Objectives This study aimed to evaluate the efficacy and safety of AngioJet rheolytic thrombectomy with the adjunctive use of glycoprotein IIb/IIIa inhibitors (GPI) in the setting of ST-segment elevation myocardial infarction (STEMI). Methods We conducted a retrospective cohort study of 877 consecutive patients with STEMI. Propensity score matching (PSM) was employed to balance the baseline characteristics between the group receiving AngioJet rheolytic thrombectomy plus GPI (the AT + GPI group) and those receiving routine treatment (the RT group). The primary endpoint was major adverse cardiovascular and cerebrovascular events (MACCE) at 1 year. Safety endpoints comprised any bleeding and major bleeding events. Results Ninety-seven patients received AngioJet rheolytic thrombectomy and GPI. No significant differences were observed between the two groups regarding in-hospital mortality, reinfarction, stent thrombosis, stroke, or bleeding. After propensity-score matching, the cumulative incidence of MACCE at 1 year did not differ significantly between the AT + GPI group and the RT group (8.2% vs 9.3%; hazard ratio, 0.894; 95% CI, 0.345 to 2.318; p = 0.818). The incidence rates of all individual safety endpoints—including stroke and bleeding—showed no significant differences between the two groups. Conclusions In this observational cohort of STEMI patients, the strategy of combining AngioJet rheolytic thrombectomy with GPI was not associated with improved 1-year outcomes compared to routine treatment, though it did not increase bleeding or stroke risk.
Objectives This study aimed to identify clinical predictors of initial TIMI thrombus grade 5 (TG 5) and to evaluate its association with one‑year major adverse cardiovascular and cerebrovascular events (MACCE) in patients with ST‑segment elevation myocardial infarction (STEMI). Methods This single‑center retrospective cohort study enrolled 823 consecutive STEMI patients between October 2014 and April 2019, of whom 554 presented with initial TG 5 and 269 did not. Inverse probability of treatment weighting (IPTW) was applied to balance baseline covariates. Multivariable logistic regression was used to identify predictors of TG 5, and Cox proportional hazards models were fitted to assess the association between TG 5 and one‑year clinical outcomes. Results Delayed PCI (> 12 hours) (OR: 4.219; 95% CI: 2.915–6.098; P < 0.001), smoking history (OR: 1.606; 95% CI: 1.177–2.190; P = 0.003), and higher BMI (OR per 1 kg/m² increase: 1.070; 95% CI: 1.021–1.121; P = 0.004) were independently associated with initial TG 5. After IPTW adjustment, there were no significant differences between the TG 5 and non‑TG 5 groups in one‑year MACCE (adjusted OR: 0.782; 95% CI: 0.501–1.220; P = 0.278) or all‑cause mortality (adjusted OR: 0.797; 95% CI: 0.473–1.341; P = 0.393). Although the TG 5 group had a higher crude incidence of heart failure, the difference was attenuated after adjustment (P = 0.054). Rehospitalization for ischemic events was significantly lower in the TG 5 group after adjustment (adjusted OR: 0.395; 95% CI: 0.184–0.850; P = 0.018). Initial Killip class ≥ II (HR: 5.099; 95% CI: 3.509–7.408; P < 0.001), delayed PCI (HR: 1.697; 95% CI: 1.025–2.810; P = 0.040), and older age (HR: 1.038; 95% CI: 1.021–1.056; P < 0.001) were independently associated with MACCE, whereas TG 5 was not (HR: 0.765; 95% CI: 0.507–1.156; P = 0.204). Conclusions Delayed PCI, smoking, and higher BMI are strong independent predictors of initial TG 5 in STEMI patients. Although this angiographic phenotype reflects severe coronary occlusion, it is not independently associated with increased one‑year MACCE or all‑cause mortality after rigorous adjustment.
BACKGROUND:High-altitude cerebral edema (HACE) leads to cognitive decline, but the underlying cellular and molecular mechanisms remain unclear. METHODS:We established a mouse model of HACE under hypobaric hypoxia (simulating at an altitude of 6000 m) and analyzed hippocampal changes using single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) at 3 days and 7 days post-exposure. RESULTS:Hypobaric hypoxia induced HACE and cognitive decline by altering the transcriptomic profiles and interactions of oligodendrocytes (MOL and MOL2) and neurons (ExN-L6-CT-2). Early upregulation of PI3K/mTOR in oligodendrocytes mitigated Rps29-bax-mediated ribosomal stress and oxidative phosphorylation, promoting survival and myelin repair. Prolonged hypoxia suppressed PI3K/mTOR, triggering apoptosis/autophagy via oxidative phosphorylation and ribosomal stress. Enhanced Tnfrsf21-App interactions between MOL2 and ExN-L6-CT-2 exacerbated neuroinflammation and cognitive decline. CONCLUSIONS:Our study reveals that HACE-induced cognitive impairment is closely associated with dysregulated ribosomal stress and oxidative phosphorylation and impaired neuroactive ligand-receptor interactions. Furthermore, we identify PI3K/mTOR dynamics, Rps29-bax-axis, and Tnfrsf21-App as novel regulators, offering potential therapeutic targets.
Tracheal reconstruction presents a significant global clinical challenge due to the unique structure and function of the trachea, which complicates its repair. Key challenges include restoring tracheal function post-transplantation, managing surgical complications, and ensuring the long-term survival of transplanted tissue. Furthermore, adequate vascularization of the transplanted trachea, along with the repair of cartilage and epithelial cells, is critical for facilitating functional recovery and successful reconstruction. In this study, a decellularized tracheal matrix was extracted to preserve its natural bioactivity. Nanoclay and GelMA were then employed as carrier materials to integrate with the decellularized tracheal matrix, forming a hydrogel scaffold. Both nanoclay and GelMA offer tunable porous structures and surface properties that promote cell adhesion and proliferation, while providing sufficient mechanical support. By leveraging the biological functions of endothelial progenitor cell-derived exosomes, we successfully loaded exosomes onto the decellularized extracellular matrix, creating a novel cell-free tracheal scaffold for investigating tracheal defect repair. The scaffold exhibited excellent biocompatibility, promoting graft vascularization and facilitating the repair of tracheal cartilage and epithelium. These findings hold significant promise for advancing tracheal reconstruction surgery and offer valuable insights for future research in this area.
BackgroundChronic high-altitude hypobaric hypoxia leads to high-altitude heart disease and heart failure. Recent research has indicated that WJMSCs (Wharton’s jelly-derived mesenchymal stem cells, WJMSCs) can alleviate ischemic myocardial injury and improve cardiac dysfunction, and macrophage polarization may have been involved. However, few studies have focused on the cardioprotective effects of WJMSCs against HAHI (high-altitude-induced heart injury, HAHI). Here, our research focused on how WJMSCs regulate macrophage polarization impacted myocardial repair in HAHI.MethodsC57/BL6J mice were fed for 28 days at a hypobaric chamber that had a comparable altitude of 6000 m, and WJMSCs were injected intravenously before HH (hypobaric hypoxia, HH) exposure. To assess cardiac function, echocardiography was carried out. Blood and heart tissue were collected for subsequent analysis. We simulated anoxic environment in vitro by inducing BMDMs (bone marrow-derived macrophages, BMDMs) with 1% O2, and employed co-culture system to investigate how WJMSCs affect macrophage polarization.ResultsAbnormal myocardial fibrosis and cardiomyocyte apoptosis, cardiac inflammation and dysfunction were exhibited in the Chronic HAHI mouse model. WJMSCs infusion maintained the cardiac structure and function in HAHI mice. Furthermore, WJMSCs infusion was effective in elevating the M2 macrophages proportion and decreasing inflammation in the heart. In vitro studies revealed that hypoxia stimulation elevated the ratio of M1 macrophages in comparison to those in the Control group and coculturing with WJMSCs encouraged the shift of M1 to M2 macrophages. Surprisingly, the anti-inflammatory effects of WJMSCs on M2 polarization were negated with pretreatment of a COX2 (Cyclooxygenase-2, COX2) inhibitor, which could be reversed with PGE2 (prostaglandin E2, PGE2) addition.ConclusionsIn conclusions, our findings indicated that WJMSCs infusions may enhance M2 macrophage polarization through the COX2-PGE2 pathway, and therefore safeguard against cardiac damage in HAHI mice.
The impact of incorporating immune checkpoint inhibitors (ICIs) into standard chemotherapy on the severity and risk of myelosuppression in advanced non-small cell lung cancer (NSCLC) patients remains uncertain. We conducted a systematic review and meta-analysis of phase 3 randomized controlled trials (RCTs) that evaluated ICIs in people with NSCLC. A comprehensive search of four databases, PubMed, Web of Science, Embase, and the Cochrane Library, was carried out from inception to 30 October 2023. Pooled analyses assessed the risk ratios (RR) for treatment-related hematological adverse events greater than or equal to grade 3. The protocol is registered with PROSPERO and has the CRD42024500056 registration number. Twenty-three phase 3 RCTs were contained, involving 15,844 people with NSCLC receiving ICIs with or without chemotherapy. Compared with chemotherapy alone, ICI monotherapy or dual immunotherapy reduced treatment-associated leukopenia (relative risk (RR) 0.03, 95
BackgroundCardiovascular diseases caused by atherosclerosis (AS) are the leading causes of disability and death worldwide. Apolipoprotein B (ApoB), the core protein of low-density lipoproteins, is a major contributor to cardiovascular disease-related morbidity and mortality, with apolipoprotein B (ApoB) playing a critical role in its pathogenesis. However, no bibliometric studies on the involvement of ApoB in AS have been published. This study aimed to conduct a comprehensive bibliometric analysis to explore the current and future trends regarding the role of ApoB in AS.MethodsUtilizing the Web of Science Core Collection, a thorough search was conducted for ApoB in AS-related papers related to research on ApoB in the field of AS during 1991-2023. The analysis focused on annual publication trends, leading countries/regions and institutions, influential authors, journal and key journals. CiteSpace and VOSviewer were employed to visualize reference co-citations, and keyword co-occurrences, offering insights into the research landscape and emerging trends.ResultsThis bibliometric analysis employed network diagrams for cluster analysis of a total of 2105 articles and reviews, evidencing a discernible upward trend in annual publication volume. This corpus of research emanates from 76 countries/regions and 2343 organizations, illustrating the widespread international engagement in ApoB-related AS studies. Notably, the United States and the University of California emerge as the most prolific contributors, which underscores their pivotal roles in advancing this research domain. The thematic investigation has increasingly focused on elucidating the mechanistic involvement of ApoB in atherosclerosis, its potential as a diagnostic biomarker, and its implications for therapeutic strategies.ConclusionThis bibliometric analysis provides the first comprehensive perspective on the evolving promise of ApoB in AS-related research, emphasizing the importance of this molecule in opening up new diagnostic and therapeutic avenues. This study emphasizes the need for continued research and interdisciplinary efforts to strengthen the fight against AS. Furthermore, it emphasizes the critical role of international collaboration and interdisciplinary exploration in leveraging new insights to achieve clinical breakthroughs, thereby addressing the complexities of AS by focusing on ApoB.
BACKGROUND:The ratio of nonhigh-density lipoprotein cholesterol (non-HDL-C) to high-density lipoprotein cholesterol (HDL-C) has been shown associated with various metabolic diseases and atherosclerosis in primary prevention. However, there is limited evidence on the relationship between the non-HDL-C/HDL-C ratio and progression of nonculprit coronary lesion (NCCL) after percutaneous coronary intervention (PCI). HYPOTHESIS:Our study aimed to investigate the potential association between the non-HDL-C/HDL-C ratio and NCCL progression in patients with acute coronary syndrome (ACS) undergoing PCI. METHODS:We conducted a retrospective analysis of ACS patients who underwent coronary angiography twice at a single center from 2016 to 2022. Lipid measurements, demographic, clinical, and other laboratory data were collected from electronic medical records. NCCLs were evaluated using quantitative coronary angiography. The primary outcome was the progression of NCCL. Patients were categorized based on NCCL progression and tertiles of the non-HDL-C/HDL-C ratio. Associations were analyzed using univariate and multivariate logistic regression analysis. RESULTS:The study included 329 ACS patients who underwent PCI, with a median follow-up angiography of 1.09 years. We found NCCL progression in 95 (28.9%) patients with acceptable low-density lipoprotein cholesterol control (median: 1.81 mmol/L). Patients in the top tertile of the non-HDL-C/HDL-C ratio had a higher risk of NCCL progression. After adjusting for potential confounding factors, the non-HDL-C/HDL-C ratio remained a significant predictor for NCCL progression (adjusted odds ratio: 1.45; 95% confidence interval: 1.14-1.86; p < 0.05). CONCLUSIONS:The non-HDL-C/HDL-C ratio predicts NCCL progression in ACS patients following PCI, providing a valuable tool for risk assessment and enhancing secondary prevention of atherosclerotic cardiovascular disease.
Acute myocardial infarction (AMI) causes acute cardiac cell death when oxygen supply is disrupted. Improving oxygen flow to the damaged area could potentially achieve the to prevent cell death and provide cardiac regeneration. Here, we describe the production of oxygen-producing injectable bio-macromolecular hydrogels from natural polymeric components including gelatin methacryloyl (GelMA), hyaluronic acid (HA) loaded with catalase (CAT). Under hypoxic conditions, the O-2-generating hydrogels (O-2 (+) hydrogel) encapsulated with Mesenchymal stem cells (MSCs)-derived-exosomes (Exo- O-2 (+) hydrogel) released substantial amounts of oxygen for >5 days. We demonstrated that after 7 days of in vitro cell culture, exhibits identical production of paracrine factors compared to those of culture of rat cardiac fibroblasts (RCFs), rat neonatal cardiomyocytes (RNCs) and Human Umbilical Vein Endothelial Cells (HUVECs), demonstrating its ability to replicate the natural architecture and function of capillaries. Four weeks after treatment with Exo-O-2 (+) hydrogel, cardiomyocytes in the peri-infarct area of an in vivo rat model of AMI displayed substantial mitotic activity. In contrast with infarcted hearts treated with O-2 (-) hydrogel, Exo- O-2 (+) hydrogel infarcted hearts showed a considerable increase in myocardial capillary density. The outstanding therapeutic advantages and quick, easy fabrication of Exo- O-2 (+) hydrogel has provided promise favourably for potential cardiac treatment applications.
BACKGROUND:Type 2 diabetes mellitus (T2DM), characterized by β-cell dysfunction and insulin resistance (IR), presents considerable treatment challenges. Apelin is an adipocyte-derived factor that shows promise in improving IR; however, it is limited by poor targeting and a short half-life. In the present study, engineered small extracellular vesicles (sEVs) derived from Wharton's jelly-derived mesenchymal stem cells (WJ-MSCs) loaded with apelin were used to address the limitations of the therapeutic application of apelin.METHODS:WJ-MSCs were transduced to obtain engineered sEVs loaded with overexpressed apelin (apelin-MSC-sEVs) and the control sEVs (MSC-sEVs). T2DM mice were injected with apelin-MSC-sEVs and MSC-sEVs, and blood glucose monitoring, glucose and insulin tolerance tests, confocal microscopy, and immunocytochemical analysis were performed. IR models of 3T3-L1 adipocytes were employed to detect GLUT4 expression in each group using western blotting; the affected pathways were determined by measuring the changes in Akt and AMPK signaling and phosphorylation.RESULTS:Upon successful engineering, WJ-MSCs demonstrated significant overexpression of apelin. The genetic modification did not adversely impact the characteristics of sEVs, ranging from surface protein markers, morphology, to particle size, but generated apelin-overexpressed sEVs. Apelin-MSC-sEVs treatment resulted in notable enhancement of Akt and AMPK pathway activities within 3T3-L1 adipocytes and adipose tissues of T2DM mice. Furthermore, the apelin-loaded sEVs significantly reduced plasma glucose levels, increased pancreatic β-cell proliferation, improved insulin and glucose tolerance, and modulated pro-inflammatory cytokine profiles, compared to mice treated with the control sEVs.CONCLUSION:Our study developed novel genetically engineered apelin-loaded sEVs derived from WJ-MSCs, and demonstrated their potent role in augmenting insulin sensitivity and regulating inflammatory responses, highlighting their therapeutic promise in T2DM management. The findings open new avenues for the development of clinically viable treatments for T2DM in humans using the apelin-loaded sEVs.
OBJECTIVE:Polydopamine nanoparticles (PDA NPs) are a promising topic in the fields of drug delivery, tissue engineering, bioimaging, etc. The present study aims to explore the impact of PDA NPs carrying ferroptosis inhibitor ferstatin-1 (Fer-1) on myocardial ischemia-reperfusion injury (MIRI).METHODS:After establishment of a rat model of MIRI and PDA NPs, the rats were divided into 4 groups: model group, sham operation group, Fer-1 group, and nano+Fer-1 group (n=8). To detect the effect of PDA NPs encapsulating Fer-1 on ferroptosis in MIRI rats, we further set up NOX4 overexpression group (pc-NOX4 group), NOX4 inhibitor group (Fulvene-5 group), nano+Fer-1+pc-NOX4 group, and nano+Fer-1+Fulvene-5 group (n=8). A CCK-8 assay was conducted to assess cell viability and staining to detect cardiomyocyte apoptosis and observe myocardial infraction.RESULTS:PDA NPs loaded with Fer-1 were successfully prepared with good safety and biocompatibility. Administration of PDA NPs carrying Fer-1 notably alleviated myocardial injury and hindered the process of ferroptosis in MIRI rats when inducing downregulation of NOX4 expression. Additionally, overexpression of GPX4 significantly attenuated myocardial injury in MIRI rats. While Fer-1 was shown to inhibit the expression of NOX4, the NOX4 inhibitor Fulvene-5 greatly elevated GPX4 and FTH1 expression in cardiomyocytes, and down-regulated the content of Fe2+, especially in the nanometer+Fer-1+Fulvene-5 group.CONCLUSION:With promising safety and biocompatibility, PDA NPs encapsulated Fer-1 decrease GPX4 and FTH1 expression by inhibiting the level of NOX4 in myocardial cells of MIRI rats, thereby suppressing ferroptosis of cardiomyocytes and alleviating myocardial injury.
Cardiovascular diseases (CVDs) constitute a significant global health concern with a profound impact on mortality rates. Recent advancements in artificial intelligence (AI) have facilitated the successful application of automated classification methods for cardiac arrhythmias. This paper introduces “Auto-FS-Cardiac,” an innovative automated feature selection model. Leveraging Automated Machine Learning (Au-toML) and the Tree-based Pipeline Optimization Tool (TPOT) framework, the model constructs a classification pipeline aimed at distinguishing between five distinct heartbeats in electro-cardiogram (ECG) data sourced from the MIT-BIH database. The study evaluates the performance of Auto-FS-Cardiac under both automated and predefined human-expert feature selection scenarios. Additionally, a comparative analysis with traditional feature selection models provides insights into the proficiency of Auto-FS-Cardiac in generating optimal pipelines for precise ECG heartbeat classification. Auto-FS-Cardiac performance, achieved an accuracy level of 0.9569 with a rapid execution time of 1.9857 seconds. Notably, when utilizing predefined features, the model maintains a consistent accuracy score of 0.9522, albeit with a longer execution time of 14.7836 seconds. This highlights the model's adaptability in balancing high accuracy and efficiency when autonomously managing the feature selection process. The observed tradeoff between efficiency and interpretability suggests that interventions in feature selection may impact these factors.
Using wearable devices to extract physiological information to identify and classify human emotion is a common research problem in human-computer interaction. From a computational point of view, emotion is difficult to quantify, estimate, and understand. However, indications of human cognitive and emotional related processes affect a variety of derived changes in many human psychological signals. These signals can help to build a quantitative model of emotion. We design and build a set of wearable hardware to acquisit, extract and process Multi-layer Electrodermal activity(MEDA) physiological signal data,and bulid neural network models based on the MEDA data. We build the dataset useing videos that can trigger happiness, sadness, anger, etc. For the annotated and sorted data set, we build a multilayer neural network model to perform feature extraction, mapping, and recognition from MEDA to emotions. Ablation experiments and results comparison are carried out for each model. Experiments show the hybrid model: end-to-end convolutional neural network with bidirectional long short-term memory network(MEDA-CBLSTM) achieves the best result. The model trained by the train set of testers achieves an average accuracy of 92.31% in their corresponding test set, but the accuracy reduces when it is tested on the other test sets. Therefore, we get the conclusion:the EDA emotion data has the characteristics of highly subject dependence.
Background: Apelin, an emerging endogenous peptide ligand, has been associated with insulin resistance, but the precise mechanism of its influence remains unclear. This study aims to determine the effect of Apelin on insulin resistance and glucose metabolism in 3T3-L1 adipocytes.Methods: Insulin resistance was induced in 3T3-L1 adipocytes through tumor necrosis factor-alpha treatment, followed by infection with Apelin-containing lentivirus particles. Apelin gene expression was confirmed by fluorescence microscope, reverse transcription polymerase chain reaction (RT-PCR), and western blot analysis. Glucose utilization was measured by a glucose uptake assay. The expressions of protein kinase B (AKt) and endothelial nitric oxide synthase (eNOS) were detected by RT-PCR and western blot. The RT-PCR evaluated the inflammatory cytokines interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and anti-inflammatory factors adiponectin.Results: The translocation of glucose transporter 4 (GLUT4) was detected by flow cytometry. Apelin overexpression in insulin resistant 3T3-L1 adipocytes resulted in a 35% (p < 0.01) increase in glucose uptake when stimulated with insulin. Apelin over expression facilitated the translocation of GLUT4 from the cytoplasm to the plasma membrane and elevated AKt and eNOS levels. Furthermore, Apelin overexpression led to an up-regulation of adiponectin mRNA and reduced TNF-alpha and IL-6 mRNA expressions.Conclusions: This study shows that Apelin stimulates GLUT4 translocation and improves glucose utilization through the AKt and eNOS pathways. Apelin can potentially enhance the mechanism of insulin resistance by mediating the inflammatory response in 3T3-L1 adipocytes.
患者女性,93岁,因完全房室传导阻滞入院.在植入起搏器的过程中,遇到双侧锁骨下静脉迂曲,导丝没能通过.为了绕过迂曲部分,尝试在右侧锁骨中线内侧穿刺,静脉造影显示穿刺针进入了上腔静脉.经讨论后决定,采用上腔静脉植入,手术成功完成,没有围手术期并发症.2个月后随访,起搏器工作良好.提示在通过传统路径植入起搏电极导线困难时,直接穿刺上腔静脉植入是可能的.
The safety and effectiveness of remote guidance of percutaneous coronary interventions (PCI) have not been fully appraised in controlled studies. We hereby presented the results of a study on remote guidance (vs on-site guidance) of PCI to explore its feasibility, safety, and effectiveness. Patients were recruited from those who received PCI procedures from January 2018 to June 2019 in a secondary hospital (Jincheng, Shanxi, China), in collaboration with a tertiary medical center (Beijing, China) approximately 680 km away. According to the type of guidance during the procedure, the patients were assigned to two groups: the remote guidance group and the on-site guidance group. Remote guidance was assisted with an advanced commercial telemedicine system. Interventional strategies, procedural success rate, peri-procedural complications, procedural duration, radiation doses, and the amount of contrast medium were compared between the two groups. A total of 352 patients were included in this study, with a total of 411 PCI procedures and 446 target lesions. The baseline clinical characteristics, as well as the distribution and characteristics of coronary artery lesions, did not differ significantly between the two groups. No significant differences were noticed in procedural success rate, peri-procedural complications, procedural duration, radiation dose, and in-hospital major adverse cardiovascular events. However, the amount of contrast medium was slightly higher in the remote guidance group. The results of the present pilot study showed the feasibility of remotely guided PCI, with safety and effectiveness measures at acceptable levels comparable to the traditional on-site guidance. Randomized studies with long-term follow-up are warranted to further confirm our findings.
Objective This study aimed to evaluate predictors for adverse cardiovascular outcomes in patients with atrial fibrillation (AF) undergoing coronary stenting. Methods We retrospectively recruited consecutive patients with previously documented non-valvular AF who underwent coronary stenting between January 2010 and June 2015 in 12 hospitals of Beijing, China. Major adverse cardiac/cerebrovascular events (MACCE) were a composite of all-cause death, non-fatal myocardial infarction, repeat revascularization, and ischaemic stroke/systemic thromboembolism (IS/STE). Major bleeding referred to grade 2 or higher of Bleeding Academic Research Consortium criteria. Results A total of 2394 patients (men: 72.3% vs. women: 27.7%, median age: 67 years) were included. The CHA(2)DS(2)-VASc and HAS-BLED were 3.6 +/- 1.6 and 1.9 +/- 0.7, respectively. The median follow-up duration was 36.2 months. There were 230 (9.6%) deaths, 96 (4.0%) IS/STE, 426 (17.8%) MACCE, and 72 (3.0%) major bleeding. Multivariate Cox regression yielded predictive models for (1) all-cause death: diabetes, prior myocardial infarction, chronic kidney disease (CKD), ST-segment elevation myocardial infarction (STEMI) at presentation, heart failure, no use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and statins; (2) IS/STE: advanced age, prior history of ischaemic stroke and intracranial haemorrhage; (3) MACCE: prior history of myocardial infarction and ischaemic stroke, CKD, STEMI, heart failure, and no statin use; (4) major bleeding: prior major bleeding, prior myocardial infarction, CKD and use of oral anticoagulants. Conclusion Chinese patients with AF and coronary stenting had high mortality and incidence of MACCE. We compiled separate predictive models for all-cause death, IS/STE, MACCE, and major bleeding.
Objective Our aim was to evaluate the efficacy and safety of intracoronary autologous bone marrow mesenchymal stem cell (BM-MSC) transplantation in patients with ST-segment elevation myocardial infarction (STEMI). Methods In this randomized, single-blind, controlled trial, patients with STEMI (aged 39–76 years) were enrolled at 6 centers in Beijing (The People’s Liberation Army Navy General Hospital, Beijing Armed Police General Hospital, Chinese People’s Liberation Army General Hospital, Beijing Huaxin Hospital, Beijing Tongren Hospital, Beijing Chaoyang Hospital West Hospital). All patients underwent optimum medical treatment and percutaneous coronary intervention and were randomly assigned in a 1:1 ratio to BM-MSC group or control group. The primary endpoint was the change of myocardial viability at the 6th month’s follow-up and left ventricular (LV) function at the 12th month’s follow-up. The secondary endpoints were the incidence of cardiovascular event, total mortality, and adverse event during the 12 months’ follow-up. The myocardial viability assessed by single-photon emission computed tomography (SPECT). The left ventricular ejection fraction (LVEF) was used to assess LV function. All patients underwent dynamic ECG and laboratory evaluations. This trial is registered with ClinicalTrails.gov, number NCT04421274. Results Between March 2008 and July 2010, 43 patients who had underwent optimum medical treatment and successful percutaneous coronary intervention were randomly assigned to BM-MSC group ( n = 21) or control group ( n = 22) and followed-up for 12 months. At the 6th month’s follow-up, there was no significant improvement in myocardial activity in the BM-MSC group before and after transplantation. Meanwhile, there was no statistically significant difference between the two groups in the change of myocardial perfusion defect index ( p = 0.37) and myocardial metabolic defect index ( p = 0.90). The LVEF increased from baseline to 12 months in the BM-MSC group and control group (mean baseline-adjusted BM-MSC treatment differences in LVEF 4.8% (SD 9.0) and mean baseline-adjusted control group treatment differences in LVEF 5.8% (SD 6.04)). However, there was no statistically significant difference between the two groups in the change of the LVEF ( p = 0.23). We noticed that during the 12 months’ follow-up, except for one death and one coronary microvascular embolism in the BM-MSC group, no other events occurred and alanine transaminase (ALT) and C-reactive protein (CRP) in BM-MSC group were significantly lower than that in the control group. Conclusions The present study may have many methodological limitations, and within those limitations, we did not identify that intracoronary transfer of autologous BM-MSCs could largely promote the recovery of LV function and myocardial viability after acute myocardial infarction.
目的 探讨西藏不同海拔高度地区生活的儿童,先天性心脏病患病率及患病种类的差别.方法 选择2012年10月至2016年10月在西藏自治区不同海拔地区进行先心病筛查的年龄在3~17岁的12878例藏族儿童,根据居住地海拔不同分为3组:L组、H组、VH组.由临床医生进行体格检查和听诊筛选出疑似病例,再由心脏专科医生进行全面超声心动图检查确诊,最后将患病数据进行统计分析.结果 随着海拔的升高,先心病的患病率从4.37/1000升高至13.35/1000;女性与男性患病率的比值从1.3升高至3.1.其中,PDA的患病率升高7倍,ASD的患病率升高1.5倍,ASD是海拔<4200 m最常见的先天性心脏病(56.3%),而PDA是海拔>4200 m最常见的先心病(60.9%).结论 显示西藏地区先心病的患病率因海拔的不同而存在很大差异(4.37/1000~13.35/1000).而且提示ASD是海拔<4200 m最常见的先心病,而PDA是>4200 m最主要的先心病类型.随着海拔的升高,女性患病率的升高更加显著.