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      Depression and Heart Disease: Therapeutic Implications

      a , b

      Cardiology

      S. Karger AG

      Depression, Coronary artery disease, Platelet abnormalities

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          Abstract

          The consequences of depression and coronary artery disease (CAD) were reviewed in the literature. The comorbidity of depression and CAD results in an increased cardiovascular mortality. We reviewed possible explanations for this increased morbidity, which include: toxicity of tricyclic antidepressants that can cause cardiac arrhythmias, abnormalities in platelet function leading to increased platelet aggregation due to abnormalities in serotonin in the platelet (an abnormality that possibly causes depression in the central nervous system), diffuse atherosclerosis causing central nervous system abnormalities including depression (vascular depression), as well as the possibility that depressed patients are less compliant with their medications and physician-directed health recommendations. Recent reports of selective serotonin reuptake inhibitors (SSRIs) causing a reduced cardiovascular mortality may be related to serotonin platelet abnormalities in depressed patients that are effectively treated by SSRIs (SADHART and ENRICHD trial). It is possible that these trials reveal a mechanism of depression that also effects platelet function and can be improved with SSRI therapy, suggesting a preferential therapeutic pathway for the treatment of depressed patients with CAD.

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          Most cited references 39

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          Pelvic organ prolapse.

          Pelvic organ prolapse is downward descent of female pelvic organs, including the bladder, uterus or post-hysterectomy vaginal cuff, and the small or large bowel, resulting in protrusion of the vagina, uterus, or both. Prolapse development is multifactorial, with vaginal child birth, advancing age, and increasing body-mass index as the most consistent risk factors. Vaginal delivery, hysterectomy, chronic straining, normal ageing, and abnormalities of connective tissue or connective-tissue repair predispose some women to disruption, stretching, or dysfunction of the levator ani complex, connective-tissue attachments of the vagina, or both, resulting in prolapse. Patients generally present with several complaints, including bladder, bowel, and pelvic symptoms; however, with the exception of vaginal bulging, none is specific to prolapse. Women with symptoms suggestive of prolapse should undergo a pelvic examination and medical history check. Radiographic assessment is usually unnecessary. Many women with pelvic organ prolapse are asymptomatic and do not need treatment. When prolapse is symptomatic, options include observation, pessary use, and surgery. Surgical strategies for prolapse can be categorised broadly by reconstructive and obliterative techniques. Reconstructive procedures can be done by either an abdominal or vaginal approach. Although no effective prevention strategy for prolapse has been identified, considerations include weight loss, reduction of heavy lifting, treatment of constipation, modification or reduction of obstetric risk factors, and pelvic-floor physical therapy.
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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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              Even minimal symptoms of depression increase mortality risk after acute myocardial infarction.

              Mild to moderate levels of depressive symptoms as characterized by Beck Depression Inventory (BDI) scores of > or =10 are associated with decreased survival after acute myocardial infarction (AMI). We investigated whether lower levels of depressive symptoms are also associated with increased mortality risk after AMI. We prospectively studied 285 patients with AMI who survived to discharge for evidence, at the time of hospitalization, of a DSM-IIIR mood disorder (using a structured clinical interview) and for symptoms of depression (using the BDI). The overall mortality rate at 4 months was 6.7%. Multiple logistic regression (chi-square 35.79, p or =65 years, left ventricular ejection fraction or =10) present at the time of AMI. Among patients > or =65 years old with left ventricular ejection fraction or =65 years, the mortality according to BDI scale grouping 0 to 3, 4 to 9, and 10+ was 2.6%, 17.1%, and 23.3%, respectively (p <0.002). Highest mortality rates were observed in patients with most severe depressive symptoms. However, compared with those without depression, higher mortality was also observed at very low levels of depressive symptoms (BDI 4 to 9) not generally considered clinically significant and below the level usually considered predictive of increased post-AMI mortality.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2008
                August 2008
                31 March 2008
                : 111
                : 2
                : 75-81
                Affiliations
                aGeorge Washington University, Washington, D.C., and bDivision of Cardiology, The Chicago Medical School, Roslyn Franklin University of Health Sciences, Chicago, Ill., USA
                Article
                119692 Cardiology 2008;111:75–81
                10.1159/000119692
                18376116
                © 2008 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Tables: 2, References: 58, Pages: 7
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