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Randomized Controlled Trial
. 2011 Jul;71(1):13-7.
doi: 10.1016/j.jpsychores.2010.11.006. Epub 2011 Jan 15.

Inflammation and treatment response to sertraline in patients with coronary heart disease and comorbid major depression

Mariska Bot  1 , Robert M Carney, Kenneth E Freedland, Eugene H Rubin, Michael W Rich, Brian C Steinmeyer, Douglas L Mann
Affiliations
Randomized Controlled Trial

Inflammation and treatment response to sertraline in patients with coronary heart disease and comorbid major depression

Mariska Bot et al. J Psychosom Res. 2011 Jul.

Abstract

Objective: Treatment-resistant depression has recently emerged as a marker of increased risk for morbidity and mortality in patients with coronary heart disease (CHD). Studies in depressed patients without CHD suggest that elevated markers of inflammation predict poor response to treatment. This may help to explain the increased risk of cardiac events associated with depression. We therefore studied the relationship between pretreatment markers of inflammation and treatment response in patients with CHD and major depression.

Methods: This was a planned, secondary analysis of a clinical trial in which 122 patients with CHD and comorbid major depression were randomly assigned to 50 mg of sertraline plus 2 g/day omega-3 fatty acids or to 50 mg of sertraline plus 2 g/day corn oil placebo capsules for ten weeks. Depressive symptoms were assessed with the Beck Depression Inventory-II (BDI-II). Blood samples were collected at baseline to determine levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α). The primary outcome was the post-treatment BDI-II depression score.

Results: Baseline levels of hs-CRP, IL-6, and TNF-α were not associated with the 10-week post-treatment depression score (P=.89, P=.88, and P=.31, respectively). Treatment responders (>50% reduction from baseline BDI-II score) did not differ from non-responders in either baseline hs-CRP, IL-6, or TNF-α (P=.83, P=.93, and P=.24, respectively). Similarly, depression remitters (BDI-II ≤8 at post-treatment) did not differ from non-remitters on the three baseline inflammation markers.

Conclusion: These findings do not support the hypothesis that elevated baseline inflammatory markers predict poor response to sertraline in patients with CHD and major depression. The explanation for the increased risk of cardiac events associated with poor response to depression treatment remains unclear.

Trial registration: ClinicalTrials.gov NCT00116857.

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References

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