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

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 sympt...

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Veröffentlicht in:Journal of affective disorders 2012-02, Vol.136 (3), p.567-576
Hauptverfasser: Kupper, Nina, Widdershoven, Jos W, Pedersen, Susanne S
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creator Kupper, Nina
Widdershoven, Jos W
Pedersen, Susanne S
description 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.
doi_str_mv 10.1016/j.jad.2011.10.029
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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 &lt; 0.05) and IL-1ra (β = 0.28, p &lt; 0.01). Somatic/affective depressive symptoms were independently related to sTNFR2 (β = 0.21, p &lt; 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 &lt; 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.</description><identifier>ISSN: 0165-0327</identifier><identifier>EISSN: 1573-2517</identifier><identifier>DOI: 10.1016/j.jad.2011.10.029</identifier><identifier>PMID: 22134045</identifier><identifier>CODEN: JADID7</identifier><language>eng</language><publisher>Oxford: Elsevier B.V</publisher><subject>Adult and adolescent clinical studies ; Affective Symptoms - blood ; Aged ; Biological and medical sciences ; Biomarkers - blood ; Cardiology. 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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 &lt; 0.05) and IL-1ra (β = 0.28, p &lt; 0.01). Somatic/affective depressive symptoms were independently related to sTNFR2 (β = 0.21, p &lt; 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 &lt; 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.</description><subject>Adult and adolescent clinical studies</subject><subject>Affective Symptoms - blood</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>Cardiology. Vascular system</subject><subject>Cognitive/affective and somatic/affective depressive symptoms</subject><subject>Depression</subject><subject>Depression - blood</subject><subject>Female</subject><subject>Heart</subject><subject>Heart failure</subject><subject>Heart Failure - blood</subject><subject>Heart Failure - psychology</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - blood</subject><subject>Inflammation - psychology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mood disorders</subject><subject>Prospective Studies</subject><subject>Psychiatry</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. 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Vascular system</topic><topic>Cognitive/affective and somatic/affective depressive symptoms</topic><topic>Depression</topic><topic>Depression - blood</topic><topic>Female</topic><topic>Heart</topic><topic>Heart failure</topic><topic>Heart Failure - blood</topic><topic>Heart Failure - psychology</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - blood</topic><topic>Inflammation - psychology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mood disorders</topic><topic>Prospective Studies</topic><topic>Psychiatry</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Receptors, Tumor Necrosis Factor, Type I - blood</topic><topic>Receptors, Tumor Necrosis Factor, Type II - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kupper, Nina</creatorcontrib><creatorcontrib>Widdershoven, Jos W</creatorcontrib><creatorcontrib>Pedersen, Susanne S</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of affective disorders</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kupper, Nina</au><au>Widdershoven, Jos W</au><au>Pedersen, Susanne S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cognitive/affective and somatic/affective symptom dimensions of depression are associated with current and future inflammation in heart failure patients</atitle><jtitle>Journal of affective disorders</jtitle><addtitle>J Affect Disord</addtitle><date>2012-02-01</date><risdate>2012</risdate><volume>136</volume><issue>3</issue><spage>567</spage><epage>576</epage><pages>567-576</pages><issn>0165-0327</issn><eissn>1573-2517</eissn><coden>JADID7</coden><abstract>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 &lt; 0.05) and IL-1ra (β = 0.28, p &lt; 0.01). Somatic/affective depressive symptoms were independently related to sTNFR2 (β = 0.21, p &lt; 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 &lt; 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.</abstract><cop>Oxford</cop><pub>Elsevier B.V</pub><pmid>22134045</pmid><doi>10.1016/j.jad.2011.10.029</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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subjects Adult and adolescent clinical studies
Affective Symptoms - blood
Aged
Biological and medical sciences
Biomarkers - blood
Cardiology. Vascular system
Cognitive/affective and somatic/affective depressive symptoms
Depression
Depression - blood
Female
Heart
Heart failure
Heart Failure - blood
Heart Failure - psychology
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Humans
Inflammation
Inflammation - blood
Inflammation - psychology
Male
Medical sciences
Middle Aged
Mood disorders
Prospective Studies
Psychiatry
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Receptors, Tumor Necrosis Factor, Type I - blood
Receptors, Tumor Necrosis Factor, Type II - blood
title Cognitive/affective and somatic/affective symptom dimensions of depression are associated with current and future inflammation in heart failure patients
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