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      Cardiovascular Considerations in Antidepressant Therapy: An Evidence-Based Review

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          Abstract

          There is a definite correlation between cardiovascular diseases and depressive disorders. Nevertheless, many aspects of this association have yet to be fully elucidated. Up to half of coronary artery disease patients are liable to suffer from some depressive symptoms, with approximately 20% receiving a diagnosis of major depressive disorders. Pharmacotherapy is a key factor in the management of major depression, not least in patients with chronic diseases who are likely to fail to show proper compliance and response to non-pharmacological interventions. Antidepressants are not deemed completely safe. Indeed, numerous side effects have been reported with the administration of antidepressants, among which cardiovascular adverse events are of paramount importance owing to their disabling and life-threatening nature. We aimed to re-examine some of the salient issues in antidepressant therapy vis-à-vis cardiovascular considerations, which should be taken into account when prescribing such medications.

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          Most cited references99

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          Depression in heart failure a meta-analytic review of prevalence, intervention effects, and associations with clinical outcomes.

          This article describes a meta-analysis of published associations between depression and heart failure (HF) in regard to 3 questions: 1) What is the prevalence of depression among patients with HF? 2) What is the magnitude of the relationship between depression and clinical outcomes in the HF population? 3) What is the evidence for treatment effectiveness in reducing depression in HF patients? Key word searches of the Medline and PsycInfo databases, as well as reference searches in published HF and depression articles, identified 36 publications meeting our criteria. Clinically significant depression was present in 21.5% of HF patients, and varied by the use of questionnaires versus diagnostic interview (33.6% and 19.3%, respectively) and New York Heart Association-defined HF severity (11% in class I vs. 42% in class IV), among other factors. Combined results suggested higher rates of death and secondary events (risk ratio = 2.1, 95% confidence interval 1.7 to 2.6), trends toward increased health care use, and higher rates of hospitalization and emergency room visits among depressed patients. Treatment studies generally relied on small samples, but also suggested depression symptom reductions from a variety of interventions. In sum, clinically significant depression is present in at least 1 in 5 patients with HF; however, depression rates can be much higher among patients screened with questionnaires or with more advanced HF. The relationship between depression and poorer HF outcomes is consistent and strong across multiple end points. These findings reinforce the importance of psychosocial research in HF populations and identify a number of areas for future study.
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            Effects of citalopram and interpersonal psychotherapy on depression in patients with coronary artery disease: the Canadian Cardiac Randomized Evaluation of Antidepressant and Psychotherapy Efficacy (CREATE) trial.

            Few randomized controlled trials have evaluated the efficacy of treatments for major depression in patients with coronary artery disease (CAD). None have simultaneously evaluated an antidepressant and short-term psychotherapy. To document the short-term efficacy of a selective serotonin reuptake inhibitor (citalopram) and interpersonal psychotherapy (IPT) in reducing depressive symptoms in patients with CAD and major depression. The Canadian Cardiac Randomized Evaluation of Antidepressant and Psychotherapy Efficacy, a randomized, controlled, 12-week, parallel-group, 2 x 2 factorial trial conducted May 1, 2002, to March 20, 2006, among 284 patients with CAD from 9 Canadian academic centers. All patients met Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for diagnosis of major depression of 4 weeks' duration or longer and had baseline 24-item Hamilton Depression Rating Scale (HAM-D) scores of 20 or higher. Participants underwent 2 separate randomizations: (1) to receive 12 weekly sessions of IPT plus clinical management (n = 142) or clinical management only (n = 142) and (2) to receive 12 weeks of citalopram, 20 to 40 mg/d (n = 142), or matching placebo (n = 142). The primary outcome measure was change between baseline and 12 weeks on the 24-item HAM-D, administered blindly during centralized telephone interviews (tested at alpha = .033); the secondary outcome measure was self-reported Beck Depression Inventory II (BDI-II) score (tested at alpha = .017). Citalopram was superior to placebo in reducing 12-week HAM-D scores (mean difference, 3.3 points; 96.7% confidence interval [CI], 0.80-5.85; P = .005), with a small to medium effect size of 0.33. Mean HAM-D response (52.8% vs 40.1%; P = .03) and remission rates (35.9% vs 22.5%; P = .01) and the reduction in BDI-II scores (difference, 3.6 points; 98.3% CI, 0.58-6.64; P = .005; effect size = 0.33) also favored citalopram. There was no evidence of a benefit of IPT over clinical management, with the mean HAM-D difference favoring clinical management (-2.26 points; 96.7% CI, -4.78 to 0.27; P = .06; effect size, 0.23). The difference on the BDI-II did not favor clinical management (1.13 points; 98.3% CI, -1.90 to 4.16; P = .37; effect size = 0.11). This trial documents the efficacy of citalopram administered in conjunction with weekly clinical management for major depression among patients with CAD and found no evidence of added value of IPT over clinical management. Based on these results and those of previous trials, citalopram or sertraline plus clinical management should be considered as a first-step treatment for patients with CAD and major depression. isrctn.org Identifier: ISRCTN15858091.
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              Effect of celecoxib add-on treatment on symptoms and serum IL-6 concentrations in patients with major depressive disorder: randomized double-blind placebo-controlled study.

              It has been proposed that the mechanism of the antidepressant effect of celecoxib is linked to its anti-inflammatory action and particularly its inhibitory effect on pro-inflammatory cytokines (e.g. interleukin-6(IL-6)). We measured changes in serum IL-6 concentrations and depressive symptoms following administration of celecoxib in patients with major depressive disorder (MDD). In a randomized double-blind placebo-controlled study, 40 patients with MDD and Hamilton Depression Rating Scale-17 items (Ham-D) score ≥18 were randomly assigned to either celecoxib (200mg twice daily) or placebo in addition to sertraline (200mg/day) for 6 weeks. Outcome measures were serum IL-6 concentrations at baseline and week 6, and Ham-D scores at baseline and weeks 1, 2, 4, and 6. The celecoxib group showed significantly greater reduction in serum IL-6 concentrations (mean difference (95%CI)=0.42(0.30 to 0.55) pg/ml, t(35)=6.727, P<0.001) as well as Ham-D scores (mean difference (95%CI)=3.35(1.08 to 5.61), t(38)=2.99, P=0.005) than the placebo group. The patients in the celecoxib group experienced more response (95%) and remission (35%) than the placebo group (50% and 5%, P=0.003 and 0.04 respectively). Baseline serum IL-6 levels were significantly correlated with baseline Ham-D scores (r=0.378, P=0.016). Significant correlation was observed between reduction of Ham-D scores and reduction of serum IL-6 levels at week 6 (r=0.673, P<0.001). We did not measure other inflammatory biomarkers. We showed that the antidepressant activity of celecoxib might be linked to its capability of reducing IL-6 concentrations. Moreover, supporting previous studies we showed that celecoxib is both safe and effective as an adjunctive antidepressant (Registration number: IRCT138903124090N1). Copyright © 2012 Elsevier B.V. All rights reserved.
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                Author and article information

                Journal
                J Tehran Heart Cent
                J Tehran Heart Cent
                JTHC
                The Journal of Tehran University Heart Center
                Tehran University of Medical Sciences
                1735-5370
                2008-2371
                28 October 2013
                : 8
                : 4
                : 169-176
                Affiliations
                Psychiatric Research Center, Roozbeh Hospital, Tehran University of Medical Sciences, Tehran, Iran
                Author notes
                [* ]Corresponding Author: Shahin Akhondzadeh, Professor of Neuroscience, Psychiatric Research Center, Roozbeh Psychiatric Hospital, Tehran University of Medical Sciences, South Kargar Street, Tehran, Iran. 1333754652. Tel: +98 21 55412222. Fax: +98 21 55419113. s.akhond@ 123456neda.net
                Article
                4434967
                26005484
                5363f699-1d73-4834-82e3-a087a595f9c8
                Copyright: © The Journal of Tehran University Heart Center & Tehran University of Medical Sciences

                This work is licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License which allows users to read, copy, distribute and make derivative works for non-commercial purposes from the material, as long as the author of the original work is cited properly.

                History
                : 23 July 2013
                : 17 August 2013
                Categories
                Medical Sciences

                Cardiovascular Medicine
                cardiovascular diseases,antidepressive agents,depressive disorder, major

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