Objective
The 30‐day readmission is associated with increased medical costs, which has become an important quality metric in several medical institutions. This current study is aimed at clarifying the prevalence, the underlying risk factors, and reasons of the 30‐day readmission after acute myocardial infarction (AMI).
Methods
PubMed, Cochrane Library, and EMBASE were systematically searched to identify eligible studies. Random‐effect models were employed to perform pooled analyses. Means and 95% confidence intervals (CIs) were used to estimate prevalence and reasons for 30‐day readmission. We also used Odds ratios (ORs) to explore the potential significant predictors of risk factors of 30‐day readmission after AMI. Potential publication bias was assessed using funnel plot and Begg'test.
Results
A total of 14 relevant studies were included in this systematic review and meta‐analysis. The pooled 30‐day readmission rate of AMI was 12% (95% CI 0.11‐0.14). Acute coronary syndrome (ACS), angina and acute ischemic heart disease, and heart failure (HF) were the principal cardiovascular reasons of 30‐day readmission. Meanwhile, non‐specific chest pain was regarded as the significant cause among non‐cardiovascular reasons. The common co‐morbidities kidney disease, HF and diabetes mellitus were significant risk factors for 30‐day readmission. No significant publication bias was found by funnel plot and statistical tests.
Conclusions
The 30‐day readmission rate of post‐AMI ranged from 11% to 14% and can be mainly attributed to cardiovascular and non‐cardiovascular events. The common co‐morbidities, such as kidney disease, HF, and diabetes mellitus were significant risk factors for 30‐day readmission.
Myocardial infarction (MI) is a severe cardiovascular disease. Some M1 macrophage-derived extracellular vesicles (EVs) are involved in the inhibition of angiogenesis and acceleration dysfunction during MI. However, the potential mechanism of M1 phenotype bone marrow-derived macrophages- (BMMs-) EVs (M1-BMMs-EVs) in MI is largely unknown. This study sought to investigate whether M1-BMMs-EVs increased CDC42 expression and activated the MEK/ERK pathway by carrying lncRNA MALAT1 and competitively binding to miR-25-3p, thus inhibiting angiogenesis and myocardial regeneration after MI. After EV treatment, the cardiac function, infarct size, fibrosis, angiogenesis, and myocardial regeneration of MI mice and the viability, proliferation and angiogenesis of oxygen-glucose deprivation- (OGD-) treated myocardial microvascular endothelial cells (MMECs) were assessed. MALAT1 expression in MI mice, cells, and EVs was detected. MALAT1 downstream microRNAs (miRs), genes, and pathways were predicted and verified. MALAT1 and miR-25-3p were intervened to evaluate EV effects on OGD-treated cells. In MI mice, EV treatment aggravated MI and inhibited angiogenesis and myocardial regeneration. In OGD-treated cells, EV treatment suppressed cell viability, proliferation, and angiogenesis. MALAT1 was highly expressed in MI mice, OGD-treated MMECs, M1-BMMs, and EVs. Silencing MALAT1 weakened the inhibition of EV treatment on OGD-treated cells. MALAT1 sponged miR-25-3p to upregulate CDC42. miR-25-3p overexpression promoted OGD-treated cell viability, proliferation, and angiogenesis. The MEK/ERK pathway was activated after EV treatment. Collectively, M1-BMMs-EVs inhibited angiogenesis and myocardial regeneration following MI via the MALAT1/miR-25-3p/CDC42 axis and the MEK/ERK pathway activation.
The aim of this study is to determine miR-22 expression levels in peripheral blood mononuclear cells (PBMCs) of patients with coronary artery disease (CAD) and to investigate whether MCP-1 expression is regulated by miR-22. miR-22 expression in PBMCs from 60 CAD patients including stable angina pectoris (SAP) (n = 29), unstable angina pectoris (UAP) or non-ST elevation myocardial infarction (NSTEMI) (n = 17), or ST-elevation MI (STEMI) (n = 14) and 20 non-CAD subjects by real-time polymerase chain reaction (qRT-PCR). The luciferase activity assays were employed to determine whether miR-22 binds to 3′UTR of MCP-1. miR-22 mimics and inhibitors were transfected into healthy PBMCs. MCP-1 mRNA and protein levels were determined by qRT-PCR and enzyme-linked immuno sorbent assay, respectively. The qRT-PCR results showed that miR-22 levels in PBMCs were decreased in CAD patients, and MCP-1 was augmented in CAD patients and was inversely correlated with miR-22 levels. The luciferase activity assays indicated that MCP-1 was a target of miR-22. Overexpression of miR-22 could significantly repress MCP-1 expression at both mRNA and protein levels in PBMCs, whereas inhibition of miR-22 showed the opposite effects. This study revealed that miR-22 is downregulated in PBMCs from patients with CAD and that miR-22 may participate in inflammatory response by targeting MCP-1, therefore contributing CAD.
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