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Frontiers in Cardiovascular Medicine 2022To explore the associations between different types and doses of statins and adverse events in secondary prevention of cardiovascular disease.
Associations between statins and adverse events in secondary prevention of cardiovascular disease: Pairwise, network, and dose-response meta-analyses of 47 randomized controlled trials.
OBJECTIVES
To explore the associations between different types and doses of statins and adverse events in secondary prevention of cardiovascular disease.
METHODS
We searched PubMed, Embase, and Cochrane databases for randomized controlled trials that compared statins with non-statin controls or different types or doses of statins. The primary outcomes included muscle condition, transaminase elevations, renal insufficiency, gastrointestinal discomfort, cancer, new onset or exacerbation of diabetes, cognitive impairment, and eye condition. We also analyzed myocardial infarction (MI), stroke, death from cardiovascular diseases (CVD), and all-cause death as the secondary outcomes to compare the potential harms with the benefits of statins. We conducted pairwise meta-analyses to calculate the odds ratio (OR) and 95% confidence intervals (CIs) for each outcome. Network meta-analyses were performed to compare the adverse effects of different statins. An Emax model was used to examine the dose-response relationships of the adverse effects of each statin.
RESULTS
Forty-seven trials involving 107,752 participants were enrolled and followed up for 4.05 years. Compared with non-statin control, statins were associated with an increased risk of transaminase elevations [OR 1.62 (95% CI 1.20 to 2.18)]. Statins decreased the risk of MI [OR 0.66 (95% CI 0.61 to 0.71), < 0.001], stroke [OR 0.78 (95% CI 0.72 to 0.84), < 0.001], death from CVD [OR 0.77 (95% CI 0.72 to 0.83), < 0.001] and all-cause death [OR 0.83 (95% CI 0.79 to 0.88), < 0.001]. Atorvastatin showed a higher risk of transaminase elevations than non-statin control [OR 4.0 (95% CI 2.2 to 7.6)], pravastatin [OR 3.49 (95% CI 1.77 to 6.92)] and simvastatin [OR 2.77 (95% CI 1.31 to 5.09)], respectively. Compared with atorvastatin, simvastatin was associated with a lower risk of muscle problems [OR 0.70 (95% CI 0.55 to 0.90)], while rosuvastatin showed a higher risk [OR 1.75 (95% CI 1.17 to 2.61)]. An Emax dose-response relationship was identified for the effect of atorvastatin on transaminase elevations.
CONCLUSION
Statins were associated with increased risks of transaminases elevations in secondary prevention. Our study provides the ranking probabilities of statins that can help clinicians make optimal decisions when there is not enough literature to refer to.
SYSTEMATIC REVIEW REGISTRATION
[https://www.crd.york.ac.uk/prospero/], identifier [CRD42021285161].
PubMed: 36093163
DOI: 10.3389/fcvm.2022.929020 -
BMC Gastroenterology Mar 2021There is increased interest in the therapeutic use of statins in cirrhosis, but preferred statin and safety outcomes are still not well known. In this systematic review...
BACKGROUND/AIMS
There is increased interest in the therapeutic use of statins in cirrhosis, but preferred statin and safety outcomes are still not well known. In this systematic review we aimed to address pharmacokinetics (PK), safety, and effects on cardiovascular (CV) outcomes of statins in cirrhosis.
METHODS
Our systematic search in several electronic databases and repositories of two regulatory bodies up to 2020-06-11 yielded 22 articles and 2 drug monographs with relevant data.
RESULTS
Rosuvastatin and pitavastatin showed minimal PK changes in Child-Pugh A cirrhosis. Only rosuvastatin was assessed in a repeated dosing PK study. Atorvastatin showed pronounced PK changes in cirrhosis. No PK data was found for simvastatin, the most commonly used statin in cirrhosis trials. There was insufficient data to assess CV effects of statins in cirrhosis. Clinical trials in cirrhosis were limited to simvastatin, atorvastatin, and pravastatin. In patients taking simvastatin 40 mg, pooled frequency of rhabdomyolysis was 2%, an incidence 40-fold higher than that reported in non-cirrhosis patients, while this was no rhabdomyolysis observed in patients on simvastatin 20 mg, atorvastatin 20 mg, or pravastatin 40 mg. Drug-induced liver injury was of difficult interpretation due to co-existence of muscle damage. No overt liver failure was reported.
CONCLUSIONS
Simvastatin 40 mg should be avoided in decompensated cirrhosis. Safety data on simvastatin 20 mg or other statins are based on small study sample size. This rarity of evidence combined with lack of data in dose adjustment methods in cirrhosis is a barrier for using statins for CV indications or for investigational use for liver indications.
Topics: Atorvastatin; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Liver Cirrhosis; Pravastatin; Simvastatin
PubMed: 33726685
DOI: 10.1186/s12876-021-01704-w -
Lipids in Health and Disease Oct 2018Although there were many studies reporting the combination therapy of Ezetimibe and Atorvastatin's efficacy and Atorvastatin monotherapy's, the conclusions were... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Although there were many studies reporting the combination therapy of Ezetimibe and Atorvastatin's efficacy and Atorvastatin monotherapy's, the conclusions were controversial. Therefore, a systematic review and meta analysis of combination therapy and monotherapy were conducted.
METHODS
PubMed, Cochrane Library and Embase were searched for studies of the combination therapy of Ezetimibe and Atorvastatin and Atorvastatin monotherapy published up to October 20, 2017. Two investigators assessed the articles for eligibility and evaluated quality.The changed values and the efficacy of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), Total Cholesterol (TC) and Triglyceride (TG) indicators were the outcomes. Four doses of the comparisons were included: the combination therapy of Ezetimibe (10 mg) and Atorvastatin (10 mg) (E10 + A10) versus Atorvastatin (20 mg) monotherapy (A20); E10 + A10 vs. A10; E10 + A20 vs. A40; E10 + A40 vs. A80. Review manager software 5.1 was used for quality assessment and Stata version 12.0 software was used for statistical analysis.
RESULTS
eventeen studies (11 publications) were included in the meta analysis. Compared with Atorvastatin monotherapy, the overall efficacy of combination therapy of Ezetimibe and Atorvastatin on lowering LDL-C (MD = - 15.38, 95% CI: -16.17 to - 14.60; I = 26.2%, n = 17), TC (MD = - 9.51, 95% CI: -10.28 to - 8.74; I = 33.7%, n = 17) and TG (MD = - 6.42, 95% CI: -7.78 to - 5.06; I = 0%, n = 15) and raising HDL-C (MD = 0.95, 95% CI: 0.34 to 1.57; I = 0%, n = 17) was significant. The efficacy of the comparison on HDL-C was largely significant for the different doses.
CONCLUSIONS
The overall efficacy and subgroup's efficacy of combination therapy of Ezetimibe and Atorvastatin on lowering LDL-C, TC and TG was significantly better than Atorvastatin monotherapy's. The overall and the E10 + A10/A20 group's effectiveness of combination therapy on rasing HDL-C were significantly.
Topics: Atorvastatin; Cholesterol, HDL; Cholesterol, LDL; Drug Therapy, Combination; Ezetimibe; Female; Humans; Hypercholesterolemia; Male; Triglycerides
PubMed: 30326894
DOI: 10.1186/s12944-018-0880-8 -
PloS One 2017Acute coronary syndrome (ACS) is an important disease threatening human life and health. Many studies have shown that the loading dose of atorvastatin can significantly... (Meta-Analysis)
Meta-Analysis Review
Effect of high-dose rosuvastatin loading before percutaneous coronary intervention in Chinese patients with acute coronary syndrome: A systematic review and meta-analysis.
BACKGROUND
Acute coronary syndrome (ACS) is an important disease threatening human life and health. Many studies have shown that the loading dose of atorvastatin can significantly improve the prognosis of patients with ACS, and reduce the mortality. However, this conclusion is not consistent. Thus, we aimed to evaluate the effect of high-dose rosuvastatin loading before percutaneous coronary intervention (PCI) in Chinese patients with ACS using a meta-analysis based on a systematic review of published articles.
METHODS
We systematically reviewed published studies, evaluating the effect of high-dose rosuvastatin loading before percutaneous coronary intervention in Chinese patients with ACS. The retrieval time is limited from inception to 2 November 2016, and the retrieved databases included PubMed, Embase, the Cochrane Library, Web of Science, CBM, CNKI, the VIP database and the Wang Fang database. Two researchers independently assessed the quality of the included studies and then extracted the data. Stata 11.0 was used for data analysis.
RESULTS
In total, 11 articles, which included 802 patients, were included in our meta-analysis. Among these patients, 398 patients were in the high-dose group (20 mg/day) and 404 patients were in the conventional dose group (10 mg/day). Meta-analysis results showed that compared with the conventional dose group: 1) The loading dose of rosuvastatin can significantly reduce the hs-CRP level after PCI, including at 24 hours (SMD = -0.65, 95%CI -0.84 ~ -0.47, P = 0.000), 48 hours (SMD = -0.40, 95%CI -0.68 ~ -0.11, P = 0.006), and four weeks (SMD = -1.64, 95%CI -2.01 ~ -1.26, P = 0.000). 2) The loading dose of rosuvastatin can significantly reduce the levels of LDL-C and cTnT, including the level of LDL-C at 30 d after PCI (SMD = -0.89, 95%CI -1.10 ~ -0.69, P = 0.000), and the level of cTnT at 24 h after PCI (SMD = -1.93, 95%CI -2.28 ~ -1.59, P = 0.000), and increase the level of HDL-C at 48 h after PCI (SMD = 0.61, 95%CI 0.34 ~ 0.88, P = 0.000). 3) The loading dose of rosuvastatin can significantly reduce the levels of TG and TC, including the level of TG at 30 d after PCI (SMD = -0.94, 95%CI -1.17 ~ -0.71, P = 0.000), the level of TC at 48 h after PCI (SMD = -0.35, 95%CI -0.68 ~ -0.01, P = 0.043), and the level of TC at 30 d after PCI (SMD = -0.77, 95%CI -0.98 ~ -0.56, P = 0.000).
CONCLUSIONS
Our systematic review and meta-analysis showed that, compared with the conventional dose, the loading dose of rosuvastatin was more beneficial to patients with ACS in China and is suitable for clinical application. Due to the limitations of the quality and quantity of included articles, this conclusion still needs to be confirmed by multicenter clinical trials.
Topics: Acute Coronary Syndrome; Anticholesteremic Agents; China; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Percutaneous Coronary Intervention; Rosuvastatin Calcium
PubMed: 28231287
DOI: 10.1371/journal.pone.0171682 -
Cureus Sep 20213-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors are commonly used drugs in the management of elevated lipid levels and cardiovascular disease. In... (Review)
Review
3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors are commonly used drugs in the management of elevated lipid levels and cardiovascular disease. In cardiovascular diseases, among other common chronic conditions, inflammatory biomarkers are used to monitor disease progression and the risk of recurrent adverse events. We explored whether or not there was a positive effect on these biomarkers using HMG-CoA reductase inhibitors. The systematic review was conducted by gathering relevant papers mainly from three databases, identified through a generated Medical Subject Headings (MeSH) strategy. Identification of papers was subsequently followed by applying a selected inclusion and exclusion criteria to narrow the papers chosen for review. Post the application of stipulated criteria, 12 papers remained. They were subsequently assessed for risk of bias using a Cochrane risk analysis tool, identifying most as having some concerns of bias or low risk of bias. We found that HMG-CoA reductase inhibitors exhibit both a lipid-lowering effect addition to an anti-inflammatory effect.
PubMed: 34722051
DOI: 10.7759/cureus.18273 -
Medicine Jun 2021Atorvastatin treatment has been suggested as a therapeutic method for women with polycystic ovary syndrome (PCOS) in many clinical studies. Nonetheless, the effects of... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Atorvastatin treatment has been suggested as a therapeutic method for women with polycystic ovary syndrome (PCOS) in many clinical studies. Nonetheless, the effects of atorvastatin on insulin resistance in PCOS patients still remain controversial.
OBJECTIVE
The aim of this report was to evaluate the effects of atorvastatin therapy on the insulin resistance in the treatment of PCOS compared to that of placebo, in order to confer a reference for clinical practice.
METHODS
Randomized controlled trials (RCTs) of atorvastatin for PCOS published up to August, 2020 were searched. Standardized mean difference (SMD) and 95% confidence interval (CI) were calculated, and heterogeneity was measured by the I2 test. Sensitivity analysis was also carried out. The outcomes of interest were as follows: fasting glucose concentration, fasting insulin level, homeostasis model assessment of insulin resistance (HOMA-IR) or body mass index (BMI) value.
RESULTS
Nine RCTs with 406 participants were included. The difference of fasting glucose concentration in PCOS patients between atorvastatin group and placebo group was not statistically significant (8 trials; SMD -0.06, 95% CI -0.31 to 0.20, P = .66). PCOS patients in atorvastatin group had lower fasting insulin level than those in placebo group (7 trials; SMD -1.84, 95% CI -3.06 to -0.62, P < .003). The homeostasis model assessment of insulin resistance (HOMA-IR) value showed significant decrease in the atorvastatin therapy compared to placebo (6 trials; SMD -4.12, 95% CI -6.00 to -2.23, P < .0001). In contrast to placebo, atorvastatin therapy did not decrease the BMI value significantly in PCOS patients (7 trials; SMD 0.12, 95% CI -0.07 to 0.31, P = .22).
CONCLUSIONS
Atorvastatin therapy can reduce insulin resistance in the treatment of patients with PCOS. In addition, further large-sample, multi-center RCTs are needed to identify these findings.
Topics: Adolescent; Adult; Atorvastatin; Blood Glucose; Body Mass Index; Fasting; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Insulin; Insulin Resistance; Polycystic Ovary Syndrome; Randomized Controlled Trials as Topic; Treatment Outcome; Young Adult
PubMed: 34128863
DOI: 10.1097/MD.0000000000026289 -
Atherosclerosis Oct 2016The effect of statin therapy on plasma adiponectin levels has not been conclusively studied. Therefore, we aimed to evaluate this effect through a systematic review and... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND AND AIMS
The effect of statin therapy on plasma adiponectin levels has not been conclusively studied. Therefore, we aimed to evaluate this effect through a systematic review and meta-analysis of available randomized controlled trials (RCTs).
METHODS
Quantitative data synthesis was performed using a random-effects model with weighted mean difference (WMD) and 95% confidence interval (CI) as summary statistics.
RESULTS
In 30 studies (43 study arms) with 2953 participants, a significant increase in plasma adiponectin levels was observed after statin therapy (WMD: 0.57 μg/mL, 95% CI: 0.18, 0.95, p = 0.004). In subgroup analysis, atorvastatin, simvastatin, rosuvastatin, pravastatin and pitavastatin were found to change plasma adiponectin concentrations by 0.70 μg/mL (95% CI: -0.26, 1.65), 0.50 μg/mL (95% CI: -0.44, 1.45), -0.70 μg/mL (95% CI: -1.08, -0.33), 0.62 μg/mL (95% CI: -0.12, 1.35), and 0.51 μg/mL (95% CI: 0.30, 0.72), respectively. With respect to duration of treatment, there was a significant increase in the subset of trials lasting ≥12 weeks (WMD: 0.88 μg/mL, 95% CI: 0.19, 1.57, p = 0.012) but not in the subset of <12 weeks of duration (WMD: 0.18 μg/mL, 95% CI: -0.23, 0.58, p = 0.390). Random-effects meta-regression suggested a significant association between statin-induced elevation of plasma adiponectin and changes in plasma low density lipoprotein cholesterol levels (slope: 0.04; 95% CI: 0.01, 0.06; p = 0.002).
CONCLUSIONS
The meta-analysis showed a significant increase in plasma adiponectin levels following statin therapy. Although statins are known to increase the risk for new onset diabetes mellitus, our data might suggest that the mechanism for this is unlikely to be due to a reduction in adiponectin expression.
Topics: Adiponectin; Adult; Aged; Atorvastatin; Cardiovascular Diseases; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Pravastatin; Quinolines; Randomized Controlled Trials as Topic; Regression Analysis; Rosuvastatin Calcium; Simvastatin
PubMed: 27498397
DOI: 10.1016/j.atherosclerosis.2016.07.897 -
Frontiers in Pharmacology 2022We aim to compare the effectiveness of different drug treatments in improving recurrence in patients with chronic subdural hematoma (CSDH). Eligible randomized...
We aim to compare the effectiveness of different drug treatments in improving recurrence in patients with chronic subdural hematoma (CSDH). Eligible randomized controlled trials (RCTs) and prospective trials were searched in PubMed, Cochrane Library, and Embase, from database inception to December 2021. After the available studies following inclusion and exclusion criteria were screened, the main outcome measures were strictly extracted. Taking the random-effects model, dichotomous data were determined and extracted by odds ratio (OR) with 95% credible interval (CrI), and a surface under the cumulative ranking curve (SUCRA) was generated to calculate the ranking probability of comparative effectiveness among each drug intervention. Moreover, we used the node-splitting model to evaluate inconsistency between direct and indirect comparisons of our network meta-analysis (NMA). Funnel plots were used to evaluate publication bias. From the 318 articles found during initial citation screening, 11 RCTs and 3 prospective trials ( = 3,456 participants) were ultimately included in our study. Our NMA results illustrated that atorvastatin + dexamethasone (ATO+DXM) (OR = 0.06, 95% CrI 0.01, 0.89) was the most effective intervention to improve recurrence in patients with CSDH (SUCRA = 89.40%, 95% CrI 0.29, 1.00). Four drug interventions [ATO+DXM (OR = 0.06, 95% CrI 0.01, 0.89), DXM (OR = 0.18, 95% CrI 0.07, 0.41), tranexamic acid (TXA) (OR = 0.26, 95% CrI 0.07, 0.41), and ATO (OR = 0.41, 95% CrI 0.12, 0.90)] achieved statistical significance in improving recurrence in CSDH patients compared with the placebo (PLB) or standard neurosurgical treatment (SNT) group. Our NMA showed that ATO+DXM, DXM, ATO, and TXA had definite efficacy in improving recurrence in CSDH patients. Among them, ATO+DXM is the best intervention for improving recurrence in patients with CSDH in this particular population. Multicenter rigorous designed prospective randomized trials are still needed to evaluate the role of various drug interventions in improving neurological function or outcome. (https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=299491), identifier (CRD 42022299491).
PubMed: 35401183
DOI: 10.3389/fphar.2022.845386 -
The Cochrane Database of Systematic... May 2015Primary percutaneous coronary intervention (PPCI) is the preferred treatment for ST-segment elevation myocardial infarction. Although coronary flow is restored after... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Primary percutaneous coronary intervention (PPCI) is the preferred treatment for ST-segment elevation myocardial infarction. Although coronary flow is restored after PPCI, impaired myocardial perfusion (known as no-reflow) related to poor clinical outcomes is frequently observed. To overcome this phenomenon, drugs, such as atorvastatin, abciximab and others, have been tried as adjunctive treatment to PPCI. Among these drugs, verapamil and adenosine are among the most promising. No other systematic reviews have examined use of these two drugs in people with acute myocardial infarction (AMI) undergoing PPCI. This is an update of the version previously published (2013, Issue 6), for which the people of interest in the review were those treated with PPCI - not those given fibrinolytic therapy.
OBJECTIVES
To study the impact of adenosine and verapamil on no-reflow during PPCI in people with AMI.
SEARCH METHODS
We updated searches of the following databases in June 2014 without language restriction: the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, Web of Science and BIOSIS, China National Knowledge Infrastructure and clinical trials registers (ClinicalTrials.gov, Current Controlled Trials, Australian and New Zealand Clinical Trials Registry, the World Health Organization (WHO) International Clinical Trials Registry Platform). We also handsearched The American Journal of Cardiology.
SELECTION CRITERIA
We selected randomised controlled trials (RCTs) in which adenosine or verapamil was the primary intervention. Participants were individuals diagnosed with AMI who were undergoing PPCI.
DATA COLLECTION AND ANALYSIS
Two review authors collected studies and extracted data. When necessary, we contacted trial authors to obtain relevant information. We calculated risk ratios (RRs), P values and 95% confidence intervals (CIs) of dichotomous data.
MAIN RESULTS
We included in our review 11 RCTs (one new study with 59 participants) involving 1027 participants. Ten RCTs were associated with adenosine and one with verapamil. We considered the overall risk of bias of included studies to be moderate. We found no evidence that adenosine reduced short-term all-cause mortality (RR 0.61, 95% CI 0.25 to 1.48, P value = 0.27), long-term all-cause mortality (RR 0.78, 95% CI 0.22 to 2.74, P value = 0.70), short-term non-fatal myocardial infarction (RR 1.32, 95% 0.33 to 5.29, P value = 0.69) or myocardial blush grade (MBG) 0 to 1 after PPCI (RR 0.96, 95% CI 0.76 to 1.22, P value = 0.75). The incidence of thrombolysis in myocardial infarction (TIMI) flow grade < 3 after PPCI (RR 0.62, 95% CI 0.42 to 0.91, P value = 0.01) was decreased. Conversely, adverse events with adenosine, such as bradycardia (RR 6.32, 95% CI 2.98 to 13.41, P value < 0.00001), hypotension (RR 11.43, 95% CI 2.75 to 47.57, P value = 0.0008) and atrioventricular (AV) block (RR 6.78, 95% CI 2.15 to 21.38, P value = 0.001), were significantly increased.Meta-analysis of verapamil as treatment for no-reflow during PPCI was not performed because data were insufficient.
AUTHORS' CONCLUSIONS
It is difficult to draw conclusions because of the insufficient quality and quantity of current research studies. We considered the overall risk of bias of included studies to be moderate. Adenosine as treatment for no-reflow during PPCI could reduce angiographic no-reflow (TIMI flow grade < 3) but was found to increase adverse events. What's more, no evidence could be found to suggest that adenosine reduced all-cause mortality, non-fatal myocardial infarction or the incidence of myocardial blush grade 0 to 1. Additionally, the efficacy of verapamil for no-reflow during PPCI could not be analysed because data were insufficient. Further clinical research into adenosine and verapamil is needed because of the limited numbers of available trials and participants.
Topics: Adenosine; Cause of Death; Humans; Myocardial Infarction; No-Reflow Phenomenon; Percutaneous Coronary Intervention; Randomized Controlled Trials as Topic; Vasodilator Agents; Verapamil
PubMed: 25985145
DOI: 10.1002/14651858.CD009503.pub3 -
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