Early detection of coronary microvascular dysfunction (CMD) in ST-segment elevation myocardial infarction (STEMI) patients undergoing percutaneous coronary intervention (PCI), is challenging. The index of microcirculatory resistance (caIMR), derived from computational pressure-fluid dynamics (CPFD), allows practical assessment of CMD using only routine coronary angiography. However, the prognostic implications of combining caIMR with microvascular obstruction (MVO) identified through cardiac magnetic resonance (CMR) imaging are unclear. This retrospective study investigates the utility of CPFD-caIMR and CMR-derived MVO in predicting major adverse cardiovascular events (MACEs) in 292 STEMI patients who underwent primary PCI, followed by caIMR and CMR evaluations. Patients were stratified into four groups based on caIMR thresholds (≤ 40 U or > 40 U) and the presence/absence of MVO. The primary endpoint was MACEs, defined as cardiac death, recurrent myocardial infarction, target vessel revascularization, or heart failure readmission. Overall, 101/292 patient exhibited discordant caIMR and MVO results. Specifically, 103 patients had caIMR ≤ 40 U without MVO, while 88 patients showed caIMR > 40 U with MVO. Multivariate analysis identified both caIMR > 40 U and MVO as independent predictors of MACEs, with an HR of 3.572 for each unit increase in CPFD-caIMR > 40 U. Combination of CPFD-caIMR and MVO significantly enhanced predictive accuracy. CPFD-caIMR is a reliable, minimally invasive tool for identifying microvascular dysfunction. Combination with CMR-derived MVO improves risk stratification in STEMI patients following PCI, holding promise for the early identification of high-risk patients, enabling targeted and personalized management.

ObjectiveThis research is to analyze the connection between NHHR and CKD occurrence using NHANES from 2001 to 2018. It will evaluate the feasibility of NHHR as a tool for predicting CKM syndrome and offer valuable insights for personalized treatment approaches within the U.S. population.MethodsData from 16,575 individuals aged 20 to 69 years were analyzed, having excluded those who were pregnant and individuals with incomplete data. CKM syndrome was characterized by the simultaneous presence of CKD and Cardiometabolic Syndrome (CMS). For the statistical analysis, weighted logistic regression models were applied, accounting for variables such as age, gender, ethnicity, educational background, marital status, lifestyle factors, and preexisting health conditions. Differently, restricted cubic splines (RCS) were applied to investigate any possible nonlinear relationships between NHHR and CKM in the study.ResultsThe research revealed that the occurrence of CKM syndrome was more prevalent among individuals aged 60 and older, with women representing 55.36% of those affected. Additionally, NHHR levels were notably elevated in CKM patients when compared to those without CKM (p < 0.0001). As NHHR increased, the prevalence of CKM also rose, with the highest prevalence in the highest NHHR quartile (Q4: 36.06%). A positive connection between NHHR and CKM was indicated by multivariable logistic regression, especially in the upper quartiles of NHHR (Q3 and Q4). Moreover, RCS analysis displayed a noteworthy nonlinear connection between NHHR and CKM occurrence. The subgroup analysis uncovered significant interactions influenced by BMI and Hypertension.ConclusionWith the rising global prevalence of CKM syndrome, early identification of high-risk individuals using NHHR could inform targeted prevention and intervention strategies. Future research should focus on validating NHHR in diverse populations and exploring its clinical utility, as well as examining its relationship with other biomarkers of metabolic dysfunction to better understand CKM syndrome’s complex pathophysiology.

Epicardial adipose tissue (EAT) is associated with microvascular obstruction (MVO). However, its association with new-onset atrial arrhythmias after percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI) is unclear. We investigated the correlation of cardiac magnetic resonance (CMR)-measured EAT with MVO and its effect on new-onset atrial arrhythmias after PCI in patients with STEMI. This study employed a single-centre retrospective design. Patients diagnosed with STEMI who underwent CMR after PCI between January 2019 and January 2023 were consecutively included and followed-up regularly. Participants were categorised based on whether they developed new-onset atrial arrhythmia after PCI. In comparison to the non-arrhythmia group, the atrial arrhythmia group exhibited higher values for age, heart rate, peak hs-TnT, peak NT-proBNP, EATV, LAES, LAED, and MVO, alongside reduced LVEF. A positive association was identified between EATV and MVO. Univariate analysis using logistic regression revealed that age, heart rate, hs-TnT level, NT-proBNP level, LVEF, EATV, LAES, LAED, and MVO were significant risk factors for atrial arrhythmia. Multivariate logistic regression analysis further identified age, LAES, EATV, and MVO as independent predictors of atrial arrhythmia. ROC curve analysis produced AUC values of 0.690 for age, 0.584 for LAES, 0.607 for MVO, and 0.769 for EATV. The EATV demonstrated a strong positive relationship with MVO after PCI in patients with STEMI. Age, LAES, EATV, and MVO were independent predictors of new-onset atrial arrhythmias and exhibited substantial prognostic significance.

目的 探讨快速情绪释放技术(FEFT)对老年慢性病患者焦虑、抑郁情绪的影响.方法 将伴有焦虑、抑郁情绪的90例老年慢性病患者随机分成观察组和对照组,每组45例,对照组进行常规治疗和护理,观察组在此基础上自行运用FEFT轻轻快速敲击眉头、眼侧、眼下、锁骨下、手腕,10-15 min/次,3次/d,干预4周,分别采用焦虑自评量表(SAS)、抑郁自评量表(SDS)评价干预前后两组患者的焦虑、抑郁水平.结果 观察组干预后SAS、SDS得分较对照组显著下降(均P＜0.01),较干预前显著下降(均P＜0.01).结论 快速情绪释放技术可有效降低老年慢性病患者焦虑、抑郁水平.

AD是老年人痴呆的主要种类.痴呆的治疗目前尚无特效药物,早发现、早干预从而减慢痴呆进程具有重要临床意义.研究表明, AD病人脑脊液中磷酸化Tau181(p-Tau181);β淀粉样蛋白1-42(Aβ1-42)水平明显高于正常病人,且上述2项指标的水平可以用来区分AD和其他形式的痴呆[ 1-2].但是,脑脊液检查是一种有创检查,大多数病人不愿意配合.本研究旨在分析血浆中p-Tau181、Aβ1-42浓度和AD病人认知之间的关系,供临床参考,报道如下.

随着中国步入老龄化社会,作为威胁老年人身体健康的两大主要疾病DM和心脏病,发病率也在逐年上升,很多老年人二者并存.老年T2DM病人合并心功能不全的发生率比非DM病人更高,约近1/4的DM病人合并心功能不全[1].如何选择安全且疗效好的降糖药物是我们临床工作者面临的难题.达格列净作为新型的降糖药物,主要成分为钠-葡萄糖协同运转体2( SGLT-2)抑制剂,既能降糖又能改善心功能不全,对病人预后有益[2].本研究主要观察达格列净应用于老年T2DM合并心功能不全病人的临床治疗效果.

目的 考察血浆脂蛋白相关磷脂酶(Lp-PL)A2及氨基末端B型利钠肽前体(NT-proBNP)水平与老年ST段抬高型心肌梗死(STEMI)患者PCI后30 d和1年内主要不良心血管事件(MACE)发生率的相关性.方法 选取接受PCI的STEMI患者248例,根据年龄分为老年组(146例)和非老年组(102例).比较两组基线数据、测量Lp-PLA2及NT-proBNP水平,分析两者水平与PCI后30 d和1年内MACE发生率的关系.老年组又根据Lp-PLA2及NT-proBNP水平分为低危、中危、高危3组,分析各组与MACE发生率关系.结果 Lp-PLA2及NT-proBNP与患者PCI术后30 d和1年内MACE发生率具有显著相关性(P<0.05).Lp-PLA2及NT-proBNP与年龄呈显著正相关(P<0.05),老年组血Lp-PLA2及NT-proBNP水平较非老年组水平高(P<0.05),且老年组30 d和1年MACE发生率逐渐升高(P<0.05).老年组亚组发现随着Lp-PLA2及NT-proBNP水平的增高,MACE发生率也逐渐增加,高危组事件发生率高于其他两组,差异均有统计学意义(P<0.05).结论 Lp-PLA2联合NT-proBNP是老年STEMI患者PCI后30 d和1年内MACE发生率的敏感预测指标.

Background/Aims: Lipopolysaccharide (LPS) is a potent activator of vascular smooth muscle cells (VSMCs) proliferation, but the underlying mechanism remains unknown. In this study, we knocked down Toll-like receptor 4 (TLR4) and Ras-related C3 botulinum toxin substrate 1 (Rac1) expression using small interfering RNA (siRNA) in order to investigate the effects and possible mechanisms of LPS-induced VSMCs proliferation. Methods: VSMCs proliferation was monitored by 5-ethynyl-2’-deoxyuridine staining, and Rac1 activity was measured via Glutathione S-transferase pull-down assay. mRNAs encoding proliferating cell nuclear antigen (PCNA), smooth muscle 22α (SM22α), myosin heavy chain (MYH) and transient receptor potential channel 1 (TRPC1) were detected by qRT-PCR. The expression of total Akt, p-Akt (308), p-Akt (473), SM22α, MYH and TRPC1 protein was analysed by Western blot. Results: Treatment with TLR4 siRNA (siTLR4) or Rac1 siRNA (siRac1) significantly decreased LPS-induced VSMCs proliferation. Moreover, LPS-induced activation of Rac1 through TLR4 was observed. Western blot analysis revealed that transfection with siTLR4 or siRac1 inhibited LPS-induced Akt phosphorylation. We discovered that LPS stimulated VSMCs proliferation via phenotypic modulation and that this effect was partially inhibited by pre-treatment with siTLR4 or siRac1. Further, TLR4 and Rac1 are involved in LPS-induced activation of TRPC1. Conclusion: This study suggests that LPS exerts an effect on VSMCs proliferation and that the TLR4/Rac1/Akt signalling pathway mediates this effect.