Nina Kupper1, Jos W Widdershoven, Susanne S Pedersen. 1. 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
Abstract
BACKGROUND: Little 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. AIM: To examine the association between depressive symptom dimensions in HF patients with inflammatory markers cross-sectionally and prospectively, while adjusting for appropriate confounders. RESULTS: Consecutive 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. CONCLUSIONS: Baseline 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.
BACKGROUND: Little 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. AIM: To examine the association between depressive symptom dimensions in HF patients with inflammatory markers cross-sectionally and prospectively, while adjusting for appropriate confounders. RESULTS: Consecutive 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. CONCLUSIONS: Baseline 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.
Authors: Diana A Chirinos; Ronald Goldberg; Marc Gellman; Armando J Mendez; Miriam Gutt; Judith R McCalla; Maria M Llabre; Neil Schneiderman Journal: Ann Behav Med Date: 2013-08
Authors: April Taylor-Clift; Lucie Holmgreen; Stevan E Hobfoll; James I Gerhart; DeJuran Richardson; James E Calvin; Lynda H Powell Journal: J Affect Disord Date: 2015-10-22 Impact factor: 4.839
Authors: Jennifer M Loftis; Alexander L Patterson; Clare J Wilhelm; Henry McNett; Benjamin J Morasco; Marilyn Huckans; Timothy Morgan; Shira Saperstein; Aliya Asghar; Peter Hauser Journal: J Psychosom Res Date: 2012-11-21 Impact factor: 3.006
Authors: Paul J Mills; Kathleen Wilson; Navaid Iqbal; Fatima Iqbal; Milagros Alvarez; Meredith A Pung; Katherine Wachmann; Thomas Rutledge; Jeanne Maglione; Sid Zisook; Joel E Dimsdale; Ottar Lunde; Barry H Greenberg; Alan Maisel; Ajit Raisinghani; Loki Natarajan; Shamini Jain; David J Hufford; Laura Redwine Journal: J Behav Med Date: 2014-12-23
Authors: Seongkum Heo; Debra K Moser; Susan J Pressler; Sandra B Dunbar; Rebecca L Dekker; Terry A Lennie Journal: Am J Crit Care Date: 2014-09 Impact factor: 2.228
Authors: Michael L Alosco; Mary Beth Spitznagel; Naftali Raz; Ronald Cohen; Lawrence H Sweet; Sarah Garcia; Richard Josephson; Manfred van Dulmen; Joel Hughes; Jim Rosneck; John Gunstad Journal: Psychosom Med Date: 2013-07-19 Impact factor: 4.312