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Volume 68, Issue 2, Pages 109-116 (February 2010)


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Hostility and physiological responses to laboratory stress in acute coronary syndrome patients

Lena BrydonaCorresponding Author Informationemail address, Philip C. Strikea, Mimi R. Bhattacharyyaa, Daisy L. Whiteheada, Jean McEwanb, Ian Zacharyb, Andrew Steptoea

Received 6 November 2008; received in revised form 7 April 2009; accepted 9 June 2009. published online 24 September 2009.

Abstract 

Objective

Evidence suggests that emotional stress can trigger acute coronary syndromes in patients with advanced coronary artery disease (CAD), although the mechanisms involved remain unclear. Hostility is associated with heightened reactivity to stress in healthy individuals, and with an elevated risk of adverse cardiac events in CAD patients. This study set out to test whether hostile individuals with advanced CAD were also more stress responsive.

Methods

Thirty-four men (aged 55.9±9.3 years) who had recently survived an acute coronary syndrome took part in laboratory testing. Trait hostility was assessed by the Cook Medley Hostility Scale, and cardiovascular activity, salivary cortisol, and plasma concentrations of interleukin-6 were assessed at baseline, during performance of two mental tasks, and during a 2-h recovery.

Results

Participants with higher hostility scores had heightened systolic and diastolic blood pressure (BP) reactivity to tasks (both P<.05), as well as a more sustained increase in systolic BP at 2 h post-task (P=.024), independent of age, BMI, smoking status, medication, and baseline BP. Hostility was also associated with elevated plasma interleukin-6 (IL-6) levels at 75 min (P=.023) and 2 h (P=.016) poststress and was negatively correlated with salivary cortisol at 75 min (P=.034).

Conclusion

Hostile individuals with advanced cardiovascular disease may be particularly susceptible to stress-induced increases in sympathetic activity and inflammation. These mechanisms may contribute to an elevated risk of emotionally triggered cardiac events in such patients.

a Psychobiology Group, Department of Epidemiology and Public Health, University College London, London, United Kingdom

b Centre for Cardiovascular Biology and Medicine, Department of Medicine, The Rayne Institute, University College London, London, United Kingdom

Corresponding Author InformationCorresponding author. Psychobiology Group, Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 6BT, London, United Kingdom. Tel.: +44 207 679 5973; fax: +44 207 916 8542.

 This research was funded by the British Heart Foundation.

PII: S0022-3999(09)00260-8

doi:10.1016/j.jpsychores.2009.06.007


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