• J Affect Disord · Feb 2012

    Cognitive/affective and somatic/affective symptom dimensions of depression are associated with current and future inflammation in heart failure patients.

    • Nina Kupper, Jos W Widdershoven, and Susanne S Pedersen.
    • Department of Medical Psychology and Neuropsychology, Center of Research on Psychology in Somatic diseases, Tilburg University, and Department of Cardiology, TweeSteden Hospital, Tilburg, The Netherlands. h.m.kupper@uvt.nl
    • J Affect Disord. 2012 Feb 1;136(3):567-76.

    BackgroundLittle is known about whether cognitive/affective depressive symptoms or somatic/affective depressive symptoms are associated with inflammation in heart failure (HF), or that the relation is confounded with disease severity.AimTo examine the association between depressive symptom dimensions in HF patients with inflammatory markers cross-sectionally and prospectively, while adjusting for appropriate confounders.ResultsConsecutive HF patients completed the Beck Depression Inventory at inclusion and at 12 month follow-up. Cytokines were assessed at both occasions. Cross-sectional--multivariate linear regression analysis (n=110) demonstrated that cognitive/affective depressive symptoms were independently associated with increased levels of sTNFR2 (β=0.20, p<0.05) and IL-1ra (β=0.28, p<0.01). Somatic/affective depressive symptoms were independently related to sTNFR2 (β=0.21, p<0.05). Prospective--(n=125) the level of cognitive/affective depressive symptoms at inclusion was prospectively associated with increased levels of sTNFR1 and sTNFR2 (β=0.21 and 0.25 resp. p<0.05), independent of covariates. Change in somatic/affective depressive symptoms over the 12 month period was associated with sTNFR2 (β=0.30, p=0.008). At symptom level, core depressive cognitions such as hopelessness and guilt drove the relation between the sTNF receptors and the cognitive/affective component, while having sleep problems was the most important associate of the somatic/affective dimension.ConclusionsBaseline cognitive/affective depressive symptoms were prospectively associated with sTNFR1 and sTNFR2 in HF patients, while change in somatic/affective depressive symptoms was associated with sTNFR2, independent from clinical and demographic covariates. Further studies are warranted to replicate these findings and to examine the association between depression dimensions, inflammation and prognosis in HF.Copyright © 2011 Elsevier B.V. All rights reserved.

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