Influence of prediabetes on the prognosis of patients with myocardial infarction: a meta-analysis.

BACKGROUND: Previous studies evaluating the association between prediabetes the prognosis of patients with acute myocardial infarction (AMI) showed inconsistent results. The aim of the meta-analysis was to compare the long-term incidence of major adverse cardiovascular events (MACEs) between AMI patients with prediabetes and normoglycemia. METHODS: Relevant prospective cohort studies were obtained by searching Medline, Web of Science, and Embase databases. Only studies with follow-up duration of at least one year were included. A random-effects model was utilized to pool the results by incorporating the influence of heterogeneity. RESULTS: Twelve studies with 6972 patients with AMI were included. Among them, 2998 were with prediabetes and 3974 were with normoglycemia. During a mean follow-up of 52.6 months, 2100 patients developed MACEs. Compared to those with normoglycemia, AMI patients with prediabetes were associated with a higher incidence of MACEs (risk ratio [RR]: 1.30, 95% confidence interval: 1.07 to 1.58, p = 0.008; I2 = 67%). Subgroup analysis showed a stronger association between prediabetes and MACEs in studies of patients with mean age ≥ 60 years compared to < 60 years (RR: 1.66 versus 1.10, p for subgroup difference = 0.04), with proportion of men < 75% compared to ≥ 75% (RR: 1.87 versus 1.08, p for subgroup difference = 0.01), and in prediabetes evaluated at or after discharge compared to that evaluated within three days of AMI onset (RR: 1.39 versus 0.78, p for subgroup difference = 0.01). CONCLUSIONS: Prediabetes may be associated with a higher risk of MACEs in patients with AMI.

Efficacy of Psycho-Cardiology therapy in patients with acute myocardial infarction complicated with mild anxiety and depression.

Objective: To evaluate the efficacy of Psycho-Cardiology therapy among patients with acute myocardial infarction (AMI) complicated with mild anxiety and depression. Methods: Two hundred and fifty-six patients with AMI who were admitted to the Cardiovascular Department of Chenzhou First People's Hospital from January 2018 to January 2020 were selected as subjects, and randomly divided into the control group (n = 128) and the Psycho-Cardiology treatment group (n = 128). Prior to the intervention, the general clinical data of the enrolled patients, such as gender, age, comorbidities (hypertension, diabetes) and smoking history, were compared, which revealed no statistical differences between the two groups (P > 0.05). The control group was given routine treatments such as reperfusion and secondary prevention of coronary heart disease, while the treatment group was given Psycho-Cardiology intervention in addition to the aforementioned treatments. Results: No significant differences in PHQ-9 and GAD-7 scores were observed between the control and treatment groups at admission (P > 0.05). After the Psycho-Cardiology treatment, the PHQ-9 and GAD-7 scores of the treatment group decreased significantly. Based on the 1-year post-treatment comparison, the left ventricular ejection fraction was improved more significantly in the Psycho-Cardiology treatment group, showing statistical significance (P < 0.05). The treatment group exhibited statistically significantly low incidences of adverse cardiovascular events, such as recurrent angina pectoris, heart failure, malignant arrhythmia, recurrent myocardial infarction and death (P < 0.05). Conclusions: Psycho-Cardiology therapy is remarkably efficacious in improving the anxiety, depression, cardiac function and reducing the occurrence of adverse cardiovascular events, which can better improve the long-term prognosis of patients with AMI compared to the traditional treatments.

Visceral adipose tissue-derived serine protease inhibitor accelerates cholesterol efflux by up-regulating ABCA1 expression via the NF-κB/miR-33a pathway in THP-1 macropahge-derived foam cells.

Atherosclerosis is a dyslipidemia disease characterized by foam cell formation driven by the accumulation of lipids. Visceral adipose tissue-derived serine protease inhibitor (vaspin) is known to suppress the development of atherosclerosis via its anti-inflammatory properties, but it is not yet known whether vaspin affects cholesterol efflux in THP-1 macrophage-derived foam cells. Here, we investigated the effects of vaspin on ABCA1 expression and cholesterol efflux, and further explored the underlying mechanism. We found that vaspin decreased miR-33a levels, which in turn increased ABCA1 expression and cholesteorl efflux. We also found that inhibition of NF-κB reduced miR-33a expression and vaspin suppressed LPS-mediated NF-κB phosphorylation. Our findings suggest that vaspin is not only a regular of inflammasion but also a promoter of cholesterol efflux.

Apolipoprotein A-1 binding protein promotes macrophage cholesterol efflux by facilitating apolipoprotein A-1 binding to ABCA1 and preventing ABCA1 degradation.

RATIONALE: Previous studies have shown that apolipoprotein-1 (apoA-1) binding protein (AIBP) is highly associated with the regulation of apoA-1 metabolism, suggesting its role in the treatment of atherosclerosis. However, how AIBP regulates foam cell formation remains largely unexplored. OBJECTIVE: To investigate the mechanisms underlying AIBP inhibition of foam cell formation from macrophages. METHODS AND RESULTS: THP-1-derived macrophages were incubated without or with apoA-1 and AIBP, followed by assessing the formation of foam cells and the potential mechanisms. Our results showed that AIBP and apoA-1 enhanced cholesterol efflux, altered the levels of cellular free cholesterol and cholesterol ester and prevented lipid accumulation so as to reduce the formation of foam cells. Meanwhile, lack of AIBP 115-123 amino acids resulted in the loss of AIBP binding to apoA-1. Moreover, our chemiluminescent analysis showed that AIBP promoted biotin-labeled apoA-1 binding to macrophages. Besides with AIBP, more apoA-1 bound to ABCA1, a key transporter responsible for cholesterol efflux to apoA-1, as indicated by our co-immunoprecipitation assay. Our results also showed that AIBP did not regulate ABCA1 mRNA expression, but stabilized its protein from CSN2-mediated degradation. CONCLUSIONS: AIBP promotes apoA-1 binding to ABCA1 on the cell membrane of macrophages and prevents ABCA1 protein from CSN2-mediated degradation so as to prevent foam cell formation. AIBP 115-123 amino acids is at least partially responsible for its binding to apoA-1.

Urotensin II increases foam cell formation by repressing ABCA1 expression through the ERK/NF-κB pathway in THP-1 macrophages.

OBJECTIVE: Foam cell formation in the arterial wall plays a key role in the development of atherosclerosis. Recent studies showed that Urotensin II (U II) is involved in the pathogenesis of atherosclerosis. Here we examined the effects of human U II on ATP-binding cassette transporter A1 (ABCA1) expression and the underlying mechanism in THP-1 macrophages. METHODS AND RESULTS: Cultured THP-1 macrophages were treated with U II, followed by measuring the intracellular lipid contents, cholesterol efflux and ABCA1 levels. The results showed that U II dramatically decreased ABCA1 levels and impaired cholesterol efflux. However, the effects of U II on ABCA1 protein expression and cellular cholesterol efflux were partially reversed by inhibition of extracellular signal regulated kinase 1/2 (ERK1/2) and nuclear factor kappa B (NF-κB) activity, suggesting the potential roles of ERK1/2 and NF-κB in ABCA1 expression, respectively. CONCLUSION: Our current data indicate that U II may have promoting effects on the progression of atherosclerosis, likely through suppressing ABCA1 expression via activation of the ERK/NF-κB pathway and reducing cholesterol efflux to promote macrophage foam cell formation.

Interleukin-27 inhibits foam cell formation by promoting macrophage ABCA1 expression through JAK2/STAT3 pathway.

The purpose of this study is to determine whether IL-27 regulates macrophage ABCA1 expression, foam cell formation, and also explore the underlying mechanisms. Here, we revealed that IL-27 decreased lipid accumulation in THP-1 derived macrophages through markedly enhancing cholesterol efflux and increasing ABCA1 expression at both protein and mRNA levels. Our study further demonstrated that IL-27 increased ABCA1 level via activation of signal transducer and activator of transcription 3 (STAT3). Inhibition of Janus kinase 2, (JAK2)/STAT3 suppressed the stimulatory effects of IL-27 on ABCA1 expression. The present study concluded that IL-27 reduces lipid accumulation of foam cell by upregulating ABCA1 expression via JAK2/STAT3. Therefore, targeting IL-27 may offer a promising strategy to treat atherosclerotic vascular disease.