism, or negative affect was associated with decreased cardiovascular reactivity. General life stress and anxiety, neuroticism, or negative affect were associated with poorer cardiovascular recovery. However, regarding the sympathetic nervous system and parasympathetic nervous system, there were no associations between the chronic psychosocial factors and stress reactivity or recovery. The results largely reflect an integrated stress response pattern of hypo- or hyperactivity depending on the specific nature of the psychosocial background.
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              Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council: cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: the American Academy of Neurology affirms the value of this guideline.

              This guideline provides an overview of the evidence on various established and potential stroke risk factors and provides recommendations for the reduction of stroke risk. Writing group members were nominated by the committee chair on the basis of each writer's previous work in relevant topic areas and were approved by the American Heart Association Stroke Council's Scientific Statement Oversight Committee. The writers used systematic literature reviews (covering the time period since the last review published in 2001 up to January 2005), reference to previously published guidelines, personal files, and expert opinion to summarize existing evidence, indicate gaps in current knowledge, and when appropriate, formulate recommendations based on standard American Heart Association criteria. All members of the writing group had numerous opportunities to comment in writing on the recommendations and approved the final version of this document. The guideline underwent extensive peer review before consideration and approval by the AHA Science Advisory and Coordinating Committee. Schemes for assessing a person's risk of a first stroke were evaluated. Risk factors or risk markers for a first stroke were classified according to their potential for modification (nonmodifiable, modifiable, or potentially modifiable) and strength of evidence (well documented or less well documented). Nonmodifiable risk factors include age, sex, low birth weight, race/ethnicity, and genetic factors. Well-documented and modifiable risk factors include hypertension, exposure to cigarette smoke, diabetes, atrial fibrillation and certain other cardiac conditions, dyslipidemia, carotid artery stenosis, sickle cell disease, postmenopausal hormone therapy, poor diet, physical inactivity, and obesity and body fat distribution. Less well-documented or potentially modifiable risk factors include the metabolic syndrome, alcohol abuse, drug abuse, oral contraceptive use, sleep-disordered breathing, migraine headache, hyperhomocysteinemia, elevated lipoprotein(a), elevated lipoprotein-associated phospholipase, hypercoagulability, inflammation, and infection. Data on the use of aspirin for primary stroke prevention are reviewed. Extensive evidence is available identifying a variety of specific factors that increase the risk of a first stroke and providing strategies for reducing that risk.
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                Author and article information

                Journal
                Int J Hypertens
                IJHT
                International Journal of Hypertension
                Hindawi Publishing Corporation
                2090-0384
                2090-0392
                2012
                3 January 2012
                : 2012
                : 268013
                Affiliations
                1Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, NC 27707, USA
                2School of Business, North Carolina Central University, Durham, NC 27707, USA
                3Department of Psychology, North Carolina Central University, Durham, NC 27707, USA
                Author notes
                *Mildred A. Pointer: mpointer@ 123456nccu.edu

                Academic Editor: Tavis S. Campbell

                Article
                10.1155/2012/268013
                3259484
                22263105
                31f02867-064a-4c66-91fd-daf97108ebdf
                Copyright © 2012 Mildred A. Pointer et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 1 August 2011
                : 7 October 2011
                : 21 November 2011
                Categories
                Research Article

                Cardiovascular Medicine
                Cardiovascular Medicine

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