Directionality of the Relationship Between Depressive Symptom Dimensions and C-Reactive Protein in Patients With Acute Coronary Syndromes

Bibliographic Data

ID19308484
AuthorsJonathan A Shaffer (0000-0002-4749-2183, National Heart Lung and Blood Institute, corresponding author), Donald Edmondson (0000-0002-4518-8196, National Heart Lung and Blood Institute), William F Chaplin (0000-0001-8221-4093, National Heart Lung and Blood Institute), J E Schwartz (0000-0002-8944-3566, Columbia University Irving Medical Center), Daichi Shimbo (0000-0001-6302-8834, Columbia University Irving Medical Center), Matthew M Burg (0000-0002-1263-2385, Columbia University Irving Medical Center), Nina Rieckmann (0000-0002-6870-451X, Columbia University Irving Medical Center), Karina W Davidson (0000-0002-9162-477X, National Heart Lung and Blood Institute)
Year2011
Volume73
Issue5
Pages370-377
Publication date2011-06-01
Peer ReviewedYes
Open AccessNo
TypeARTICLE
VenuePsychosomatic Medicine (JOURNAL)
Journal identifiersISSN: 0033-3174 • E-ISSN: 1534-7796
PublisherOvid Technologies (Wolters Kluwer Health) (PUBLISHER)
DOI10.1097/psy.0b013e31821deafd
PMID21636659
PMCIDPMC3110525
OpenAlexW2073529494
LanguageEN
Citations received3
References cited54

OBJECTIVE: Previous theoretical models predict that elevated inflammation may predict later depressive symptoms, but bidirectional associations are possible. We examined whether depressive symptoms or inflammation predicts change in the other for a 3-month period in a sample of adults with acute coronary syndromes (ACS). METHODS: During hospitalization for their index ACS event (baseline) and then again 1 and 3 months later, 163 post-ACS patients completed the Beck Depression Inventory, a measure of depressive symptom severity with cognitive-affective and somatic-affective subscales. C-reactive protein (CRP) was also assessed at each visit; known correlates of depression and CRP were assessed at baseline. Path analyses were conducted to evaluate prospective associations between depressive symptoms and log-transformed CRP values and whether strength and/or directionality varied by specific depressive symptom dimensions. RESULTS: Baseline total depressive symptom severity predicted a smaller decrease in CRP from baseline to 1 month (unstandardized parameter estimates [B] = 0.04, p < .001) controlling for all covariates, as did baseline cognitive-affective depressive symptom severity (B = 0.10, p = .02). Baseline somatic-affective depressive symptom severity did not predict change in CRP (B = -0.002, p = .94). CRP did not predict 1- or 3-month change in total, cognitive-affective, or somatic-affective depressive symptom severity. The results did not differ for men and women. CONCLUSIONS: Greater cognitive-affective and total depressive symptom severity at the time of a cardiac event predicts a smaller decrease in CRP 1 month later, but there was no evidence in this study that CRP predicts change in depressive symptoms

Anxiety · Beck Depression Inventory · C-reactive protein · Cognition · Depression (economics) · Depressive symptoms · Inflammation · Major depressive disorder · Prospective cohort study · Psychiatry · Cardiac Health and Mental Health · Clinical Psychology · Internal Medicine · Medicine · Psychology · Stress Responses and Cortisol · Tryptophan and brain disorders

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