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- ACS, acute coronary syndrome
- BDI, Beck Depression Inventory
- COPES, Coronary Psychosocial Patient Evaluation Study
- CRP, C reactive protein
Although depression symptoms are associated with an increased risk of recurrent cardiovascular disease in patients who have experienced an acute coronary syndrome (ACS) event, the exact mechanisms remain poorly understood. Inflammation has been suggested to be a mechanism in the depression–ACS prognosis link, as raised concentrations of inflammatory biomarkers, especially C reactive protein (CRP), are associated with recurrent cardiovascular events.1 In the few studies that have examined the relation between depression status and CRP concentrations after an ACS event, depression and CRP concentrations were assessed 2–6 months after the index ACS event, when the rate of depression remission would already be relatively high.2–4 The objective of this study was to examine the relation between the course of depression and CRP concentrations after an ACS event.
Patients were enrolled from an ancillary study of COPES (Coronary Psychosocial Patient Evaluation Study), a multisite, observational cohort study designed to investigate the aetiology and naturalistic course of depressive symptoms in the three-month period after an ACS event. Patients were eligible for inclusion in COPES if they had been hospitalised for an ACS event (either acute myocardial infarction with or without ST segment elevation or unstable angina) and scored between 0 and 4 (indicative of no depressive symptoms) or ⩾ 10 (at least mild depressive symptoms) on the Beck Depression Inventory (BDI) within one week after the index ACS event. The BDI is a self-report measure of depressive symptom severity, and a score of ⩾ 10 is associated with increased mortality risk after an ACS event.5 The BDI was readministered three months after enrolment.
Of the 275 patients enrolled in …
↵* Also the Zena and Michael A Wiener Cardiovascular Institute, Department of Medicine, Mount Sinai School of Medicine, New York, USA
This work was supported by grants HC25197, HL072866, HL04458 and HL76857 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. The funding source supported the collection and analyses of data, but had no direct role in the interpretation of data, the writing of the report and the decision to submit the paper for publication.
Competing interests: None declared.
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