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BMC Family Practice Dec 2003Statins alter lipid concentrations. This systematic review determined the efficacy of particular statins, in terms of their ability to alter cholesterol. (Comparative Study)
Comparative Study Meta-Analysis Review
BACKGROUND
Statins alter lipid concentrations. This systematic review determined the efficacy of particular statins, in terms of their ability to alter cholesterol.
REVIEW METHODS
PubMed, the Cochrane Library, references lists of reports, and reviews were searched (September 2001) for randomised, double blind trials of statins for cholesterol in trials of 12 weeks or longer. Mean change in total cholesterol, LDL-cholesterol, HDL-cholesterol, and triglycerides was calculated using pooled data for particular statins, and for particular doses of a statin. Pre-planned sensitivity analyses were used to determine the effects of initial concentration of total cholesterol, study duration, the effects of major trials, and effects in placebo versus active controlled trials. Information was not collected on adverse events.
RESULTS
Different statins at a range of doses reduced total cholesterol by 17-35% and LDL-cholesterol by 24-49% from baseline. Lower doses of statins generally produced less cholesterol lowering, though for most statins in trials of 12 weeks or longer there was at best only a weak relationship between dose and cholesterol reduction. Duration of treatment and baseline total cholesterol concentration did not alter the amount of the benefit attained.
CONCLUSIONS
Statins are effective medicines and confer benefit to patients in terms of primary and secondary prevention of coronary heart disease. Reductions in total cholesterol of 25% or more and LDL cholesterol of more than 30% were recorded for fixed doses of simvastatin 40 mg, atorvastatin 10 mg, and rosuvastatin 5 mg and 10 mg.
Topics: Atorvastatin; Cholesterol; Cholesterol, HDL; Cholesterol, LDL; Dose-Response Relationship, Drug; Fatty Acids, Monounsaturated; Female; Fluorobenzenes; Fluvastatin; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Indoles; Lovastatin; Male; Pravastatin; Pyridines; Pyrimidines; Pyrroles; Randomized Controlled Trials as Topic; Rosuvastatin Calcium; Simvastatin; Sulfonamides; Triglycerides
PubMed: 14969594
DOI: 10.1186/1471-2296-4-18 -
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 -
Asian Journal of Andrology 2017The aim of this study is to investigate the effect of statins type or even when grouping statins by hydrophilic or hydrophobic nature on prostate cancer risk. A... (Meta-Analysis)
Meta-Analysis Review
The aim of this study is to investigate the effect of statins type or even when grouping statins by hydrophilic or hydrophobic nature on prostate cancer risk. A literature search was performed without language restrictions using the databases of PubMed (1984.1-2015.3), MEDLINE (1984.1-2015.3), and EMBASE (1990.1-2015.3). Two independent reviewers appraised eligible studies and extracted data. Weighted averages were reported as relative risk (RR) with 95% confidence intervals (CI). Statistic heterogeneity scores were assessed with the standard Cochran's Q-test and I2 statistic. Publication bias was detected using the Begg's and Egger's tests. All statistical analyses were conducted by STATA version 10. Finally, fourteen studies were included in the meta-analysis. Both hydrophilic and hydrophobic statins showed no association with incidence of prostate cancer (RR = 1.00, 95% CI: 0.82-1.17; RR = 0.90, 95% CI: 0.73-1.08, respectively). Meanwhile, the risk of prostate cancer was not reduced in simvastatin (RR = 0.89, 95% CI: 0.72-1.05), pravastatin (RR = 1.02, 95% CI: 0.94-1.11), atorvastatin (RR = 0.89, 95% CI: 0.76-1.02), fluvastatin (RR = 0.99, 95% CI: 0.97-1.01), or lovastatin users (RR = 0.94, 95% CI: 0.79-1.08). The funnel plot showed that there was no publication bias. The results showed that statins had a neutral effect on prostate cancer risk; hydrophilic and hydrophobic statins as well as any subtype of statins did not affect the risk of prostate cancer.
Topics: Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Incidence; Male; Prostatic Neoplasms; Risk
PubMed: 27924788
DOI: 10.4103/1008-682X.190327 -
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 -
BMJ Open May 2015To evaluate the efficacy and safety of high-intensity statin therapy in patients with chronic kidney disease (CKD). (Meta-Analysis)
Meta-Analysis Review
OBJECTIVE
To evaluate the efficacy and safety of high-intensity statin therapy in patients with chronic kidney disease (CKD).
DESIGN
A systematic review and meta-analysis.
DATA SOURCES
Randomised controlled trials (RCTs) comparing high-intensity statin therapy (atorvastatin 80 mg or rosuvastatin 20/40 mg) with moderate/mild statin treatment or placebo were derived from the databases (PubMed, Embase, Ovid, the Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library, and ISI Web of Knowledge).
OUTCOME MEASURE
Primary end points: clinical events (all-cause mortality, stroke, myocardial infarction and heart failure); secondary end points: serum lipid, renal function changes and adverse events.
RESULTS
A total of six RCTs with 10,993 adult patients with CKD were included. A significant decrease in stroke was observed in the high-intensity statin therapy group (RR 0.69, 95% CI 0.56 to 0.85). However, the roles of high-intensity statin in decreasing all-cause mortality (RR 0.85, 95% CI 0.67 to 1.09), myocardial infarction (RR 0.69, 95% CI 0.40 to 1.18) and heart failure (RR 0.73, 95% CI 0.48 to 1.13) remain unclear with low evidence. High-intensity statin also had obvious effects on lowering the LDL-C level but no clear effects on renal protection. Although pooled results showed no significant difference between the intervention and control groups in adverse event occurrences, it was still insufficient to put off the doubts that high-intensity statin might increase adverse events because of limited data sources and low quality evidences.
CONCLUSIONS
High-intensity statin therapy could effectively reduce the risk of stroke in patients with CKD. However, its effects on all-cause mortality, myocardial infarction, heart failure and renal protection remain unclear. Moreover, it is hard to draw conclusions on the safety assessment of intensive statin treatment in this particular population. More studies are needed to credibly evaluate the effects of high-intensity statin therapy in patients with CKD.
Topics: Drug Administration Schedule; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Myocardial Infarction; Randomized Controlled Trials as Topic; Renal Insufficiency, Chronic; Stroke
PubMed: 25979868
DOI: 10.1136/bmjopen-2014-006886 -
International Journal of Preventive... 2021Cardiovascular diseases impose a burden of disease and economic burden on society. With regard to different drugs are used to treat cardiovascular disease; these... (Review)
Review
Cardiovascular diseases impose a burden of disease and economic burden on society. With regard to different drugs are used to treat cardiovascular disease; these interventions should be economically evaluated and them that the most cost-effective were selected. The aim of this study was to investigate the studies carried on the cost-effectiveness and cost-utility of statin drugs for the treatment of patients with cardiovascular disease between 2004 and 2020. Quality assessment of the articles was examined by Drummond's checklist. Given that the inclusion criteria, 26 articles included in the review. The results of this review showed that many articles related to the economic evaluation of statin drugs adhered international standards for performing economic evaluation studies. All the studies mentioned the source of effectiveness (the second criteria) and alternative options for the comparison (the third criteria). Atorvastatin and rosuvastatin drugs were the main options for the comparison in the studies. Although the results of the studies were different in some aspects, such as the type of modeling, costs items and the study perspective, they reached the same results which the use of statin drugs versus no-drug can decrease cost, cardiovascular events and deaths and increase QALY. The results were nearly different due to study design, time horizon, efficacy, and drug prices.
PubMed: 34249288
DOI: 10.4103/ijpvm.IJPVM_125_20 -
International Journal of Endocrinology 2018Current evidence indicates that statins increase the risk of new onset diabetes mellitus (NOD) and also deteriorate the glycemic control in patients with known diabetes... (Review)
Review
BACKGROUND
Current evidence indicates that statins increase the risk of new onset diabetes mellitus (NOD) and also deteriorate the glycemic control in patients with known diabetes mellitus (DM) after high-dose statin therapy.
AIMS
The aim of this review was to explore the effect of atorvastatin in causing NOD or deteriorating glycemic control in patients with DM.
METHODS
Two independent reviewers conducted the literature search, through PubMed database searching for articles published in English until April 2015, and only primary studies were included.
RESULTS
Of the 919 articles identified in our original search, 33 met the criteria for this review encompassing 1,951,113 participants. Twenty articles examined dysregulation of DM due to atorvastatin. Half of them showed that there was no significant change in glycemic control in patients treated with atorvastatin. Other studies showed that fasting plasma glucose and HbA1c levels were increased by atorvastatin. Thirteen articles examined if atorvastatin causes NOD. The majority of these articles showed that patients who used atorvastatin had a higher dose-dependent risk of developing NOD.
CONCLUSION
This systematic review suggests that there is an association between atorvastatin treatment and NOD. Moreover, it showed that atorvastatin in high dose causes worsening of the glycemic control in patients with DM.
PubMed: 30425742
DOI: 10.1155/2018/8380192 -
Medical Science Monitor : International... Jan 2019BACKGROUND Currently, statins are used to treat polycystic ovary syndrome (PCOS). This systematic review and meta-analysis aimed to investigate the... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND Currently, statins are used to treat polycystic ovary syndrome (PCOS). This systematic review and meta-analysis aimed to investigate the effect of statins on serum or plasma levels of dehydroepiandrosterone (DHEA) in women with PCOS. MATERIAL AND METHODS Databases that were searched included PubMed, Embase, and the Cochrane Library from their inception to August of 2018. Published randomized controlled trials (RCTs) were identified that evaluated the impact of statins on plasma DHEA levels in women with PCOS. The Cochrane risk of bias tool was used to assess the quality of the included RCTs. A random-effects model was used to analyze the pooled results. RESULTS Meta-analysis was performed on data from ten published studies that included 735 patients and showed that statin treatment could significantly reduce plasma DHEA levels when compared with controls (SMD, -0.43; 95% CI, -0.81-0.06; p=0.02; I²=82%). Statins were significantly more effective than placebo in reducing the levels of DHEAs. Subgroup analysis based on statin type showed that atorvastatin significantly reduced DHEA levels (SMD, -0.63; 95% CI, -1.20 - -0.05; p=0.03; I²=38%) but simvastatin did not significantly reduce DHEA levels (SMD: -0.14; 95% CI, -0.49-0.28; p=0.43; I²=77%). Subgroup analysis based on duration of treatment showed no significant difference between 12 weeks of statin treatment (SMD, -0.61; 95% CI, -1.23-0.02; p=0.06; I²=85%) and 24 weeks (SMD, -0.34; 95% CI -0.95-0.28; p=0.29; I²=83%). CONCLUSIONS Meta-analysis showed that statins significantly reduced the levels of DHEA when compared with placebo in patients with PCOS.
Topics: Adult; Atorvastatin; China; Dehydroepiandrosterone; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypoglycemic Agents; Metformin; Middle Aged; Polycystic Ovary Syndrome; Simvastatin
PubMed: 30698163
DOI: 10.12659/MSM.914128 -
Annals of Translational Medicine Dec 2019Pulmonary hypertension (PH) is a multi-causal disease and no satisfactory therapeutic strategies for it. Statins have been suggested as potential drugs in PH, whose...
BACKGROUND
Pulmonary hypertension (PH) is a multi-causal disease and no satisfactory therapeutic strategies for it. Statins have been suggested as potential drugs in PH, whose effects in different clinic types of PH have not been conclusive. In this study, we included randomized controlled clinical trials (RCTs) evaluating the efficacy and safety of statins therapy in PH.
METHODS
We searched databases including Medline, Embase, Cochrane, PubMed and Web of science, with time up to January 1, 2019. With 95% confidence interval (CI), weighted mean difference (WMD) or standardized mean difference (SMD) was pooled and calculated in a random or fixed effect model according to I2 statistic.
RESULTS
A total of nine RCTs with 657 patients were included. Four types of statins (atorvastatin, pravastatin, rosuvastatin and simvastatin) were used at different doses (10-80 mg daily) for up to 6 months. In the pooled-data analysis, compared with placebo, there were significant improvements in pulmonary arterial pressure (PAP), in addition to low-density lipoprotein (LDL) in patients treated with statins, but not in 6-minute walking distance (6MWD), cardiac index (CDI). No more adverse events and all-cause mortality were revealed. Subgroup analysis indicated that statins could decrease PAP in the subtype of PH due to chronic obstructive pulmonary disease (COPD), but not pulmonary arterial hypertension (PAH).
CONCLUSIONS
This study indicates that statins can efficiently and safely reduce PAP in PH, especially in the subtype due to COPD. Further RCTs are needed to focus on the efficacy and safety of statin therapy in different subtypes of PH.
PubMed: 32042802
DOI: 10.21037/atm.2019.11.19 -
Mayo Clinic Proceedings. Innovations,... Jun 2019To assess the effect of statins compared with placebo on the risk of developing hypertransaminasemia.
OBJECTIVE
To assess the effect of statins compared with placebo on the risk of developing hypertransaminasemia.
PATIENTS AND METHODS
We performed a systematic review of electronic databases and included articles published between January 1, 1965, and April 10, 2017. Randomized clinical trials (RCTs) comparing statins vs placebo were included. Odds ratios (ORs) were pooled in random-effect meta-analyses according to established methods recommended by the Cochrane Collaboration.
RESULTS
Seventy-three eligible RCTs, comprising 123,051 patients, were identified. Statins associated with a significantly risk of hypertransaminasemia (OR 1.45; 95% confidence interval [CI], 1.24-1.69; <.001). Atorvastatin showed the highest odds (OR 2.66; 95% CI, 1.74-4.06; <.001) followed by rosuvastatin (OR 1.35; 95% CI, 1.06-1.70; =.01) and lovastatin (OR 1.53; 95% CI, 1.03-2.28; =.04). Pravastatin, fluvastatin, and simvastatin yielded no statistically different odds compared with placebo.
CONCLUSIONS
A dose-dependent risk of developing hypertransaminasemia occurs in patients taking atorvastatin, rosuvastatin, and lovastatin.
PubMed: 31193835
DOI: 10.1016/j.mayocpiqo.2019.01.003