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Alimentary Pharmacology & Therapeutics Mar 2012Noncardiac chest pain (NCCP) is a common condition, affecting approximately 25% of the general population. The cause of NCCP can be classified as gastro-oesophageal... (Review)
Review
BACKGROUND
Noncardiac chest pain (NCCP) is a common condition, affecting approximately 25% of the general population. The cause of NCCP can be classified as gastro-oesophageal reflux disease (GERD)-related NCCP, where antireflux therapy is the main treatment modality or alternatively as non-GERD-related NCCP, where pain modulators, including antidepressants, are utilised.
AIM
To provide a systematic review evaluating the evidence for the use of antidepressants in the treatment of non-GERD-related NCCP.
METHODS
A computerised literature and manual search was conducted to identify relevant randomised, placebo-controlled studies, published in any language for the evaluation of the effectiveness of antidepressant as a therapeutic intervention for NCCP.
RESULTS
Six randomised placebo-controlled trials of antidepressant treatment for NCCP were identified. The medications included were selective serotonin reuptake inhibitors [paroxetine (n = 2), sertraline (n = 1)], tricyclic antidepressant [impramine (n = 1)], serotonin-norepinephrine reuptake inhibitor [venlafaxine (n = 1)] and a triazolopyridine [trazodone (n = 1)]. The percentage reduction in chest pain was statistically significant with venlafaxine (50% vs. 10%; P < 0.001), sertraline (63% vs. 15%; P = 0.02) and imipramine (52% vs. 1%; P = 0.03). The improvement in chest pain symptoms was independent of improvement in depression scores. Clinical global improvement also significantly improved in patients on venlafaxine, sertraline, paroxetine and trazodone. The percentage of patients in treatment groups reporting adverse effects were relatively high compared with those in placebo groups, although majority were statistically insignificant or significance was not reported. Nonetheless, adverse events were the reported reason for discontinuation of trials in 53% of patients from the antidepressant groups compared with 29% from the placebo group.
CONCLUSIONS
There is modest evidence for the benefit of antidepressants in reducing NCCP and improving patients' general health. However, there is significant heterogeneity amongst the studies with several study limitations to warrant more rigorous trials and to assess the usefulness of low-dose antidepressants in non-GERD NCCP.
Topics: Antidepressive Agents; Chest Pain; Diagnosis, Differential; Gastroesophageal Reflux; Humans; Pain Measurement; Severity of Illness Index
PubMed: 22239853
DOI: 10.1111/j.1365-2036.2011.04978.x -
American Journal of Alzheimer's Disease... Mar 2014The objective of this review is to summarize the current data on the pharmacological treatments for frontotemporal dementias from randomized controlled trials. A... (Review)
Review
The objective of this review is to summarize the current data on the pharmacological treatments for frontotemporal dementias from randomized controlled trials. A systematic search of 4 major databases, PubMed, Medline, PsychINFO and Cochrane, found a total of 9 randomized controlled, double-blinded clinical trials. Of these, 2 trials used the selective serotonin reuptake inhibitor (SSRI), paroxetine; 1 trial used trazodone; 2 trials used stimulants (methylphenidate and dextroamphetamine); 1 trial used the acetylcholinesterase inhibitor, galantamine; 2 trials used the N-methyl-d-aspartate antagonist, memantine; and 1 trial used the neuropeptide oxytocin. The analysis of the available data indicates that SSRIs, trazodone, and the amphetamines may be effective in reducing some behavioral symptoms, but none of these medications had an impact on cognition. Available data indicate that these medications were well tolerated in all the trials.
Topics: Cognition; Dopamine Agents; Frontotemporal Dementia; Humans; Memantine; Randomized Controlled Trials as Topic; Selective Serotonin Reuptake Inhibitors; Treatment Outcome
PubMed: 24164931
DOI: 10.1177/1533317513507375 -
Frontiers in Neuroendocrinology Oct 2022Postpartum depression is a common mental disease in obstetric puerperium. Its etiology is not completely clear, and its clinical manifestations are complex. It has... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Postpartum depression is a common mental disease in obstetric puerperium. Its etiology is not completely clear, and its clinical manifestations are complex. It has serious adverse effects on the body and mind of mothers and infants. Treatment should also follow the principle of individualization. Preliminary studies have shown that traditional chinese medicine prescriptions combined with paroxetine is effective in treating postpartum depression. In order to better determine the therapeutic effect, further exploration was carried out.
HYPOTHESIS
Does the study better evaluate the therapeutic effect and provide data support for clinical promotion?
STUDY DESIGN
The search comes from using the following electronic databases established until January 2022.
STUDY RESULTS
The meta analysis results show that paroxetine combined with traditional chinese medicine prescriptions can reduce the Hamilton Depression Scale (HAMD) score [WMD = -7.35, 95 % CI (-10.84, -3.87), P<0.001] and Edinburgh Postpartum Depression Scale (EPDS) score [WMD = -3.24, 95 % CI (-5.96, -0.53), P < 0.001].And better than paroxetine treatment alone in terms of improving clinical efficacy [RR = 1.22, 95 % CI (1.16, 1.30), P < 0.001].
CONCLUSIONS
Based on the combination of paroxetine and traditional chinese medicine prescriptions in the treatment of postpartum depression, there is a certain clinical effect, and a strong research design and a certain number of RCTs are required at the same time. Future research should clarify the specific composition and composition of traditional Chinese medicine prescriptions.
Topics: Female; Humans; Paroxetine; Depression, Postpartum; Medicine, Chinese Traditional; Randomized Controlled Trials as Topic; Prescriptions; Depression
PubMed: 35926637
DOI: 10.1016/j.yfrne.2022.101019 -
Annals of Internal Medicine Dec 2009In primary care settings, prevalence estimates of major depressive disorder range from 5% to 13% in all adults, with lower estimates in those older than 55 years (6% to... (Review)
Review
BACKGROUND
In primary care settings, prevalence estimates of major depressive disorder range from 5% to 13% in all adults, with lower estimates in those older than 55 years (6% to 9%). In 2002, the U.S. Preventive Services Task Force (USPSTF) recommended screening adults for depression in clinical practices that have systems to ensure accurate diagnosis, effective treatment, and follow-up.
PURPOSE
To conduct a targeted, updated systematic review for the U.S. Preventive Services Task Force about the benefits and harms of screening adult patients for depression in a primary care setting, the benefits of depression treatment in older adults, and the harms of depression treatment with antidepressant medications.
DATA SOURCES
MEDLINE, the Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, Database of Abstracts of Reviews of Effects, PsycINFO (1998 to 2007), expert suggestions, and bibliographies of recent systematic reviews.
STUDY SELECTION
Fair- to good-quality randomized clinical trials or controlled clinical trials; systematic reviews; meta-analyses; and large observational studies of serious adverse events and early discontinuation due to adverse effects. All studies were published in English.
DATA EXTRACTION
Two investigators abstracted, critically appraised, and synthesized 33 articles that met inclusion criteria.
DATA SYNTHESIS
Nine fair- or good-quality trials indicate that primary care depression screening and care management programs with staff assistance, such as case management or mental health specialist involvement, can increase depression response and remission. Benefit was not evident in screening programs without staff assistance in depression care. Seven regulatory reviews or meta-analyses and 3 large cohort studies indicate no increased risk for completed suicide deaths with antidepressant treatment. Risk for suicidal behaviors was increased in young adults (aged 18 to 29 years) who received antidepressants, particularly those who received paroxetine, but was reduced in older adults.
LIMITATION
Examination of harms was limited to serious adverse events, and existing systematic reviews were primarily used. Additional studies published from 2007 to 2008 extend this review.
CONCLUSION
Depression screening programs without substantial staff-assisted depression care supports are unlikely to improve depression outcomes. Close monitoring of all adult patients who initiate antidepressant treatment, particularly those younger than 30 years, is important both for safety and to ensure optimal treatment.
Topics: Adolescent; Adult; Age Factors; Antidepressive Agents; Depression; Feedback; Humans; Mass Screening; Middle Aged; Patient Care Team; Primary Health Care; Psychotherapy; Risk Assessment; Selective Serotonin Reuptake Inhibitors; Suicide; Young Adult
PubMed: 19949145
DOI: 10.7326/0003-4819-151-11-200912010-00007 -
The Cochrane Database of Systematic... Jan 2015Anxiety disorders are a potentially disabling group of disorders that frequently co-occur with alcohol use disorders. Comorbid anxiety and alcohol use disorders are... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Anxiety disorders are a potentially disabling group of disorders that frequently co-occur with alcohol use disorders. Comorbid anxiety and alcohol use disorders are associated with poorer outcomes, and are difficult to treat with standard psychosocial interventions. In addition, improved understanding of the biological basis of the conditions has contributed to a growing interest in the use of medications for the treatment of people with both diagnoses.
OBJECTIVES
To assess the effects of pharmacotherapy for treating anxiety in people with comorbid alcohol use disorders, specifically: to provide an estimate of the overall effects of medication in improving treatment response and reducing symptom severity in the treatment of anxiety disorders in people with comorbid alcohol use disorders; to determine whether specific medications are more effective and tolerable than other medications in the treatment of particular anxiety disorders; and to identify which factors (clinical, methodological) predict response to pharmacotherapy for anxiety disorders.
SEARCH METHODS
Review authors searched the specialized registers of The Cochrane Collaboration Depression, Anxiety and Neurosis Review Group (CCDANCTR, to January 2014) and the Cochrane Drugs and Alcohol Group (CDAG, to March 2013) for eligible trials. These registers contain reports of relevant randomized controlled trials (RCT) from: the Cochrane Central Register of Controlled Trials (CENTRAL, all years), MEDLINE (1950 to date), EMBASE (1974 to date) and PsycINFO (1967 to date). Review authors ran complementary searches on EMBASE, PubMed, PsycINFO and the Alcohol and Alcohol Problems Science Database (ETOH) (to August 2013). We located unpublished trials through the National Institutes of Health (NIH) RePORTER service and the World Health Organization (WHO) International Clinical Trials Registry Platform (to August 2013). We screened reference lists of retrieved articles for additional studies.
SELECTION CRITERIA
All true RCTs of pharmacotherapy for treating anxiety disorders with comorbid alcohol use disorders. Trials assessing drugs administered for the treatment of drinking behaviour, such as naltrexone, disulfiram and acomprosate were not eligible for inclusion in this systematic review.
DATA COLLECTION AND ANALYSIS
A systematic review is a standardised evaluation of all research studies that address a particular clinical issue.Two review authors independently assessed RCTs for inclusion in the review, collated trial data and assessed trial quality. We contacted investigators to obtain missing data. We calculated categorical and continuous treatment effect estimates and their 95% confidence intervals (CI) for treatment using a random-effects model with effect-size variability expressed using Chi(2) and I(2) heterogeneity statistics.
MAIN RESULTS
We included five placebo-controlled pharmacotherapy RCTs (with 290 participants) in the review. Most of the trials provided little information on how randomization was performed or on whether both participants and study personnel were blinded to the intervention. Two of the three trials reporting superiority of medication compared with placebo on anxiety symptom outcomes were industry funded. We regarded one trial as being at high risk of bias due to selective reporting.Study participants had Diagnostic and Statistical Manual (DSM) III- and DSM IV-diagnosed alcohol use disorders and post-traumatic stress disorder (two studies), social anxiety disorder (SAD; two studies) or generalized anxiety disorder (GAD; one study). Four trials assessed the efficacy of the selective serotonin re-uptake inhibitors (SSRIs: sertraline, paroxetine); one RCT investigated the efficacy of buspirone, a 5-hydroxytryptamine (5-HT) partial agonist. Treatment duration lasted between eight and 24 weeks. Overall, 70% of participants included in the review were male.There was very low quality evidence for an effect of paroxetine on global clinical response to treatment, as assessed by the Clinical Global Impressions - Improvement scale (CGI-I). Global clinical response was observed in more than twice as many participants with paroxetine than with placebo (57.7% with paroxetine versus 25.8% with placebo; risk ratio (RR) 2.23, 95% CI 1.13 to 4.41; 2 trials, 57 participants). However, there was substantial uncertainty regarding the size of the effect of paroxetine due to the small number of studies providing data on clinically diverse patient samples. The second primary outcome measure was reduction of anxiety symptom severity. Although study investigators reported that buspirone (one trial) was superior to placebo in reducing the severity of anxiety symptoms over 12 weeks, no evidence of efficacy was observed for paroxetine (mean difference (MD) -14.70, 95% CI -33.00 to 3.60, 2 trials, 44 participants) and sertraline (one trial). Paroxetine appeared to be equally effective in reducing the severity of post-traumatic stress disorder (PTSD) symptoms as the tricyclic antidepressant desipramine in one RCT. The maximal reduction in anxiety disorder symptom severity was achieved after six weeks with paroxetine (two RCTs) and 12 weeks with buspirone (one RCT), with maintenance of medication efficacy extending to 16 with paroxetine and 24 weeks with buspirone. There was no evidence of an effect for any of the medications tested on abstinence from alcohol use or depression symptoms. There was very low quality evidence that paroxetine was well tolerated, based on drop-out due to treatment-emergent adverse effects. Nevertheless, levels of treatment discontinuation were high, with 43.1% of the participants in the studies withdrawing from medication treatment. Certain adverse effects, such as sexual problems, were commonly reported after treatment with paroxetine and sertraline.
AUTHORS' CONCLUSIONS
The evidence-base for the effectiveness of medication in treating anxiety disorders and comorbid alcohol use disorders is currently inconclusive. There was a small amount of evidence for the efficacy of medication, but this was limited and of very low quality. The majority of the data for the efficacy and tolerability of medication were for SSRIs; there were insufficient data to establish differences in treatment efficacy between medication classes or patient subgroups. There was a small amount of very low quality evidence that medication was well tolerated. There was no evidence that alcohol use was responsive to medication.Large, rigorously conducted RCTs would help supplement the small evidence-base for the efficacy and tolerability of pharmacotherapy for anxiety and comorbid alcohol use disorders. Further research on patient subgroups who may benefit from pharmacological treatment, as well as novel pharmacological interventions, is warranted.
Topics: Alcohol-Related Disorders; Anxiety; Anxiety Disorders; Buspirone; Comorbidity; Desipramine; Humans; Paroxetine; Phobia, Social; Publication Bias; Randomized Controlled Trials as Topic; Selective Serotonin Reuptake Inhibitors; Sertraline; Stress Disorders, Post-Traumatic
PubMed: 25601826
DOI: 10.1002/14651858.CD007505.pub2 -
PloS One 2022Clinical Depression and the subsequent low immunity is a comorbidity that can act as a risk factor for the severity of COVID-19 cases. Antidepressants such as Selective... (Meta-Analysis)
Meta-Analysis
INTRODUCTION
Clinical Depression and the subsequent low immunity is a comorbidity that can act as a risk factor for the severity of COVID-19 cases. Antidepressants such as Selective serotonin reuptake inhibitor and Serotonin-norepinephrine reuptake inhibitors are associated with immune-modulatory effects, which dismiss inflammatory responses and reduce lung tissue damage. The current systematic review and meta-analysis aims to evaluate the effect of antidepressant drugs on the prognosis and severity of COVID-19 in hospitalized patients.
METHODS
A systematic search was carried out in PubMed/Medline, EMBASE, and Scopus up to June 14, 2022. The following keywords were used: "COVID-19", "SARS-CoV-2", "2019-nCoV", "SSRI", "SNRI", "TCA", "MAOI", and "Antidepressant". A fixed or random-effect model assessed the pooled risk ratio (RR) with 95% CI. We considered P < 0.05 as statistically significant for publication bias. Data were analyzed by Comprehensive Meta-Analysis software, Version 2.0 (Biostat, Englewood, NJ).
RESULTS
Fourteen studies were included in our systematic review. Five of them were experimental with 2350, and nine of them were observational with 290,950 participants. Eight out of fourteen articles revealed the effect of antidepressants on reducing the severity of COVID-19. Selective serotonin reuptake inhibitors drugs, including Fluvoxamine, Escitalopram, Fluoxetine, and Paroxetine, and among the Serotonin-norepinephrine inhibitors medications Venlafaxine, are reasonably associated with reduced risk of intubation or death. Five studies showed no significant effect, and only one high risk of bias article showed the negative effect of antidepressants on the prognosis of Covid-19. The meta-analysis of clinical trials showed that fluvoxamine could significantly decrease the severity outcomes of COVID-19 (RR: 0.763; 95% CI: 0.602-0.966, I2: 0.0).
FINDINGS
Most evidence supports that the use of antidepressant medications, mainly Fluvoxamine, may decrease the severity and improve the outcome in hospitalized patients with SARS-CoV-2. Some studies showed contradictory findings regarding the effects of antidepressants on the severity of COVID-19. Further clinical trials should be conducted to clarify the effects of antidepressants on the severity of COVID-19.
Topics: Antidepressive Agents; Fluoxetine; Fluvoxamine; Humans; Norepinephrine; Paroxetine; SARS-CoV-2; Serotonin; Selective Serotonin Reuptake Inhibitors; Venlafaxine Hydrochloride; COVID-19 Drug Treatment
PubMed: 36201406
DOI: 10.1371/journal.pone.0267423 -
The Cochrane Database of Systematic... Oct 2012Although pharmacological and psychological interventions are both effective for major depression, in primary and secondary care settings antidepressant drugs remain the... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Although pharmacological and psychological interventions are both effective for major depression, in primary and secondary care settings antidepressant drugs remain the mainstay of treatment. Amongst antidepressants many different agents are available. Duloxetine hydrochloride is a dual reuptake inhibitor of serotonin and norepinephrine and has been licensed by the Food and Drug Administration in the US for major depressive disorder (MDD), generalised anxiety disorder, diabetic peripheral neuropathic pain, fibromyalgia and chronic musculoskeletal pain.
OBJECTIVES
To assess the evidence for the efficacy, acceptability and tolerability of duloxetine in comparison with all other antidepressant agents in the acute-phase treatment of major depression.
SEARCH METHODS
MEDLINE (1966 to 2012), EMBASE (1974 to 2012), the Cochrane Collaboration Depression, Anxiety and Neurosis Controlled Trials Register and the Cochrane Central Register of Controlled Trials up to March 2012. No language restriction was applied. Reference lists of relevant papers and previous systematic reviews were hand-searched. Pharmaceutical company marketing duloxetine and experts in this field were contacted for supplemental data.
SELECTION CRITERIA
Randomised controlled trials allocating patients with major depression to duloxetine versus any other antidepressive agent.
DATA COLLECTION AND ANALYSIS
Two review authors independently extracted data and a double-entry procedure was employed. Information extracted included study characteristics, participant characteristics, intervention details and outcome measures in terms of efficacy, acceptability and tolerability.
MAIN RESULTS
A total of 16 randomised controlled trials (overall 5735 participants) were included in this systematic review. Of these, three trials were unpublished. We found 11 studies (overall 3304 participants) comparing duloxetine with one selective serotonin reuptake inhibitor (SSRI) (six studies versus paroxetine, three studies versus escitalopram and two versus fluoxetine), four studies (overall 1978 participants) comparing duloxetine with a newer antidepressants (three with venlafaxine and one with desvenlafaxine, respectively) and one study (overall 453 participants) comparing duloxetine with an antipsychotic drug which is also used as an antidepressive agent, quetiapine. No studies were found comparing duloxetine with tricyclic antidepressants. The pooled confidence intervals were rather wide and there were no statistically significant differences in efficacy when comparing duloxetine with other antidepressants. However, when compared with escitalopram or venlafaxine, there was a higher rate of drop out due to any cause in the patients randomised to duloxetine (odds ratio (OR) 1.62; 95% confidence interval (CI) 1.01 to 2.62 and OR 1.56; 95% CI 1.14 to 2.15, respectively). There was also some weak evidence suggesting that patients taking duloxetine experienced more adverse events than paroxetine (OR 1.24; 95% CI 0.99 to 1.55).
AUTHORS' CONCLUSIONS
Duloxetine did not seem to provide a significant advantage in efficacy over other antidepressive agents for the acute-phase treatment of major depression. No differences in terms of efficacy were found, even though duloxetine was worse than some SSRIs (most of all, escitalopram) and newer antidepressants (like venlafaxine) in terms of acceptability and tolerability. Unfortunately, we only found evidence comparing duloxetine with a handful of other active antidepressive agents and only a few trials per comparison were found (in some cases we retrieved just one trial). This limited the power of the review to detect moderate, but clinically meaningful differences between the drugs. As many statistical tests have been used in the review, the findings from this review are better thought of as hypothesis forming rather than hypothesis testing and it would be very comforting to see the conclusions replicated in future trials. Most of included studies were sponsored by the drug industry manufacturing duloxetine. As for all other new investigational compounds, the potential for overestimation of treatment effect due to sponsorship bias should be borne in mind. In the present review no trials reported economic outcomes. Given that several SSRIs and the great majority of antidepressants are now available as generic formulation (only escitalopram, desvenlafaxine and duloxetine are still on patent), more comprehensive economic estimates of antidepressant treatment effect should be considered to better inform healthcare policy.
Topics: Antidepressive Agents; Citalopram; Cyclohexanols; Depression; Desvenlafaxine Succinate; Dibenzothiazepines; Duloxetine Hydrochloride; Fluoxetine; Humans; Paroxetine; Quetiapine Fumarate; Randomized Controlled Trials as Topic; Thiophenes; Venlafaxine Hydrochloride
PubMed: 23076926
DOI: 10.1002/14651858.CD006533.pub2 -
Alpha Psychiatry Sep 2021The aim of the article is to review systematically current researches investigating the relationship between intrauterine exposure to antidepressants and neonatal... (Review)
Review
The aim of the article is to review systematically current researches investigating the relationship between intrauterine exposure to antidepressants and neonatal hypoglycemia. This paper included studies published in electronic databases from January 2005 to July 2020. The searched keywords were as follows: antidepressants, pregnancy, selective serotonin reuptake inhibitors (SSRIs), citalopram, fluoxetine, paroxetine, escitalopram, sertraline, fluvoxamine, selective serotonin-norepinephrine reuptake inhibitors (SNRIs), venlafaxine, tricyclic antidepressants (TCAs), neonatal outcomes, neonatal hypoglycemia, imipramine, clomipramine, amitriptyline, bupropion, trazodone, and mirtazapine. This review examined 10 relevant studies. The odds ratio/risk ratio reported in the studies were 1.33-1.73 for any antidepressant, 1.30-1.35 for SSRI, 1.42-2.11 for SNRI, and 2.07 for TCAs. The risk of neonatal hypoglycemia in infants exposed to maternal TCAs appears to be slightly higher compared to infants exposed to maternal SSRIs. Data from current studies consistently show that exposure to maternal antidepressants during pregnancy may be related to increased risk of neonatal hypoglycemia in infants.
PubMed: 36447450
DOI: 10.1530/alphapsychiatry.2021.21143 -
Frontiers in Aging Neuroscience 2022Post-stroke depression (PSD) is a common complication after stroke. PSD is associated with emotional disorders and psychological dependence, which are potential risk...
Post-stroke depression (PSD) is a common complication after stroke. PSD is associated with emotional disorders and psychological dependence, which are potential risk factors for stroke recurrence and suicidality. This study aimed to perform an umbrella review of therapies for PSD through a comprehensive literature search. A systematic search was conducted in the PubMed and Web of Science by two independent authors. We examined the Hamilton Depression Scale (HAMD), Activities of daily living (ADL), Neurologic function as efficacy endpoints, and the incidence of adverse events as safety profiles. Seventeen eligible studies, including 267 clinical trials were included in this study. The results showed that High-Frequency Repetitive Transcranial Magnetic Stimulation (HfrTMS), Acupuncture/EA+conventional treatment, Escitalopram, Modified Sini San, Moxibustion, Xiaoyao Formula, Paroxetine, Chinese herbal medicine, Exercise, Citalopram, and Cognitive behavioral therapy are beneficial for improving the depression symptoms of patients with PSD. HfrTMS and Sertraline may have an impact on slowing the scores of activities of daily living or neurologic function. In addition, Acupuncture/EA+conventional, Escitalopram, Citalopram, Sertraline, and Fluoxetine showed no serious adverse events in PSD patients. Our study demonstrated that 11 treatment methods can effectively improve the condition of PSD patients.
PubMed: 36081895
DOI: 10.3389/fnagi.2022.993250 -
The Cochrane Database of Systematic... Dec 2021Depression occurs frequently in individuals with coronary artery disease (CAD) and is associated with a poor prognosis. (Review)
Review
BACKGROUND
Depression occurs frequently in individuals with coronary artery disease (CAD) and is associated with a poor prognosis.
OBJECTIVES
To determine the effects of psychological and pharmacological interventions for depression in CAD patients with comorbid depression.
SEARCH METHODS
We searched the CENTRAL, MEDLINE, Embase, PsycINFO, and CINAHL databases up to August 2020. We also searched three clinical trials registers in September 2021. We examined reference lists of included randomised controlled trials (RCTs) and contacted primary authors. We applied no language restrictions.
SELECTION CRITERIA
We included RCTs investigating psychological and pharmacological interventions for depression in adults with CAD and comorbid depression. Our primary outcomes included depression, mortality, and cardiac events. Secondary outcomes were healthcare costs and utilisation, health-related quality of life, cardiovascular vital signs, biomarkers of platelet activation, electrocardiogram wave parameters, non-cardiac adverse events, and pharmacological side effects.
DATA COLLECTION AND ANALYSIS
Two review authors independently examined the identified papers for inclusion and extracted data from the included studies. We performed random-effects model meta-analyses to compute overall estimates of treatment outcomes.
MAIN RESULTS
Thirty-seven trials fulfilled our inclusion criteria. Psychological interventions may result in a reduction in end-of-treatment depression symptoms compared to controls (standardised mean difference (SMD) -0.55, 95% confidence interval (CI) -0.92 to -0.19, I = 88%; low certainty evidence; 10 trials; n = 1226). No effect was evident on medium-term depression symptoms one to six months after the end of treatment (SMD -0.20, 95% CI -0.42 to 0.01, I = 69%; 7 trials; n = 2654). The evidence for long-term depression symptoms and depression response was sparse for this comparison. There is low certainty evidence that psychological interventions may result in little to no difference in end-of-treatment depression remission (odds ratio (OR) 2.02, 95% CI 0.78 to 5.19, I = 87%; low certainty evidence; 3 trials; n = 862). Based on one to two trials per outcome, no beneficial effects on mortality and cardiac events of psychological interventions versus control were consistently found. The evidence was very uncertain for end-of-treatment effects on all-cause mortality, and data were not reported for end-of-treatment cardiovascular mortality and occurrence of myocardial infarction for this comparison. In the trials examining a head-to-head comparison of varying psychological interventions or clinical management, the evidence regarding the effect on end-of-treatment depression symptoms is very uncertain for: cognitive behavioural therapy compared to supportive stress management; behaviour therapy compared to person-centred therapy; cognitive behavioural therapy and well-being therapy compared to clinical management. There is low certainty evidence from one trial that cognitive behavioural therapy may result in little to no difference in end-of-treatment depression remission compared to supportive stress management (OR 1.81, 95% CI 0.73 to 4.50; low certainty evidence; n = 83). Based on one to two trials per outcome, no beneficial effects on depression remission, depression response, mortality rates, and cardiac events were consistently found in head-to-head comparisons between psychological interventions or clinical management. The review suggests that pharmacological intervention may have a large effect on end-of-treatment depression symptoms (SMD -0.83, 95% CI -1.33 to -0.32, I = 90%; low certainty evidence; 8 trials; n = 750). Pharmacological interventions probably result in a moderate to large increase in depression remission (OR 2.06, 95% CI 1.47 to 2.89, I = 0%; moderate certainty evidence; 4 trials; n = 646). We found an effect favouring pharmacological intervention versus placebo on depression response at the end of treatment, though strength of evidence was not rated (OR 2.73, 95% CI 1.65 to 4.54, I = 62%; 5 trials; n = 891). Based on one to four trials per outcome, no beneficial effects regarding mortality and cardiac events were consistently found for pharmacological versus placebo trials, and the evidence was very uncertain for end-of-treatment effects on all-cause mortality and myocardial infarction. In the trials examining a head-to-head comparison of varying pharmacological agents, the evidence was very uncertain for end-of-treatment effects on depression symptoms. The evidence regarding the effects of different pharmacological agents on depression symptoms at end of treatment is very uncertain for: simvastatin versus atorvastatin; paroxetine versus fluoxetine; and escitalopram versus Bu Xin Qi. No trials were eligible for the comparison of a psychological intervention with a pharmacological intervention.
AUTHORS' CONCLUSIONS
In individuals with CAD and depression, there is low certainty evidence that psychological intervention may result in a reduction in depression symptoms at the end of treatment. There was also low certainty evidence that pharmacological interventions may result in a large reduction of depression symptoms at the end of treatment. Moderate certainty evidence suggests that pharmacological intervention probably results in a moderate to large increase in depression remission at the end of treatment. Evidence on maintenance effects and the durability of these short-term findings is still missing. The evidence for our primary and secondary outcomes, apart from depression symptoms at end of treatment, is still sparse due to the low number of trials per outcome and the heterogeneity of examined populations and interventions. As psychological and pharmacological interventions can seemingly have a large to only a small or no effect on depression, there is a need for research focusing on extracting those approaches able to substantially improve depression in individuals with CAD and depression.
Topics: Adult; Coronary Artery Disease; Depression; Escitalopram; Humans; Psychotherapy; Quality of Life
PubMed: 34910821
DOI: 10.1002/14651858.CD008012.pub4