Wolff-Parkinson-White (WPW) syndrome is a cardiac arrhythmia disorder caused by abnormal cardiac channels (accessory pathway, AP) between the atria and ventricles. The 12-lead electrocardiogram (ECG) is an essential diagnostic tool for identifying WPW syndrome. It can precisely identify abnormal electrical conduction resulting from APs in the heart. With the rapid development of artificial intelligence technology, advanced technologies are applied to classify AP locations in WPW using ECG signals. However, these studies face two main challenges: firstly, the lack of large public datasets limits the training and performance evaluation of models; secondly, due to the scarcity of data for rare AP locations, the WPW patients' data exhibits a long-tailed distribution, which results in an imbalance in categories. To tackle these challenges, we have established the largest WPW patient ECG database for developing automatic AP location algorithms. It comprises data from two hospitals with a total of 918 individual data. Moreover, we propose Tail-AwareNet to improve the classification accuracy of the tail data. Specifically, we propose a data augmentation strategy to solve the problem of category imbalance and introduce the Double Branch Channel Attention Inverted Residual Convolution (DBIRConv) module to capture the important information across different receptive fields and channels. Finally, we propose the Head-Tail Collaboration module to deal with the long-tailed distribution of data and improve the classification accuracy of each category. The results of the experiments demonstrate that the proposed method exhibits excellent performance, achieving an accuracy of 90.39 f 0.45%, an F1 score of 66.63 f 2.65%, a precision of 72.17 f 3.40%, a recall of 65.60 f 0.19%, and a sensitivity of 97.50 f 0.18%.

Myopia is a major public health concern that poses a serious threat to vision. The combination of precise monitoring of changes in the choroidal structure and blood flow, along with early prevention and control through pharmacological intervention, represents a key direction in myopia research. In the present study, swept-source optical coherence tomography angiography was used to obtain dynamic assessments of wide-field choroidal thickness and blood flow in guinea pigs before and after form-deprivation (FD). The effects of brimonidine on refraction, axial length, choroidal thickness, and perfusion in guinea pigs with form-deprivation myopia (FDM) were assessed. In addition, the choroidal expression of nitric oxide synthase (NOS), neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), transforming growth factor-beta1 (TGF-β1), and α-smooth muscle actin (α-SMA) was quantified. The choroidal changes observed in the guinea pigs with FDM showed spatial heterogeneity, with areas of lower baseline choroidal thickness and blood flow showing greater susceptibility to FD stimulation and exhibiting more significant reductions. Brimonidine significantly slowed refraction and axial elongation in the FDM guinea pigs and broadly alleviated choroidal thinning and hypoperfusion. At the molecular level, brimonidine markedly reduced the FD-induced elevated choroidal expression of NOS, nNOS, eNOS, TGF-β1, and α-SMA. Brimonidine showed anti-myopic effects by preserving choroidal thickness and perfusion in FDM guinea pigs, potentially through suppression of the abnormally elevated expression of NOS, TGF-β1, and α-SMA in the choroid. These findings offer new insights and therapeutic targets for pharmacological prevention and control of myopia.

PURPOSE:This study aims to evaluate the effects of brimonidine eye drops and intravitreal administration in guinea pigs with form-deprivation myopia (FDM) and to analyze the ocular pharmacokinetics and irritation. METHODS:The experimental guinea pigs were randomized to the normal control, FDM, FDM brimonidine topical eye drops, and FDM intravitreal injection groups. The experiment period was 13 days. Changes in ocular refraction and axial length were monitored regularly. The ocular pharmacokinetics of brimonidine and its metabolite brimonidine-2,3-dione were analyzed using ultra-performance liquid chromatography-tandem mass spectrometry. Ocular irritation was assessed by the Draize test, corneal fluorescein staining, and hematoxylin and eosin staining. RESULTS:Two administration methods of brimonidine equally inhibited the increase in refraction and axial length in FDM guinea pigs (P < 0.05). Pharmacokinetic analysis revealed significant and sustained accumulation of brimonidine in the iris and choroid. Brimonidine was preferentially distributed to the cornea, conjunctiva, and sclera when administered topically, and preferentially to the retina and vitreous when administered intravitreally. The total area under the curve values for retinal and scleral tissues demonstrated that continuous topical administration was 1.95 times and 1.36 times that of intravitreal administration, respectively. The concentration of brimonidine-2,3-dione was significantly lower than that of brimonidine. Brimonidine topical eyedrops had less ocular irritation. CONCLUSIONS:At the drug concentrations in this study, both topical and intravitreal brimonidine achieved sufficient ocular exposure to exert similar myopia-suppressing effects. Continuous topical administration can maintain higher drug concentrations in the retinal and scleral tissues with less eye irritation.

Contrast-induced acute kidney injury (CIAKI) is a common complication after contrast media administration. Growing evidences implicate microRNA (miR)-30c has a key role in renal diseases. This study aimed to investigate the role and mechanism of miR-30c in CIAKI. CIAKI rat models were established using tail vein injection of omnipaque. MiR-30c was significantly downregulated in CIAKI models both in vivo and in vitro, concomitant with increased cell apoptosis and deteriorated renal injury. Meanwhile, the cell apoptosis, renal dysfunction and renal injury under contrast exposure were alleviated after overexpression of miR-30c. Mechanistically, we demonstrated that miR-30c directly targeted SOCS1, whose downregulation reduced contrast-induced HK-2 cell apoptosis. Furthermore, the upregulation of SOCS1 abolish the protective effect of the overexpression of miR-30c on contrast-induced cell apoptosis. In summary, overexpression of miR-30c inhibited renal tubular epithelial cell apoptosis and mitigated CIAKI via inhibiting the gene of SOCS1.

BackgroundMalnutrition is increasingly recognized as a modifiable prognostic factor in myocardial infarction (MI), yet traditional nutritional assessment methods often fail to adequately capture lipid-related atherogenic risk. We introduced an innovative modified Controlling Nutritional Status (mCONUT) score, which replaces total cholesterol with non-HDL cholesterol, aiming to improve the stratification of atherosclerotic risk and to assess its prognostic utility in predicting MI outcomes.MethodsIn this retrospective cohort study, we analyzed a total of 3,730 patients diagnosed with MI, extracted from the MIMIC-IV database, and stratified them into Normal, Mild, and Worse groups based on the mCONUT score. After performing 1:1:1 propensity score matching, we selected 993 patients for comparative analysis. Multivariable Cox proportional hazards models, adjusted for clinical and demographic confounders, were employed to evaluate all-cause mortality at 180 days and 1 year.ResultsAmong 993 MI patients, the median age was 75 years (IQR 68–82) with 58.4% males (n = 580). Malnutrition severity (mCONUT ≥6) stratified prognostic risk: Worse group demonstrated progressive mortality increases (180-day: 13.9% vs. Normal 7.85%, p = 0.037; 1-year: 31.4% vs. 21.2%, p = 0.011), alongside lower BMI, extended hospitalization, reduced hypertension, higher CKD incidence, and diminished revascularization (all p < 0.05). Multivariable analyses confirmed graded mortality risk: 180-day (Model 1: adjusted HR 1.58, p = 0.009; Model 2: HR 1.46, p = 0.031) and 1-year (Model 1: HR 1.61, p = 0.002; Model 2: HR 1.52, p = 0.008). Consistency across subgroups was observed, with heightened vulnerability in males, hypertensives (interaction p = 0.004), diabetes and non-white individuals.ConclusionsThe mCONUT score has emerged as a robust multidimensional biomarker for predicting MI prognosis, with worse malnutrition (mCONUT ≥ 6) being significantly associated with a 46%–61% elevation in mortality risk, demonstrating a clear linear dose-response relationship. Routine screening and tailored nutritional interventions should be prioritized in modern MI management practices.

Fungal keratitis is a serious blinding eye disease. The development of fungal infections depends primarily on the interaction of fungal virulence with host immune defense factors. The cornea is considered an immune-privileged organ, and resident macrophages are the main immune cells that respond to the heterogeneity exhibited by the microenvironment with their polarization. In the early stage of infection, macrophages polarize towards M1, which promotes inflammation and facilitates fungal clearance but produces a cellular storm that exacerbates immune damage; in the late stage of infection, macrophages polarize towards M2, which suppresses the inflammatory response and facilitates tissue repair, but may be immunosuppressed or even immune escape to the detriment of pathogen clearance. The balance between pro-inflammatory and anti-inflammatory responses is key to maintaining the functional integrity of the cornea. Current antifungal drug therapy is limited, so it is particularly important to find a therapeutic target for the inflammatory response triggered by the immune response in addition to antifungal therapy. In this review, the functional and phenotypic characterization of macrophage subsets associated with fungal keratitis was reviewed, more in-depth research is needed to explore the specific mechanisms by which macrophage polarization and their impact on fungal keratitis. Targeted regulation of macrophage differentiation based on their phenotype and function could be an effective approach to treat and manage fungal keratitis in the future.

To evaluate ocular refractive development, choroidal thickness (ChT) and changes in choroidal blood flow in form-deprived myopia (FDM) Guinea pigs treated with repeated low-level red-light (RLRL) therapy. Twenty-eight 3-week-old male tricolour Guinea pigs were randomised into three groups: normal controls (NC, n = 10), form-deprived (FD, n = 10) and red light treated with form-deprivation (RLFD, n = 8). Interocular refraction and axial length (AL) changes were monitored. Optical coherence tomography angiography (OCTA) measured choroidal thickness, vessel area density, vessel skeleton density and blood flow signal intensity (flux) in the choriocapillaris and medium–large vessel layers. The experimental intervention lasted 3 weeks. At week 3, the FD group had higher myopia and longer axial length than the NC group (all p < 0.001). The RLFD group had higher hyperopia and shorter axial length than the FD group (all p < 0.001). At week 1, the NC group had a thicker choroidal thickness than the FD group (p < 0.05). At weeks 2 and 3, the RLFD group had a thicker choroidal thickness than the FD group (p = 0.002, p < 0.001, respectively). Additionally, the NC group had higher vessel area density, vessel skeleton density and flux in the choriocapillaris layer than the FD group at the three follow-up time points (all p < 0.05). At week 3, the vessel skeleton density and flux were higher in the RLFD group than in the FD group (all p < 0.05). Correlation analysis results showed that weekly changes in refraction and choroidal thickness were negatively correlated with changes in axial length (all p < 0.05). Choroidal thickness changes were positively correlated with alterations in the vessel area density, vessel skeleton density and flux in the choriocapillaris layer, as well as vessel skeleton density and flux changes in the medium–large vessel layers (all p < 0.05). Repeated low-level red-light (RLRL) therapy retards FDM progression in Guinea pigs, potentially through increased choroidal blood flow in the choriocapillaris layer.

BACKGROUND:Myopia is becoming a huge burden on the world's public health systems. The purpose of this study was to explore the effect of brimonidine in the treatment of form-deprivation myopia (FDM) and the relationship between intraocular pressure (IOP) and myopia development.METHODS:Monocular form deprivation myopia (FDM) was induced in three-week-old pigmented male guinea pigs. They were treated with 3 different methods of brimonidine administration (eye drops, and subconjunctival or intravitreal injections). Four different concentrations of brimonidine were tested for each method (2µg/µL, 4µg/µL, 20µg/µL, and 40µg/µL). All treatments continued for a period of 21 days. Tonometry, retinoscopy, and A-scan ultrasonography were used to monitor intraocular pressure, refractive error and axial length (AL), respectively.RESULTS:Treatment with subconjunctival brimonidine at 40µg/µL, and intravitreal brimonidine at 2µg/µL and 4µg/µL, inhibited the development of FDM. The myopic refraction, excessive axial length, and elevation of IOP were significantly decreased. Brimonidine in eye drops was ineffective.CONCLUSION:Brimonidine at appropriate doses significantly reduced the development of FD myopia in guinea pigs. The IOP may change with FD myopia.

Drug treatment studies are a focal point for identifying novel approaches to reduce myopia progression through basic science research. Here, we investigated the effects of various brimonidine administration routes and concentrations on form-deprivation myopia (FDM) progression, matrix metalloproteinase-2 (MMP-2), and collagen alpha1 chain of type I (COL1A1) expression in the retinal pigment epithelial (RPE)-choroid complex and sclera of guinea pigs. They demonstrate that brimonidine has the capacity to impede choroidal thinning induced by FDM, potentially through the induction of choroidal vasodilation. Additionally, we observed that brimonidine effectively counteracts FDM-induced downregulation of choroidal and scleral MMP-2 expression. Suppression of MMP-2 expression may reduce disruption of scleral and choroidal structural integrity which reduces declines in choroidal blood circulation and mitigates increases in ocular elongation. This research elucidates the effects of brimonidine on myopia progression, offering potential insights into therapeutic interventions for myopia.

BACKGROUND:12,13-dihydroxy-9Z-octadecenoic acid (12,13-diHOME) has shown potential in protecting against heart disease, but its relationship with atrial fibrillation (AF) remains unknown. METHODS:Coronary sinus (CS) and femoral vein blood samplings were synchronously collected from AF and non-AF subjects (paroxysmal supraventricular tachycardia or idiopathic premature ventricular complexes) who underwent catheter ablation. First, untargeted metabolomic profiling was performed in a discovery cohort (including 12 AF and 12 non-AF subjects) to identify the most promising CS or femoral vein metabolite. Then, the selected metabolite was further measured in a validation cohort (including 119 AF and 103 non-AF subjects) to confirm its relationship with left atrium remodeling and 1-year postablation recurrence of AF. Finally, the biological function of the selected metabolite was validated in a rapid-paced cultured HL-1 atrial cardiomyocytes model. RESULTS:Metabolomic analysis identified CS 12,13-diHOME as the most pronounced change metabolite correlated with left atrium remodeling in the discovery cohort. In the validation cohort, CS 12,13-diHOME was significantly lower in patients with AF than non-AF controls (84.32±20.13 versus 96.24±23.56 pg/mL; P<0.01), and associated with worse structural, functional, and electrical remodeling of left atrium. Multivariable regression analyses further demonstrated that decreased CS 12,13-diHOME was an independent predictor of 1-year postablation recurrence of AF (odds ratio, 0.754 [95% CI, 0.648-0.920]; P=0.005). Biological function validations showed that 12,13-diHOME treatment significantly protect the cell viability, improved the expression of MHC (myosin heavy chain) and Cav1.2 (L-type calcium channel α1c), and attenuated mitochondrial damage in the rapid-paced cultured HL-1 cardiomyocytes model. CONCLUSIONS:CS metabolite 12,13-diHOME is decreased in patients with AF and can serve as a novel biomarker for left atrium remodeling.

Background Type 1 diabetes (T1D) is a significant risk factor for a range of cardiovascular diseases. Nonetheless, the causal relationship between T1D and non-ischemic cardiomyopathy (NICM) remains to be elucidated. Furthermore, the mechanisms responsible for the progression from T1D to NICM have not been definitively characterized. Objective The aim of this study was to conduct a Mendelian randomization (MR) study to investigate the causal effects of T1D and its complications on the development of NICM. Additionally, this study aimed to conduct a mediation analysis to identify potential mediators within this correlation. Methods Genetic variants were used as instrumental variables for T1D. The summary data for T1D were obtained from two genome-wide association study datasets. The summary data for T1D with complications and NICM were obtained from the Finnish database. Two-sample MR, multivariable MR and mediation MR were conducted in this study. Results The study revealed a causal association between T1D, T1D with complications, and NICM (with odds ratios of 1.02, 95% CI 1.01–1.04, p = 1.17e-04 and 1.03, 95% CI 1.01–1.05, p = 3.15e-3). Even after adjusting for confounding factors such as body mass index and hypertension, T1D remained statistically significant (with odds ratio of 1.02, 95% CI 1.01–1.04, p = 1.35e-4). Mediation analysis indicated that monokine induced by gamma interferon may play a mediating role in the pathogenesis of T1D-NICM (mediation effect indicated by odds ratio of 1.005, 95% CI 1.001–1.01, p = 4.9e-2). Conclusion The study demonstrates a causal relationship between T1D, its complications, and NICM. Additionally, monokine induced by gamma interferon may act as a potential mediator in the pathogenesis of T1D-NICM.

Background: Atrial fibrillation (AF) is common among intensive care unit (ICU) patients and significantly raises the in-hospital mortality rate. Existing scoring systems or models have limited predictive capabilities for AF patients in ICU. Our study developed and validated machine learning models to predict the risk of in-hospital mortality in ICU patients with AF. Methods and Results: Medical Information Mart for Intensive Care (MIMIC)-IV dataset and eICU Collaborative Research Database (eICU-CRD) were analyzed. Among ten classifiers compared, adaptive boosting (AdaBoost) showed better performance in predicting all-cause mortality in AF patients. A compact model with 15 features was developed and validated. Both the all variable and compact models exhibited excellent performance with area under the receiver operating characteristic curves (AUCs) of 1(95%confidence interval [CI]: 1.0-1.0) in the training set. In the MIMIC-IV testing set, the AUCs of the all variable and compact models were 0.978 (95% CI: 0.973-0.982) and 0.977 (95% CI: 0.972-0.982), respectively. In the external validation set, the AUCs of all variable and compact models were 0.825 (95% CI: 0.815-0.834) and 0.807 (95% CI: 0.796-0.817), respectively. Conclusion: An AdaBoost-based predictive model was subjected to internal and external validation, highlighting its strong predictive capacity for assessing the risk of in-hospital mortality in ICU patients with AF.

心血管内科疾病危重复杂、见习周期短,给心血管内科见习教学工作带来了挑战.工作坊作为参与式、体验式及互动式的实践教学模式,可有效提升学生的综合实践能力.依据心血管内科疾病的特点及工作坊理论基础,制定"病例—任务—问题"的工作坊教学流程,按照逻辑维与时间维两个维度,提出本专业的工作坊病例设置方法;以急性心肌梗死病例为例设计工作坊任务及问题,为工作坊教学实践提供理论依据;对工作坊模式的运行方式及实施提出了建议.

目的:评估"诊断学"理论考试卷的质量,基于试卷分析改进教学策略以提高教学质量.方法:汇总中山大学2018级临床医学专业"诊断学"理论考卷177份,采用SPSS 26.0进行试卷分数的频数、均数、信度和效度统计,分别计算试题的难度及区分度.根据试卷信度、效度、难度级区分度进行试卷质量分析,并基于试卷分析提出教学策略改进方案.结果:177名学生的考试成绩为34.5～84.0分,平均为62.23±10.66分.试卷总体信度(γ)为0.778,总效度(V)为0.534,总体难度(P)为0.622,区分度(D)为0.52;学生总失分率为:38％.结论:本次考试试卷难度偏难,效度偏低,信度及区分度良好.学生在知识灵活应用方面掌握欠佳,需根据试卷分析情况,改进教学策略,以提高教学效果.

Purpose: Brimonidine is a highly alpha-2 adrenergic agonist, which provides a potential myopia control effect. This study aimed to examine the pharmacokinetics and concentration of brimonidine in the posterior segment tissue of eyes in guinea pigs. Methods: A liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was successfully used for brimonidine pharmacokinetics and tissue distribution research in guinea pigs following intravitreal administration (20 μg/eye). Results: Brimonidine concentrations in the retina and sclera were maintained at a high level (>60 ng/g) at 96 h postdosing. Brimonidine concentration peaked in the retina (377.86 ng/g) at 2.41 h and sclera (306.18 ng/g) at 6.98 h. The area under curve (AUC0-∞) was 27,179.99 ng h/g in the retina and 39,529.03 ng h/g in the sclera. The elimination half-life (T1/2e) was 62.43 h in the retina and 67.94 h in the sclera. Conclusions: The results indicated that brimonidine was rapidly absorbed and diffused to the retina and sclera. Meanwhile, it maintained higher posterior tissue concentrations, which can effectively activate the alpha-2 adrenergic receptor. This may provide pharmacokinetic evidence for the inhibition of myopia progression by brimonidine in animal experiments.

The comparison between the diagnostic criteria for cirrhotic cardiomyopathy (CCM) first proposed in 2005 (2005 Montreal criteria), and those redefined in the 2019 Cirrhotic Cardiomyopathy Consortium (2019 CCC criteria) has generated significant controversy. Importantly, the predictive value of these criteria in cirrhotic patients (CPs) remains unclear to this date. Thus, the present study aims to compare the 2 sets of criteria and investigate their predictive value in CPs. Between April 2021 and April 2023, a total of 104 CPs with an average age of 46.4 +/- 8.9 years, who had no history of other cardiac dis-eases or malignancies were enrolled in this prospective single-center observational cohort study, conducted at the Third Affiliated Hospital of Sun Yat-Sen University. Various echo-cardiographic indicators were measured and assessed for their prognostic value and asso-ciation with clinical outcomes. The prevalence of CCM was found to be comparable when evaluated using both the 2019 CCC and 2005 Montreal criteria (54.8% vs 44.2%, p = 0.161). However, the diagnosis of systolic dysfunction was significantly different between the 2 criteria (52.9% vs 1.0%, p <0.001). Among patients with systolic dysfunction, 27.9% had reduced left ventricular global longitudinal strain, while 25% had increased left ventricular global longitudinal strain. Moreover, fewer patients were diag-nosed with diastolic dysfunction (DD) using the 2019 CCC criteria (4.8% vs 44.2%, p <0.001). Multivariate Cox analysis revealed that CPs who had encephalopathy, a high model for end-stage liver disease score, and DD diagnosed using the 2019 CCC criteria exhibited a poorer prognosis. In conclusion, although the prevalence of CCM according to both criteria is similar, the consistency is poor, indicating that they are not the same group of patients. Importantly, CPs with DD diagnosed according to the 2019 CCC criteria might be associated with increased adverse events. (c) 2023 Elsevier Inc. All rights reserved. (Am J Cardiol 2023;208:180-189)

Steroid-induced glaucoma (SIG) is the most common adverse steroid-related effect on the eyes. SIG patients can suffer from trabecular meshwork (TM) dysfunction, intraocular pressure (IOP) elevation, and irreversible vision loss. Previous studies have mainly focused on the role of extracellular matrix turnover in TM dysfunction; however, whether the cellular effects of TM cells are involved in the pathogenesis of SIG remains unclear. Here, we found that the induction of cellular senescence was associated with TM dysfunction, causing SIG in cultured cells and mouse models. Especially, we established the transcriptome landscape in the TM tissue of SIG mice via microarray screening and identified ANRIL as the most differentially expressed long non-coding RNA, with a 5.4-fold change. The expression level of ANRIL was closely related to ocular manifestations (IOP elevation, cup/disc ratio, and retinal nerve fiber layer thickness). Furthermore, p15, the molecular target of ANRIL, was significantly upregulated in SIG and was correlated with ocular manifestations in an opposite direction to ANRIL. The reciprocal regulation between ANRIL and p15 was validated using luciferase reporter assay. Through depletion in cultured cells and a mouse model, ANRIL/p15 signaling was confirmed in cellular senescence via cyclin-dependent kinase activity and, subsequently, by phosphorylation of the retinoblastoma protein. ANRIL depletion imitated the SIG phenotype, most importantly IOP elevation. ANRIL depletion-induced IOP elevation in mice can be effectively suppressed by p15 depletion. Analyses of the single-cell atlas and transcriptome dynamics of human TM tissue showed that ANRIL/p15 expression is spatially enriched in human TM cells and is correlated with TM dysfunction. Moreover, ANRIL is colocalized with a GWAS risk variant (rs944800) of glaucoma, suggesting its potential role underlying genetic susceptibility of glaucoma. Together, our findings suggested that steroid treatment promoted cellular senescence, which caused TM dysfunction, IOP elevation, and irreversible vision loss. Molecular therapy targeting the ANRIL/p15 signal exerted a protective effect against steroid treatment and shed new light on glaucoma management.

Background Coronary sinus (CS) blood sampling gives an insight into the localized pathophysiology of heart diseases. However, additional specifically-designed or modified catheters were needed in most previous studies, making the convenience of clinical application unsatisfactory. This study aimed to introduce a simple method for CS blood sampling without using additional catheters during catheter ablation (CA) of arrhythmias, and to investigate its feasibility and safety. Methods A total of 119 patients undergoing CA were prospectively enrolled, including 25 with paroxysmal supraventricular tachycardia (PSVT), 30 with premature ventricular complexes (PVC), and 64 with atrial fibrillation (AF). Cannulation and sampling of CS was performed via the femoral vein using a conventional 8F SR0TM or 8.5F SL1TM introducer sheath (St. Jude Medical) guided by a 6F steerable diagnostic catheter (St. Jude Medical). The success rate and any suspicious complications were recorded. Untargeted liquid chromatograph-mass spectrometer (LC-MS)-based metabonomics of CS samples versus peripheral venous samples were also performed. Results CS blood samples were successfully collected from 114 patients, with an overall success rate of 95.8%. Among patients with different arrhythmias, the success rates were similar, with 96.0% in PSVT, 96.7% in PVC, and 95.3% in AF (P=0.223). Adverse events occurred in four (3.4%) patients, including two patients with occasional atrial ectopic beats without causing any discomfort, and two patients with new-onset paroxysmal AF lasting for about 2 min. No serious complications were noted. Metabonomics analysis showed that CS samples provided a number of different metabolites (93 in PVST, 217 in PVC, and 109 in AF) versus peripheral samples. Conclusions Our method for CS blood sampling during CA is feasible and safe, and can provide useful cardiometabolic information that is significantly different from a peripheral sample.

目的 探究人参皂苷Rb1(GRb1)对糖尿病大鼠心脏功能、心肌细胞凋亡的影响及其机制.方法 5～6周龄SPF级SD雄性大鼠24只,随机分为对照组、糖尿病组、糖尿病+低剂量GRb1(10 mg/kg)组和糖尿病+高剂量GRb1(20 mg/kg)组,每组6只.除对照组外,其他组大鼠腹腔注射40 mg/kg链脲佐菌素(STZ),1周后随机血糖大于16.7 mmol/L即为建模成功.糖尿病+低、高剂量GRb1组每天分别腹腔注射10、20 mg/kg GRb1,连续8周.通过左心室插管测定心功能,测定血清胰岛素(INS)、随机血糖(Glu)水平,计算胰岛素抵抗的稳态模型评估的对数值(lg HOMA-IR).测定凋亡及炎症相关蛋白的表达:Bax/Bcl-2、裂解的半胱氨酸-天冬氨酸特异性蛋白酶3(cleaved caspase3)、p-核转录因子κB(NF-κB)/NF-κB、p-核转录因子κB的抑制蛋白(IκB)/IκB及沉默信息调节因子2相关酶1(sirt1),原位末端标记法(TUNEL)染色测定凋亡.结果 STZ处理后大鼠随机血糖均高于16.7 mmol/L,模型构建成功.与对照组比较,糖尿病组大鼠左室舒张功能减退,差异有统计学意义(P＜0.05),GRb1未能显著改善心功能.GRb1不影响糖尿病大鼠INS、Glu和lg HOMA-IR.与糖尿病组大鼠比较,糖尿病+低、高剂量GRb1组大鼠心肌组织中Bax/Bcl-2、cleaved caspased-3蛋白的表达以及NF-κB磷酸化、乙酰化水平显著降低,差异均有统计学意义(P＜0.05).与糖尿病组大鼠比较,糖尿病+高剂量GRb1组大鼠p-IκB/IκB水平显著降低,sirt1表达水平显著提高,差异均有统计学意义(P＜0.05).结论 GRb1可以显著改善糖尿病大鼠心肌细胞的凋亡,改善糖尿病心肌病的预后.

ObjectiveThe purpose of this study was to use a large database that contains information on patient intensive care unit (ICU) admissions to study critically ill patients with cirrhosis and the relation with atrial fibrillation and short-term and 4-year mortality. MethodsThe Monitoring in Intensive Care Database III database was used to identify patients with cirrhosis hospitalized in an ICU from 2001 to 2012. Demographic and clinical data were extracted from the database. Clinical data and demographic information were collected for each patient in our study. Kaplan-Meier analysis and multivariate Cox regression models were performed to examine the relation between atrial fibrillation and in-hospital and 4-year all-cause mortality. ResultsA total of 1,481 patients (mean age 58 years, 68% male) with liver cirrhosis treated in an ICU were included in the analysis, and the prevalence of atrial fibrillation was 14.2%. The in-hospital all-cause mortality rate was 26.60%, and patients who had a significantly higher rate of atrial fibrillation (21.57% vs. 11.50%, P < 0.001). Multivariate analysis indicated that atrial fibrillation was significantly associated with in-hospital all-cause mortality (hazard ratio [HR] = 1.52, 95% confidence interval [CI]: 1.19 to 1.95; P < 0.001), and 4-year all-cause mortality (HR = 1.55, 95% CI: 1.12 to 2.13; P = 0.008). Kaplan-Meier survival analysis showed that patients with atrial fibrillation had a significantly higher in-hospital and 4-year all-cause mortality rate than patients without atrial fibrillation. ConclusionsCritically ill patients with liver cirrhosis have a significantly increased rate of atrial fibrillation, and the presence of atrial fibrillation is an independent risk for in-hospital and 4-year all-cause mortality.