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Janicki, Denise L. (2006) CHRONIC STRESS, INFLAMMATION, AND PROGRESSION OF CAROTID ARTERY ATHEROSCLEROSIS: A MEDIATION MODEL. Doctoral Dissertation, University of Pittsburgh. (Unpublished)

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Psychosocial stress might account for some of the variance in cardiovascular disease (CVD) risk that is not explained by traditional risk factors. Most studies of stress and CVD have focused on (a) stress in a single life domain, and (b) clinical CVD outcomes. Few studies have examined physiologic mechanisms that might explain the association between stress and CVD. The primary aim of the present study was to examine whether: (1) chronic stress predicts changes in carotid artery intima-media thickness (IMT) and plaque; and (2) the association between chronic stress and changes in these surrogate CVD endpoints is mediated by inflammatory processes. A secondary aim was to investigate whether individual differences in cardiovascular reactivity (CVR) moderates the association between stress and changes in IMT and plaque. The sample (n=276; M age=60.5), was a subset of the Pittsburgh Healthy Heart Project, a longitudinal investigation of the effects of psychosocial and biological risk factors on surrogate CVD endpoints among healthy older adults. Chronic stress was assessed at baseline with the Chronic Stress Scale (CSS; Norris & Uhl, 1993), a self-report survey that measures stress in 7 life domains during the preceding 6 months. Chronic stress was computed in terms of (a) scores on the 7 CSS subscales and (b) average score across all 7 subscales. Ultrasound IMT measures were taken at baseline and 3 years later. Mean IMT was derived by taking the bilateral average of far wall common, internal and bulb measures. IMT change was computed as the arithmetic difference between follow-up and baseline values. Plaque change was computed as the number of visible lesions at follow-up less the number of lesions at baseline. Blood draws for inflammatory markers and CVR testing were conducted at separate baseline visits. Results failed to support the mediation model. Only the CSS physical stress subscale was an independent predictor of IMT change (b=.02, t=2.13, p=.03). CSS scores were unrelated to plaque, or to inflammatory marker levels. Results did not differ according to CVR. Findings question the importance of chronic stress, as measured by global self-report, as a predictor of change in IMT and plaque.


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Item Type: University of Pittsburgh ETD
Status: Unpublished
CreatorsEmailPitt UsernameORCID
Janicki, Denise
ETD Committee:
TitleMemberEmail AddressPitt UsernameORCID
Committee ChairKamarck, Thomas Wtkam@pitt.eduTKAM
Committee Member Marsland, Anna Lmarsland@pitt.eduMARSLAND
Committee MemberMatthews, Karen
Committee MemberCohen,
Committee MemberOrchard, Trevor Jtjo@pitt.eduTJO
Date: 2 June 2006
Date Type: Completion
Defense Date: 13 January 2006
Approval Date: 2 June 2006
Submission Date: 18 October 2005
Access Restriction: No restriction; Release the ETD for access worldwide immediately.
Institution: University of Pittsburgh
Schools and Programs: Dietrich School of Arts and Sciences > Psychology
Degree: PhD - Doctor of Philosophy
Thesis Type: Doctoral Dissertation
Refereed: Yes
Uncontrolled Keywords: interleukin-6; psychosocial; C-reactive protein; cardiovascular disease
Other ID:, etd-10182005-141724
Date Deposited: 10 Nov 2011 20:03
Last Modified: 15 Nov 2016 13:50


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