Development and validation of a machine learning-based readmission risk prediction model for non-ST elevation myocardial infarction patients after percutaneous coronary intervention.

To investigate the factors that influence readmissions in patients with acute non-ST elevation myocardial infarction (NSTEMI) after percutaneous coronary intervention (PCI) by using multiple machine learning (ML) methods to establish a predictive model. In this study, 1576 NSTEMI patients who were hospitalized at the Affiliated Hospital of North Sichuan Medical College were selected as the research subjects. They were divided into two groups: the readmitted group and the non-readmitted group. The division was based on whether the patients experienced complications or another incident of myocardial infarction within one year after undergoing PCI. Common variables selected by univariate and multivariate logistic regression, LASSO regression, and random forest were used as independent influencing factors for NSTEMI patients' readmissions after PCI. Six different ML models were constructed using these common variables. The area under the ROC curve, accuracy, sensitivity, and specificity were used to evaluate the performance of the six ML models. Finally, the optimal model was selected, and a nomogram was created to visually represent its clinical effectiveness. Three different methods were used to select seven representative common variables. These variables were then utilized to construct six different ML models, which were subsequently compared. The findings indicated that the LR model exhibited the most optimal performance in terms of AUC, accuracy, sensitivity, and specificity. The outcome, admission mode (walking and non-walking), communication ability, CRP, TC, HDL, and LDL were identified as independent predicators of readmissions in NSTEMI patients after PCI. The prediction model constructed by the LR algorithm was the best. The established column graph model established proved to be effective in identifying high-risk groups with high accuracy and differentiation. It holds a specific predictive value for the occurrence of readmissions after direct PCI in NSTEMI patients.

The mortality for the implantable cardiac defibrillator in nonischemic cardiomyopathy: An updated systematic review and meta-analysis.

The implantable cardiac defibrillator (ICD) is common for the management of nonischemic cardiomyopathy (NICM). Mortality is a crucial issue for patients with NICM. We can understand the mortality events of ICD versus medicine treatment via a systemic review and meta-analysis of randomized clinical trials. The comparison between ICD treatment and medicine treatment was performed to find if the ICD treatment can be associated with lower relative risk and hazard ratio of mortality than the medicine treatment. In addition, the different kinds of mortality events were analyzed for the ICD treatment. After a restricted selection, 9 studies with a total of 4001 NICM patients were enrolled. The focused outcome was the events of all-cause mortality, sudden cardiac death, and cardiovascular death. The results showed that ICD treatment might be associated with lower relative risk and hazard ratio of all-cause mortality and sudden cardiac death. However, the relative risk and hazard ratio of cardiovascular mortality was not significantly different between ICD treatment and medicine treatment. In the current meta-analysis, the ICD treatment might show a lower relative risk and hazard ratio of all-cause mortality and sudden cardiac death when compared with medicine treatment. However, no significant differences were observed in cardiovascular mortality between ICD and medicine treatment.

Extracellular-vesicle containing miRNA-503-5p released by macrophages contributes to atherosclerosis.

Endothelial dysfunction, and the differentiation of smooth muscle cells (SMCs) into proliferative, secretory phenotypes, are two major pathophysiological processes in atherosclerosis. SMCs have the potential to recruit macrophages in atherosclerotic plaques, in which macrophages drive inflammatory responses. In this study, we found that microRNA-503-5p (miR-503-5p) was enriched in either extracellular vesicles (EVs), secreted by oxidized low-density lipoprotein-treated macrophages, or the EVs from peripheral blood mononuclear cells of atherosclerosis patients. miR-503-5p was transferred intercellularly from macrophages to the co-cultured human coronary artery endothelial cells (HCAECs) and HCASMCs via EVs, thus reducing the proliferative and angiogenic abilities of HCAECs and accelerating the proliferative and migrating abilities of HCASMCs. Smad family members 1, 2 and 7 were negatively regulated by miR-503-5p in HCAECs and HCASMCs. miR-503-5p was verified as an enhancer of inflammatory cytokines and adhesion molecules released by macrophages, in part via the down-regulation of smad family members 1, 2 and 7. The inhibition of miR-503-5p by lentivirus reduced atherosclerotic lesion formations in the aorta of atherosclerotic mice. Our work demonstrated a miR-503-5p- and EV-mediated mechanism for macrophage communication with HCAECs and HCASMCs in atherosclerosis. miR-503-5p is pro-atherosclerotic stimuli that may be a therapeutic target for atherosclerosis treatment.

Mechanical chest compression with LUCAS device does not improve clinical outcome in out-of-hospital cardiac arrest patients: A systematic review and meta-analysis.

BACKGROUND: Cardiac arrest (CA) is a serious threat to human health. Cardiopulmonary resuscitation (CPR) is an effective treatment for CA. Early and high-quality CPR is closely related to the survival rate of patients with CA. But manual chest compression has a lot of defects. To solve the defects and improve the quality of CPR, mechanical CPR device was invented. However, it has still controversy whether manual chest compression or mechanical chest compression is better. This systematic review was aimed to investigate the difference in clinical outcomes between manual chest compression and Lund University Cardiac Assist System (LUCAS) assisted CPR in patients with out-hospital CA. METHODS: Original research studies, conducted on adult out-of-hospital CA, were included. PubMed/Medline, EMBASE, Scopus, Cochrane Library, CNKI, and Wanfang database were searched from the setting to February 21, 2019. Odds ratio (OR) with 95% confidence interval (CI) was selected as effect scale index for evaluation of the difference in return of spontaneous circulation (ROSC), survival to hospital admission, survival to hospital discharge, and survival to 30 days. Random effects model was used in this study to estimate overall mean effects. RESULTS: A total of 6 articles, including 4 randomized controlled trials and 2 nonrandomized controlled trials, were selected. And 8501 subjects were involved to analyze the clinical outcomes of LUCAS and manual chest compression for patients with out-hospital CA. Comparisons of ROSC (33.3% vs 33.0%, P = .98; OR = 1; 95% CI: [0.89,1.13]), survival to hospital admission (22.7% vs 24.3%, P = .32; OR = 0.86; 95% CI: [0.65,1.15]), survival to hospital discharge (8.6% vs 10.7%, P = .50; OR = 0.92; 95% CI: [0.73,1.17]), and survival to 30 days (7.5% vs 8.5%, P = .50; OR = 0.92; 95% CI: [0.73,1.17]) were made. No significant difference was found. CONCLUSION: The synthesis of available evidence does not support that mechanical chest compression with LUCAS device improves clinical outcome in out-of-hospital CA patients compared with manual chest compression. Large scale studies with improved designs are still needed in the future.

Effect of paeoniflorin on cardiac remodeling in chronic heart failure rats through the transforming growth factor ß1/Smad signaling pathway.

BACKGROUND: Cardiac remodeling is an important mechanism for the occurrence and development of chronic heart failure (CHF). Paeoniflorin (Pae) is the main active ingredient of Chinese herbaceous peony and has novel anti-inflammatory effect. This study was conducted to assess the effects and mechanisms of Pae on cardiac remodeling in CHF rats. METHODS: A cardiac remodeling rat model was induced by isoprenaline (Iso). Pae (20 µg/kg/d) was administrated to CHF rats for six weeks. Cardiac ultrasound was used to assess the structure and function of CHF rats. Collagen volume fraction (CVF) and perivascular collagen volume area of myocardial tissues were calculated. With real-time polymerase chain reaction and Western blot, the protein and mRNA levels of transforming growth factor ß1 (TGF-ß1) and Smad3 were detected. RESULTS: Compared to Iso group, Pae can alleviate cardiac remodeling and improve cardiac function in CHF rats. The levels of CVF and perivascular collagen volume area reduced in Pae group (P<0.05). The expression of TGF-ß1 and Smad3 protein decreased in Pae and Cap group (P<0.05). Further, the expression of TGF-ß1 and Smad3 mRNA also decreased markedly in the Pae group (P<0.05). CONCLUSIONS: Pae could attenuate cardiac remodeling and improve cardiac function in CHF rats. The potential mechanism for the cardioprotective effect of Pae may be highly associated with the down-regulating of TGF-ß1/Smad signaling pathway.

Association between serum adropin level and coronary artery disease: a systematic review and meta-analysis.

BACKGROUND: Recent studies have found that adropin is associated with coronary artery disease (CAD). This meta-analysis sought to assess the relationship between serum adropin level and CAD. METHODS: Online databases including the Cochrane Library, PubMed, EMbase, Ovid, CBM, CNKI, VIP and WanFang Data were electronically searched for the clinical study concerning the relationship between serum adropin levels and CAD, including acute myocardial infarction (AMI), unstable angina pectoris (UAP), and stable angina pectoris (SAP). Two reviewers independently screened literature, extracted data and assessed methodological quality of included studies. Standard mean difference (SMD) with its 95% confidence interval (CI) was used as the effect size in this study. Then meta-analysis was performed using RevMan 5.2 software. RESULTS: A total of seven articles involved 945 participants were included. The results indicated that serum adropin level in CAD group was lower than healthy control group (SMD =-2.44, P=0.0008). In the subgroup analysis, the levels of serum adropin in AMI group (SMD =-2.96, P<0.00001), UAP group (SMD =-2.09, P=0.0001) and SAP group (SMD =-1.23, P=0.007) were also lower than that of healthy control. CONCLUSIONS: Serum adropin level in patients with CAD was lower than healthy individuals, indicating that the decrease of adropin concentration might play an important role in the development of CAD.