Cognitive‐behavioural stress management does not improve biological cardiovascular risk indicators in women with ischaemic heart disease: a randomized‐controlled trial

• Published in: Journal of Internal Medicine
• Main Authors: CLAESSON, M., BIRGANDER, L. S., JANSSON, J.‐H., LINDAHL, B., BURELL, G., ASPLUND, K., MATTSSON, C.
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wiley 2006
• Subjects: Northern Sweden
• Online Access: http://dx.doi.org/10.1111/j.1365-2796.2006.01691.x; https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fj.1365-2796.2006.01691.x; https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2796.2006.01691.x

Abstract. Objectives. Psychosocial factors, such as stress and vital exhaustion, are associated with an increased risk of cardiovascular events, and women report more psychosocial ill‐being after an acute myocardial infarction than men. We have earlier shown that a cognitive‐behavioural intervention in women with ischaemic heart disease (IHD) improved psychosocial well‐being. In the present study, we tested the hypothesis that the improvement in psychosocial well‐being is associated with an improvement in biochemical indicators of cardiovascular risk. Design. Randomized‐controlled trial in northern Sweden. Setting. Outpatient care. Subjects. Women with IHD were randomized to either a 1‐year cognitive‐behavioural stress management programme or usual care. Of the 159 women who completed the study, 77 were in the intervention group, and 82 in the control group. Interventions. A 1‐year cognitive‐behavioural stress management programme versus conventional care. Results. Group assignment was not found to be a determinant of waist circumference, high sensitive C‐reactive protein (hs‐CRP), fibrinogen, von Willebrand factor (vWF), plasminogen activator inhibitor type 1 (PAI‐1) activity, tissue plasminogen activator (tPA) activity, tPA antigen, tPA–PAI‐1 complex, leptin, or HOMA2 insulin resistance index (HOMA2‐IR) at follow up. Changes in psychosocial variables were not associated with changes in any of the biological risk indicators. Conclusions. Even if our cognitive‐behavioural stress management programme had effects on proximal targets, such as stress behaviour and vital exhaustion, we found no improvement in intermediate biochemical targets related to the metabolic syndrome and IHD. Our results challenge the proposition that the relationship between psychological well‐being and biological cardiovascular risk indicators is a direct cause–effect phenomenon.