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Beta Blockade after myocardial infarction: systematic review and meta regression analysis.

ABSTRACT: OBJECTIVES:To assess the effectiveness of beta blockers in short term treatment for acute myocardial infarction and in longer term secondary prevention; to examine predictive factors that may influence outcome and therefore choice of drug; and to examine the clinical importance of the results in the light of current treatment. DESIGN:Systematic review of randomised controlled trials. SETTING:Randomised controlled trials. SUBJECTS:Patients with acute or past myocardial infarction. INTERVENTION:beta Blockers compared with control. MAIN OUTCOME MEASURES:All cause mortality and non-fatal reinfarction. RESULTS:Overall, 5477 of 54 234 patients (10.1%) randomised to beta blockers or control died. We identified a 23% reduction in the odds of death in long term trials (95% confidence interval 15% to 31%), but only a 4% reduction in the odds of death in short term trials (-8% to 15%). Meta regression in long term trials did not identify a significant reduction in effectiveness in drugs with cardioselectivity but did identify a near significant trend towards decreased benefit in drugs with intrinsic sympathomimetic activity. Most evidence is available for propranolol, timolol, and metoprolol. In long term trials, the number needed to treat for 2 years to avoid a death is 42, which compares favourably with other treatments for patients with acute or past myocardial infarction. CONCLUSIONS:beta Blockers are effective in long term secondary prevention after myocardial infarction, but they are underused in such cases and lead to avoidable mortality and morbidity.

SUBMITTER: Freemantle N

PROVIDER: S-EPMC31101 | biostudies-literature | 1999 Jun

REPOSITORIES: biostudies-literature

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beta Blockade after myocardial infarction: systematic review and meta regression analysis.

Freemantle N N Cleland J J Young P P Mason J J Harrison J J

BMJ (Clinical research ed.) 19990601 7200

<h4>Objectives</h4>To assess the effectiveness of beta blockers in short term treatment for acute myocardial infarction and in longer term secondary prevention; to examine predictive factors that may influence outcome and therefore choice of drug; and to examine the clinical importance of the results in the light of current treatment.<h4>Design</h4>Systematic review of randomised controlled trials.<h4>Setting</h4>Randomised controlled trials.<h4>Subjects</h4>Patients with acute or past myocardia ...[more]

PMID: 10381708

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Project description:Background A comprehensive evaluation of the benefits of mineralocorticoid receptor antagonists (MRA) in acute myocardial infarction (AMI) patients is lacking. Objective To summarize the evidence on the efficacy and safety of MRA in patients admitted for AMI. Methods Articles were identified through PubMed, Embase, Cochrane Library, Ovid (Medline1946-2021), and ClinicalTrials.gov databases from their inception to December 31, 2020. Results 15 articles with a total of 11,861 patients were included. MRA reduced the risk of all-cause mortality by 16% (relative ratio (RR): 0.84; 95% confidence interval (CI) (0.76, 0.94); P = 0.002) and the incidence of cardiovascular adverse events by 12% (RR: 0.88, 95% CI (0.83, 0.93), P < 0.00001) in post-AMI patients, and further analysis demonstrated that early administration of MRA within 7 days after AMI resulted in a greater reduction in all-cause mortality (RR: 0.72, 95% CI (0.61, 0.85), P < 0.0001). Subgroup analyses showed that post-STEMI patients without left ventricular systolic dysfunction (LVSD) treated with MRA had a 36% reduction in all-cause mortality (RR: 0.64, 95% CI (0.46, 0.89), P = 0.007) and a 22% reduction in cardiovascular adverse events (RR: 0.78, 95% CI (0.67, 0.91), P = 0.002). Meanwhile, post-STEMI patients without LVSD treated with MRA get significant improvements in left ventricular ejection fraction (mean difference (MD): 2.69, 95% CI (2.44, 2.93), P < 0.00001), left ventricular end-systolic index (MD: -4.52 ml/m2, 95% CI (-8.21, -0.83), P = 0.02), and left ventricular end-diastolic diameter (MD: -0.11 cm, 95% CI (-0.22, 0.00), P = 0.05). The corresponding RR were 1.72 (95% CI (1.43, 2.07), P < 0.00001) for considered common adverse events (hyperkalemia, gynecomastia, and renal dysfunction). Conclusions Our findings suggest that MRA treatment reduces all-cause mortality and cardiovascular adverse events in post-AMI patients, which is more significant in patients after STEMI without LVSD. In addition, MRA treatment may exert beneficial effects on the reversal of cardiac remodeling in patients after STEMI without LVSD.

Project description:ObjectiveTo summarise existing data on the relation between the time from symptom onset until revascularisation (time to reperfusion) and the myocardial salvage index (MSI) calculated as proportion of non-necrotic myocardium inside oedematous myocardium on T2-weighted and T1-weighted late gadolinium enhancement MRI after ST-segment elevation myocardial infarction (STEMI).MethodsStudies including patients with revascularised STEMI and stating both the time to reperfusion and the MSI measured by T2-weighted and T1-weighted late gadolinium enhancement MRI were searched in MEDLINE, EMBASE and ISI Web of Science until 16 May 2020. A mixed effects model was used to evaluate the relation between the time to reperfusion and the MSI. The gender distribution and mean age in included patient groups, the timing of MRI, used MRI sequences and image interpretation methodology were included in the mixed effects model to explore between-study heterogeneity.ResultsWe included 38 studies with 5106 patients. The pooled MSI was 42.6% (95% CI: 38.1 to 47.1). The pooled time to reperfusion was 3.8 hours (95% CI: 3.5 to 4.0). Every hour of delay in reperfusion was associated with an absolute decrease of 13.1% (95% CI: 11.5 to 14.6; p<0.001) in the MSI. Between-study heterogeneity was considerable (σ2=167.8). Differences in the gender distribution, timing of MRI and image interpretation among studies explained 45.2% of the between-study heterogeneity.ConclusionsThe MSI on T2-weighted and T1-weighted late gadolinium enhancement MRI correlates inversely with the time to reperfusion, which indicates that cardioprotection achieved by minimising the time to reperfusion leads to a higher MSI. The analysis revealed considerable heterogeneity between studies. The heterogeneity could partly be explained by differences in the gender distribution, timing and interpretation of MRI suggesting that the MRI-assessed MSI is not only influenced by cardioprotective therapy but also by patient characteristics and MRI parameters.

Project description:BACKGROUND:The effect of antipsychotic (AP) drugs on risk of stroke and myocardial infarction (MI) remains unclear due to methodological limitations of, and inconsistencies across, existing studies. We aimed to systematically review studies reporting on the associations between AP drug use and stroke or MI risk, and to investigate whether associations differed among different sub-populations. METHODS:We searched Medline, EMBASE, PsychINFO and Cochrane Library (from inception to May 28, 2017) for observational studies reporting on AP drug use and MI or stroke occurrence. We performed random-effects meta-analyses for each outcome, performing sub-groups analyses by study population - specifically general population (i.e. those not restricted to patients with a particular indication for AP drug use), people with dementia only and psychiatric illness only. Where feasible we performed subgroup analyses by AP drug class. RESULTS:From 7008 articles, we included 29 relevant observational studies, 19 on stroke and 10 on MI. Results of cohort studies that included a general population indicated a more than two-fold increased risk of stroke, albeit with substantial heterogeneity (pooled HR 2.31, 95% CI 1.13, 4.74, I2 = 83.2%). However, the risk among patients with dementia was much lower, with no heterogeneity (pooled HR 1.16, 95% CI 1.00, 1.33, I2 = 0%) and there was no clear association among studies of psychiatric populations (pooled HR 1.44, 95% CI 0.90, 2.30; substantial heterogeneity [I2 = 78.8])). Associations generally persisted when stratifying by AP class, but few studies reported on first generation AP drugs. We found no association between AP drug use and MI risk (pooled HR for cohort studies: 1.29, 95% CI 0.88, 1.90 and case-control studies: 1.07, 95% CI 0.94, 1.23), but substantial methodological and statistical heterogeneity among a relatively small number of studies limits firm conclusions. CONCLUSIONS:AP drug use may be associated with an increased risk of stroke, but there is no clear evidence that this risk is further elevated in patients with dementia. Further studies are need to clarify the effect of AP drug use on MI and stroke risk in different sub-populations and should control for confounding by indication and stratify by AP drug class.

Project description:BACKGROUND:Myocardial infarction (MI) is a multifactorial disease with complex pathogenesis, mainly the result of the interplay of genetic and environmental risk factors. The regulation of thrombosis, inflammation and cholesterol and lipid metabolism are the main factors that have been proposed thus far to be involved in the pathogenesis of MI. Traditional risk-estimation tools depend largely on conventional risk factors but there is a need for identification of novel biochemical and genetic markers. The aim of the study is to identify differentially expressed genes that are consistently associated with the incidence myocardial infarction (MI), which could be potentially incorporated into the traditional cardiovascular diseases risk factors models. METHODS:The biomedical literature and gene expression databases, PubMed and GEO, respectively, were searched following the PRISMA guidelines. The key inclusion criteria were gene expression data derived from case-control studies on MI patients from blood samples. Gene expression datasets regarding the effect of medicinal drugs on MI were excluded. The t-test was applied to gene expression data from case-control studies in MI patients. RESULTS:A total of 162 articles and 174 gene expression datasets were retrieved. Of those a total of 4 gene expression datasets met the inclusion criteria, which contained data on 31,180 loci in 93 MI patients and 89 healthy individuals. Collectively, 626 differentially expressed genes were detected in MI patients as compared to non-affected individuals at an FDR q-value?=?0.01. Of those, 88 genes/gene products were interconnected in an interaction network. Totally, 15 genes were identified as hubs of the network. CONCLUSIONS:Functional enrichment analyses revealed that the DEGs and that they are mainly involved in inflammatory/wound healing, RNA processing/transport mechanisms and a yet not fully characterized pathway implicated in RNA transport and nuclear pore proteins. The overlap between the DEGs identified in this study and the genes identified through genetic-association studies is minimal. These data could be useful in future studies on the molecular mechanisms of MI as well as diagnostic and prognostic markers.

Project description:ObjectiveTo evaluate the magnitude of the association between risk factors and premature myocardial infarction (MI) (men aged 18-55 years; women aged 18-65 years).Patients and methodsWe searched MEDLINE and other databases from inception through April 30, 2020, as well as bibliography of articles selected for data extraction. We selected observational studies reporting the magnitude of the association of at least 1 risk factor (demographic characteristics, lifestyle factors, clinical risk factors, or biomarkers) with premature MI and a control group. Pooled risk estimates (random effects) from all studies unadjusted and adjusted for risk factors were reported as summary odds ratios (ORs) with 95% CIs.ResultsFrom 35,320 articles of 12.7 million participants, we extracted data on 19 risk factors from 77 studies across 58 countries. Men had a higher risk of premature MI (OR, 2.39; 95% CI, 1.71 to 3.35) than did women. Family history of cardiac disease was associated with a higher risk of premature MI (OR, 2.67; 95% CI, 2.29 to 3.27). Major modifiable risk factors associated with higher risk were current smoking (OR, 4.34; 95% CI, 3.68 to 5.12 vs no/former), diabetes mellitus (OR, 3.54; 95% CI, 2.69 to 4.65), dyslipidemia (OR, 2.94; 95% CI, 1.76 to 4.91), and hypertension (OR, 2.85; 95% CI, 2.48 to 3.27). Higher body mass index carried higher risk (OR, 1.46; 95% CI, 1.24 to 1.71 for ≥25 kg/m2 vs <25 kg/m2). Biomarkers associated with 2- to 3-fold higher risk were total cholesterol levels greater than 200 mg/dL, triglyceride levels higher than 150 mg/dL, and high-density lipoprotein cholesterol levels less than 60 mg/dL (to convert to mmol/L, multiply by 0.0259).ConclusionMajor risk factors for premature MI are mostly amenable to patient, population, and policy level interventions. Mild elevations in body mass index and triglyceride levels were associated with higher risk, which has implications for the growing worldwide epidemic of cardiometabolic diseases.

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Beta Blockade after myocardial infarction: systematic review and meta regression analysis.

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beta Blockade after myocardial infarction: systematic review and meta regression analysis.

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