BACKGROUND:Patients with severe aortic stenosis (AS) often have concomitant coronary artery disease (CAD), but optimal timing of percutaneous coronary intervention (PCI) remains unclear, especially in those with very high risk. CASE SUMMARY:A 63-year-old man with severe AS (aortic valve area 0.9 cm2), reduced left ventricular ejection fraction (40%), and triple-vessel CAD including bilateral chronic total occlusions underwent a single-session transcatheter aortic valve replacement (TAVR) plus PCI under prophylactic veno-arterial extracorporeal membrane oxygenation because of extreme risk of hemodynamic collapse. TAVR was performed first, followed by rotational atherectomy-assisted PCI. DISCUSSION:Prophylactic veno-arterial extracorporeal membrane oxygenation provided a critical safety net, allowing valve recapture and repositioning despite heavy calcification and successful chronic total occlusion revascularization. This 1-stop strategy avoided staged procedures and cumulative cardiac stress. TAKE-HOME MESSAGE:For high-risk AS with complex CAD, a 1-stop TAVR-plus-PCI strategy under prophylactic ECMO support is feasible and potentially life-saving; careful imaging and advanced intraoperative techniques are essential.

OBJECTIVE:This study was aimed at analyzing the correlation of serum γKlotho with the long-term prognosis of multivessel coronary artery disease (MVD) and develop a predictive model to predict an accurate long-term prognosis. METHODS:We enrolled 969 MVD patients and classified them into three groups: training (n = 552), internal validation (n = 224), and external validation (n = 193) groups, respectively. The training group data helped in establishing a prognostic model. Univariable Cox regression analyses were conducted using serum and clinical γKlotho levels. Thereafter, the least absolute shrinkage and selection operator (LASSO) regression model was utilized for optimizing feature selection. Additionally, we constructed a prognosis prediction nomogram with multivariate Cox regression results by incorporating features screened with the LASSO model. Moreover, the as-constructed prognosis model's discriminability, consistency, and clinical usefulness were assessed by receiver operating characteristic (ROC) curve, C-index, decision curve analysis (DCA), and calibration plot analysis, respectively. RESULT:Included in our prognosis prediction nomogram, the predictors of the long-term prognosis of MVD patients were age, BMI, diabetes mellitus (DM), antiplatelets, LDL-C, LVDD, and serum γKlotho level. Consequently, this nomogram displayed high discriminability, according to ROC and C-index analyses. Moreover, according to the calibration plot, the nomogram's probabilities exhibited high consistency with the actual levels. Based on DCA, this nomogram displayed good clinical usefulness. CONCLUSION:Higher serum γKlotho levels correlated with the poor prognosis of MVD patients, our predictive model exhibited better predictive ability and clinical usefulness.

To systematically review and analyze the impact of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors on circulating inflammation, focusing on their underlying mechanisms and clinical application prospects, this review comprehensively summarizes recent studies addressing the molecular basis, nonclassical pathologic mechanisms, clinical evidence in multisystem diseases, therapeutic advances, and combined intervention strategies associated with PCSK9 and its inhibitors, highlighting their anti-inflammatory potential and personalized management strategies. PCSK9 participates in circulating inflammation primarily through multiple signaling pathways, including the NOD-like receptor family pyrin domain containing 3 inflammasome and the Toll-like receptor 4/nuclear factor kappa B axis. Clinical evidence indicates that PCSK9 inhibitors have limited direct effects on traditional inflammatory biomarkers. However, they show benefits in improving atherosclerotic plaque stability and modulating immune-inflammatory gene expression. The anti-inflammatory effects of PCSK9 inhibitors in circulating inflammation might not be directly reflected through changes in conventional inflammatory biomarkers. Future research should further explore their nonclassical mechanisms and optimize personalized risk stratification strategies, integrating multiomics and multiple biomarkers for precise inflammation management.

Background:Published studies have reported inconsistent findings regarding the association between preprocedural red cell distribution width (RDW) and adverse outcomes after percutaneous coronary intervention (PCI), and earlier reviews no longer reflect the currently available evidence. This updated systematic review and meta-analysis was conducted to reassess the association between preprocedural RDW and adverse outcomes in patients with coronary artery disease (CAD) undergoing PCI. Methods:PubMed, Embase, Web of Science, and the Cochrane Library were searched from inception to November 22, 2025. Standard major adverse cardiovascular events (MACE), all-cause mortality (ACM), and cardiovascular mortality (CVM) were prespecified as the primary outcomes, whereas PCI-specific stent-related outcomes were analyzed separately as exploratory outcomes. Hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (CIs) were extracted for quantitative synthesis when appropriate. Results:Twenty-four studies comprising 31 comparison groups and approximately 83,000 patients were included in the meta-analysis. Elevated preprocedural RDW was associated with higher risks of ACM (HR 1.46, 95% CI 1.31-1.63) and CVM (HR 1.66, 95% CI 1.33-2.07), with the most consistent association observed for ACM. The HR-based analysis of standard MACE showed a statistically significant association (HR 1.24, 95% CI 1.06-1.45; p = 0.007), but the finding was unstable in sensitivity analysis and should therefore be interpreted cautiously. After endpoint reclassification, only one study remained eligible for the OR-based analysis of standard MACE, precluding quantitative synthesis. In-stent restenosis (ISR) was analyzed separately as an exploratory stent-related outcome when eligible studies were available. Conclusions:Elevated preprocedural RDW was associated with adverse outcomes after PCI. The most consistent association was observed for ACM, whereas the evidence for CVM and standard MACE was less certain. PCI-specific stent-related outcomes should be interpreted as exploratory. Further prospective multicenter studies with standardized endpoint definitions and harmonized RDW cutoff values are warranted. Systematic Review Registration:https://www.crd.york.ac.uk/PROSPERO/view/CRD420251249457, PROSPERO, CRD420251249457.

BACKGROUND AND AIMS:The efficacy of prophylactic mechanical circulatory support with micro-axial flow pump or veno-arterial extracorporeal membrane oxygenation (VA-ECMO) in patients with severely reduced left ventricular ejection fraction (LVEF) undergoing high-risk percutaneous coronary intervention (PCI) remains unclear. METHODS:Patients with complex three-vessel disease, unprotected left main coronary disease or last patent conduit and LVEF ≤ 35% were assigned to receive either a micro-axial flow pump (SynFlow 3.0) or VA-ECMO support during a non-emergent high-risk PCI procedure in this prospective, multicentre, randomized, open-label, non-inferiority trial. The primary endpoint was the incidence of 30-day major adverse events, defined as any of: all-cause death, myocardial infarction, stroke/transient ischaemic attack, repeat revascularization, major bleeding, acute kidney injury, cardiopulmonary resuscitation/cardioversion, cardiac surgery/limb ischaemia, or serious device-related complications. Safety endpoints included adverse events and serious adverse events. RESULTS:The primary endpoint, 30-day major adverse events, occurred in 8 of 109 patients (7.34%) in the SynFlow 3.0 group and 13 of 113 patients (11.5%) in the VA-ECMO group (absolute difference adjusted for centre effect, -4.6%; 95% confidence interval, -12.6% to 3.5%; P for non-inferiority < .001). Patients with SynFlow 3.0 had shorter post-procedural hospital stay (4.1 days vs 5.2 days on average, P = .047) and fewer device-related adverse events (3.7% vs 11.5%; P = .041). Anaemia occurred more often with VA-ECMO than with SynFlow 3.0 (20.4% vs 9.2%; P = .023). CONCLUSIONS:The prophylactic use of a micro-axial flow pump during high-risk PCI procedures was non-inferior to VA-ECMO in the incidence of 30-day major adverse events. The use of a micro-axial flow pump was associated with shorter post-procedural hospital stay and fewer device-related adverse events.

This case report describes the emergency management of a 70-year-old man who developed acute cardiac tamponade owing to right coronary artery rupture during chronic total occlusion percutaneous coronary intervention. Despite successful covered stent deployment and pericardiocentesis, iatrogenic right ventricular perforation occurred owing to a misplaced pericardial sheath. A novel dual-device strategy combining ProGlide and StarClose (Abbott) SE vascular closure devices achieved complete hemostasis under real-time transthoracic echocardiography and digital subtraction angiography. Key innovations include the first hybrid vascular closure device application for right ventricular perforation, synchronized pericardial drainage, and protocolized autotransfusion. This approach challenges surgical paradigms, demonstrating percutaneous bailout feasibility for complex iatrogenic injuries. Sustained procedural success was confirmed at 30-day follow-up.

Objectives To investigate the association between triglyceride-glucose (TyG) index levels at hospital admission and the risk of in-hospital adverse events, including all-cause mortality, in patients with acute myocardial infarction (AMI). The primary hypothesis was that higher TyG index levels are associated with greater risk of adverse in-hospital outcomes.Design Retrospective cohort study.Setting Tertiary hospital inpatient care in China. The study included consecutively hospitalised patients with AMI between 1 August 2011 and 10 January 2022.Participants A total of 3458 patients with AMI were included. The mean age was 60.8 years, and 78.4% were men. Patients were excluded if they had incomplete data for TyG index calculation or outcome ascertainment.Interventions No therapeutic intervention was assigned; the study was observational. TyG index was calculated using fasting triglycerides and fasting plasma glucose levels at admission.Primary and secondary outcome measures The primary outcome was all-cause in-hospital mortality. Secondary outcomes included cardiogenic shock and fatal rapid arrhythmia. Outcomes were identified through standardised clinical records.Results Among 3458 patients, 375 (10.84%) died during hospitalisation, 236 (6.84%) developed cardiogenic shock and 147 (4.25%) experienced fatal rapid arrhythmia. After multivariable adjustment, higher TyG index levels were significantly associated with increased odds of all-cause mortality (OR, 1.27; 95% CI, 1.02 to 1.57; p<0.05) and cardiogenic shock (OR, 1.54; 95% CI, 1.22 to 1.94; p<0.001). When categorised into quartiles, patients in the highest quartile (Q4) had greater odds of mortality (OR, 1.71; 95% CI, 1.10 to 2.65; p<0.05) and cardiogenic shock (Q2: OR, 2.18; 95% CI, 1.39 to 3.45; Q3: OR, 1.71; 95% CI, 1.06 to 2.77; Q4: OR, 2.81; 95% CI, 1.70 to 4.67; all p<0.05 vs Q1). Restricted cubic spline analysis confirmed a linear association between the TyG index and both primary and secondary outcomes.Conclusion Higher TyG index levels at admission are independently associated with an increased risk of all-cause mortality and cardiogenic shock among patients hospitalised for AMI. These findings suggest that the TyG index may serve as a useful prognostic biomarker for risk stratification in this population. Further prospective studies are warranted to validate its clinical utility.

Background:Acute coronary syndrome (ACS) is a critical cardiovascular condition with diverse clinical presentations, necessitating personalized therapeutic approaches. This study explores the genetic variation associated with ACS subtypes in the Han and Uyghur Chinese populations to support the development of precision medicine approaches tailored to ethnic-specific genetic backgrounds. Methods:A total of 985 ACS patients (668 Han and 317 Uyghur Chinese) representing different ACS subtypes were enrolled. Clinical characteristics and 66 genetic polymorphisms were analyzed. Statistical analyses were conducted to identify differences in genetic variants and clinical features across ACS subtypes and ethnic groups. Results:Significant clinical and genetic differences were observed between ACS subtypes and between ethnic groups. In the Han population, polymorphisms in CYP2D6 and PTGER3 were significantly associated with ACS subtypes (p ≤ 0.05). In the Uyghur population, six genes-ACY3, CACNA1C, CYP2C9, CYP2C19, CYP4F2, and VKORC1-showed significant associations (p ≤ 0.05). These findings indicate distinct genetic landscapes across the two ethnic groups. Furthermore, population-specific associations between genetic variants and artery narrowing were identified. Predictive models integrating clinical and genetic features achieved an area under the curve (AUC) of 0.832 [95% confidence intervals (CI): 0.774-0.889] in Uyghur patients and 0.674 (95% CI: 0.626-0.722) in Han patients, indicating a higher internal AUC of these genetic markers in the Uyghur population. Conclusion:This study highlights ethnic differences in the genetic architecture of ACS. The result also underscores the need for population-specific strategies in risk stratification and treatment. The identified genetic markers and predictive models may guide future research on ethnicity-specific risk stratification.

This case report describes the emergency management of a 70-year-old man who developed acute cardiac tamponade owing to right coronary artery rupture during chronic total occlusion percutaneous coronary intervention. Despite successful covered stent deployment and pericardiocentesis, iatrogenic right ventricular perforation occurred owing to a misplaced pericardial sheath. A novel dual-device strategy combining ProGlide and StarClose (Abbott) SE vascular closure devices achieved complete hemostasis under real-time transthoracic echocardiography and digital subtraction angiography. Key innovations include the first hybrid vascular closure device application for right ventricular perforation, synchronized pericardial drainage, and protocolized autotransfusion. This approach challenges surgical paradigms, demonstrating percutaneous bailout feasibility for complex iatrogenic injuries. Sustained procedural success was confirmed at 30-day follow-up.

BACKGROUND:The association between low-density lipoprotein (LDL) cholesterol and increased mortality risk has been well-documented, yet apolipoprotein B (apoB) is regarded as a more precise risk indicator. However, a comprehensive analysis integrating both markers in relation to mortality risk remains unreported. OBJECTIVES:This study aimed to investigate the relationship between LDL cholesterol levels and mortality across varying apoB concentrations within the general population. METHODS:Data from 15,380 participants in the 2005-2016 National Health and Nutrition Examination Survey (NHANES) were utilized to construct Cox regression models and apply restricted cubic splines, assessing the association between LDL cholesterol and mortality across distinct apoB stratifications. RESULTS:The study cohort had a median (IQR) age of 46.0 (32.0, 60.0) years, with 7949 (51.8%) males. During a median follow-up of 101.0 months (IQR: 67-137), 1771 (8.8%) all-cause mortality events were observed; 443 (2.1%) deaths were attributed to cardiovascular diseases, while 109 (0.5%) resulted from cerebrovascular diseases. Low apoB and LDL-cholesterol levels were independently linked to an elevated risk of all-cause and cardiovascular mortality. Compared with participants having apoB <90 mg/dL and LDL-cholesterol levels between 100-129 mg/dL, those with LDL-cholesterol <70 mg/dL (HR, 1.81; 95%CI: 1.39-2.36) and 70-99 mg/dL (HR, 1.28; 95%CI: 1.01-1.62) demonstrated a higher risk of all-cause mortality. Additionally, reduced apoB levels contributed to an increased risk of cardiovascular mortality among individuals with low LDL-cholesterol levels. CONCLUSIONS:Low apoB and LDL-cholesterol levels were associated with heightened all-cause and cardiovascular mortality risk in the general population. Conversely, high apoB and low LDL-cholesterol levels did not correlate with increased mortality risk.

Coronary collateral circulation (CCC) significantly impacts myocardial perfusion and clinical outcomes in coronary artery disease patients, yet the underlying molecular heterogeneity remains inadequately characterized. To identify distinct molecular phenotypes in patients with poor CCC, validate these phenotypes using clinical parameters, and evaluate their prognostic implications. This study enrolled 149 patients (80 with good CCC and 69 with poor CCC) for high-throughput proteomic profiling. Unsupervised consensus clustering identified molecular subtypes within poor CCC patients, followed by differential expression analysis and KEGG pathway enrichment. Boruta feature selection was implemented, and multiple machine learning algorithms were tested on clinical data, with XGBoost optimization (accuracy 80.0

BACKGROUND AND AIMS:The prevalence of vascular calcification and osteoporosis is increasing in the general population. We aimed to investigate the combined impact of abdominal aortic calcification (AAC) and bone mineral density (BMD) on mortality risk. METHODS AND RESULTS:Data were from the 2013-2014 National Health and Nutrition Examination Survey (NHANES). AAC was assessed using the AAC-24 scoring system (range 0-24) and categorized as none (0), mild (1-4), or severe (≥5). Bone mineral density (BMD) was classified according to WHO criteria as normal (T-score ≥ -1.0), osteopenia (T-score between -1.0 and -2.5), or osteoporosis (T-score ≤ -2.5). Among 2099 participants (median age 61.0 years; 51.2 % female), 231 (8.9 %) died over a median follow-up of 6 years, including 53 (1.9 %) from cardiovascular disease. Among those with osteoporosis, severe AAC was linked to the highest all-cause mortality risk versus no AAC (HR 2.59; 95 % CI, 1.22-5.49; P = 0.013). In contrast, among those with normal BMD, mild and severe AAC showed no significant increase in mortality. Compared with individuals with severe AAC and normal BMD, those with osteoporosis and severe AAC had higher all-cause mortality (HR 2.8; 95 % CI, 1.41-5.58; P = 0.003). The combination of osteoporosis and severe AAC was also associated with an increased cardiovascular mortality risk. Mediation analysis revealed BMD accounted for 11.64 % of the association between AAC and all-cause mortality in the fully adjusted model. CONCLUSION:Severe AAC and low BMD jointly contributed to increased all-cause and cardiovascular mortality in adults over 50, and BMD partially mediated the effect of AAC on adverse outcomes.

目的 探讨载脂蛋白A1(ApoA1)对不稳定型心绞痛(UAP)患者主要不良心血管事件(MACE)的预测作用.方法 连续选取2016 年12 月1 日至2019 年12 月15 日于新疆医科大学第一附属医院心脏中心确诊为UAP的住院患者.收集患者年龄、性别、血常规、空腹血糖、血脂等基线资料.所有患者出院后持续随访48 个月,根据MACE发生与否将患者分为MACE组和非MACE组.分析ApoA1 对UAP患者发生MACE的预测作用.结果 本研究共纳入UAP患者333 例,MACE组136 例,非MACE组197 例.MACE组男性、高血压病、糖尿病、肥胖比例、血小板计数、三酰甘油水平均高于非 MACE组,ApoA1 水平低于非 MACE组[(1.11±0.22)g/L比(1.28±0.41)g/L],差异均有统计学意义(均P<0.05).多因素Cox回归分析结果显示,ApoA1 是UAP患者发生MACE的独立保护因素(P<0.05).受试者工作特征曲线分析结果显示,ApoA1 预测UAP患者发生MACE的曲线下面积为0.631(95%置信区间:0.572~0.691,P<0.001),截断值为1.16 g/L,敏感度为 81%,特异度为 59%.根据ApoA1 截断值将 333 例患者分为低ApoA1 组(ApoA1≤1.16 g/L,168 例)和高 ApoA1 组(ApoA1>1.16 g/L,165 例).Kaplan-Meier 生存曲线分析结果显示,低ApoA1 组累积生存率明显低于高 ApoA1 组,差异有统计学意义(Log-rank P = 0.018).结论 ApoA1 对UAP患者MACE有一定的预测价值.

目的 探讨PCSK9对小鼠肝脏脂肪变性的机制.方法 以腺相关病毒8.2(adeno-associated virus 8.2,AAV8.2)为载体构建绿色荧光蛋白(green fluorescent protein,GFP)和人源PCSK9经尾静脉转染至小鼠肝脏表达.将36只C57BL/6J小鼠按照随机数字表法分为空白组、GFP组和PCSK9组,每组各12只,共饲养24周.通过苏木精-伊红(hematoxylin eosin,HE)染色观察肝脏组织形态,天狼星红染色(sirius red staining,SRS)观察肝脏纤维化程度,油红0(oil red O,ORO)染色观察肝脏脂质浸润程度.通过酶联免疫吸附试验(enzyme linked immunosorbent assay,ELISA)检测血清PCSK9、白细胞介素(interleukin,IL)-1β,流式细胞术检测肝脏单核细胞胞内炎性细胞因子,包括IL-2、IL-4、γ-干扰素(interferon-γ,INF-γ)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、颗粒酶B(granulase B,GrB).免疫组化检测肝组织巨噬细胞标志物CD68阳性细胞百分比.Western blot法检测PCSK9干预小鼠单核-吞噬细胞白血病细胞(RAW264.7)细胞胆固醇流出蛋白、清道夫受体相关蛋白、NF-κB信号通路相关蛋白表达.结果 PCSK9组小鼠肝脏组织脂滴总量、脂肪变性、空泡化、纤维化程度明显增加或增强(P＜0.001).免疫组化检测结果显示,PCSK9组巨噬细胞标志物CD68阳性细胞百分比显著高于GFP组及空白组(P＜0.05).流式细胞术检测结果显示,PCSK9组IL-2、TNF-α在CD4+、CD8+细胞亚群百分比明显高于高脂GFP组(P＜0.05),而IL-4、INF-γ,GrB在组间各细胞群中比较,差异无统计学意义(P＞0.05).Western blot法检测结果显示,与空白组比较,PCSK9显著降低LDLR水平,升高 ATP 结合盒转运体 A1(ATP-binding cassette transporter A1,ABCA1)、清道夫受体 B(scavenger receptor B,SRB 或 CD36)、Toll样受体 4(Toll-like receptor 4,TLR4)、磷酸化 IκBα 激酶(phosphorylated inhibit kappa B α kinase,p-IκBα)、磷酸化 p65 蛋白(phosphorylated p65,p-p65)蛋白水平(P＜0.05).结论 PCSK9介导NF-κB信号通路致小鼠肝脏脂肪代谢失衡及炎性细胞因子浸润加速了肝脏脂肪变性.

目的 利用人细胞株,系统研究PCSK9是否通过肝源性MIF调控单核/巨噬细胞炎症反应,进而为动脉粥样硬化(Atherosclerosis)等炎症性疾病的临床防控提供新的思路和依据.方法 利用小干扰RNA(Small interfering RNA,SiRNA)介导的MIF基因转染THLE-3细胞,将实验分为MIF低表达组(Si-MIF-THLE-3)和MIF正常表达组(Con-THLE-3),通过实时荧光定量PCR(quantitative real-time PCR,RT-qPCR)检测肝细胞中PCSK9、MIF mRNA表达.在Si-MIF-THLE-3组和Con-THLE-3组中分别给与PCSK9重组蛋白进行干预,通过Western Blot检测肝细胞中PCSK9、MIF蛋白表达,并用ELISA测定培养液中PCSK9及MIF的含量,并收集上述肝细胞的培养液,-80℃冻存.利用SiRNA介导的MIF基因转染THP-1细胞,将实验分为MIF低表达组(Si-MIF-THP-1)和MIF正常表达组(Con-THP-1),通过Western Blot检测MIF的蛋白表达.将收集的肝细胞培养液分别加入Si-MIF-THP-1和Con-THP-1组共培养48 h,其中PCSK9干预组另设TLR4特异性抑制剂TAK-242(1 μM)(P+T).通过ELISA检测炎症因子表达;Western Blot检测THP-1细胞株中TLR4—NF-κB信号通路的表达.结果 ①Si-MIF-THLE-3组较Con-THLE-3组的MIF mRNA表达显著降低,而PCSK9的mRNA表达升高(P均<0.05).②PCSK9干预后肝细胞MIF蛋白的表达以及分泌至培养液中的含量升高,而PCSK9蛋白的表达以及培养液中的含量不变(P均<0.05).③Si-MIF-THP-1组较Con-THP-1组的MIF蛋白表达显著降低(P均<0.05).④Si-MIF-THP-1组较Con-THP-1组炎症因子的表达低,PCSK9干预组较正常组和P+T组的炎症因子表达升高;PCSK9干预组较正常组和P+T组的TLR4蛋白表达升高;Si-MIF-THP-1组较Con-THP-1组的IKBα蛋白表达高,PCSK9干预组较正常组和P+T组的IKBα蛋白表达低;PCSK9干预组较正常组和P+T组的P65/P50蛋白表达高(P均<0.05).结论 PCSK9可诱导肝细胞MIF的合成与分泌,肝细胞分泌的MIF可与巨噬细胞表面受体TLR4结合,激活下游NF-κB炎症信号通路,促进TNF-α、白介-6、白介-1β、单核细胞驱化因子-1等炎症因子的分泌,激发炎症效应.

二尖瓣返流(Mitralregurgitation,MR)可分为原发性MR及继发性MR(功能性MR).2016年来自复旦大学中山医院基于该院超声科的数据调查研究表明,42.44％为轻度MR,1.63％为中度MR,1.44％为重度MR.在LVEF＜30％的人群中重度MR占比22.14％.在1948例重度MR中,原发性MR占比49.9％[1].2017年浙江二院结构性心脏病团队文献显示[2],超声检出MR在所有心脏瓣膜疾病中的占比最 高(0.68％).

目的 探讨以脉搏轮廓心输出量监测技术(PICCO)筛选使用双水平气道正压通气(BiPA P)治疗射血分数降低型心力衰竭(HFrEF)患者的临床疗效.方法 纳入2017年1月～2020年12月新疆维吾尔自治区人民医院收治的HFrEF患者358例,具备无创呼吸机辅助通气(NIPPV)患者208例,其中具有PICCO监测适应症且签署知情同意146例,测得基线资料;采用随机数字化原则分为两组:BiPAP组(n=74)和面罩吸氧组(n=72),比较干预后4 h的PICCO相关指标及转机械通气治疗的百分比.依据血管外肺水指数(EVLWI)结果,EVLWI≥10为BiPAP干预组39例(PICCO+BiPAP),面罩吸氧30例(PICCO+面罩吸氧);分别于0(基线)、4、8、12、24 h共5次测得PICCO数据.统计分析各组BNP变化、血气、CI前后、EVLWI、ITBVI前后变化.统计分析院内心源性死亡、恶性心律失常、心源性休克发生率、无创改有创插管转换率.结果 ①与面罩吸氧组相比,BiPA P组转机械通气概率更低,在4 h时氧分压恢复更快,EVLWI降低(均P<0.05).②以EVLWI≥10为界限,BiPAP辅助EVLWI≥10患者临床效果更明显,不同时间点LnBNP逐渐降低、心脏指数增加、胸腔内血容积指数降低(P<0.01);而在EVLWI<10组中上述指标无统计学差异(P>0.05).③在EVLWI≥10的HF患者中,与面罩吸氧相比,BiPAP救治效果更明显,转机械通气低、心脏脂数增加(P<0.01).结论 BiPAP模式对EVLWI≥10患者辅助通气有益于HFrEF降低BNP、增加心脏指数,减少有创机械通气,提高抢救成功率.

目的 探讨外源性补充酮体对肥胖小鼠线粒体功能及氧化应激的影响.方法 采用随机分组对照研究的方法,将C57BL/6J雄性小鼠给予普通饲料或高脂饲料喂养.12周后,除普通饲料喂养的对照组,高脂饲料喂养的小鼠随机分为模型组和酮脂灌胃组.酮脂灌胃组使用酮脂灌胃4周,对照组和模型组用相同体积0.9％NaCl溶液灌胃.统计固定时间点小鼠体质量及血糖变化,采用经皮心脏超声检测小鼠心功能,检测氧化应激相关指标,脂质过氧化终产物丙二醛(malondialdehyde,MDA)含量、超氧化物歧化酶(superoxide dismutase,SOD)活性及蛋白过氧化水平;使用Seahorse能量分析仪测定线粒体呼吸能力.结果 与对照组比较,模型组小鼠体质量增长显著;葡萄糖耐受能力明显降低;左心室射血分数和左心室短轴缩短率均下降;心肌线粒体功能受损,体现在基础呼吸和最大呼吸均显著下降.心肌组织MDA含量明显增加、SOD活性大幅降低以及蛋白质过氧化水平加深.与模型组比较,酮脂灌胃后的肥胖小鼠心肌线粒体基础呼吸和最大呼吸均增高,MDA含量有所下降,SOD活性提高,同时蛋白过氧化水平下降.结论 高脂饮食喂养诱导小鼠肥胖表型,伴随心脏线粒体功能损害及氧化应激增强,外源性补充酮体可以减轻肥胖小鼠心肌线粒体损伤,改善心脏氧化应激.

ObjectiveWe aim to investigate the prognostic effects of metabolic syndrome (MS) on patients with non-ST elevated myocardial infarction (NSTEMI) after percutaneous coronary intervention (PCI).MethodsPatients with NSTEMI undergoing PCI were consecutively collected. According to the presence or absence of MS, they were divided into two groups and followed up for 1 year. The endpoint was major adverse cardiovascular events (MACE), including all-cause death, unstable angina hospitalization, heart failure (HF) hospitalization, non-fatal recurrent myocardial infarction (MI), and target lesion revascularization. Also, six subgroups were made according to gender, age, left ventricular ejection fraction (LVEF), Global Registry of Acute Coronary Events (GRACE) score, hypersensitive troponin (hsTNT), and several diseased vessels. Cox proportional hazard model was adopted to analyze the effect of MS on MACE in all the patients and different subgroups.ResultsA total of 1,295 patients were included in the current analysis and 660 (50.97%) of them had MS. About 88 patients were lost to follow-up, and the overall average follow-up was 315 days. MS was an independent risk factor for MACE (HR 1.714, CI 1.265–2.322, p = 0.001), all-cause death, heart failure (HF) hospitalization, and non-fatal recurrent MI. In the MS component, BMI ≥28 kg/m2 was positively associated with MACE. Subgroup analysis indicated the prognostic value of MS was more striking for patients with the following: age of >60, LVEF of ≤40%, GRACE of >140, multivessel disease, or hsTNT of >0.1 ng/ml.ConclusionsThe MS was a robust adverse prognostic factor in patients diagnosed with NSTEMI, especially among those of older age and at higher ischemic risk. A BMI of ≥28 kg/m2 independently predicted the occurrence of MACE. Prognosis may be improved by controlling abdominal obesity.

Metabolic syndrome (MetS) is a major risk factor for cardiovascular disease and negatively affecting the prognosis of patients with ST elevation myocardial infarction (STEMI). Macrophage migration inhibitory factor (MIF) is a multipotent cytokine involved in various cardiovascular and inflammatory diseases. In this prospective study, we investigate the value of MIF in the long-term prognosis of STEMI combined with MetS after emergency PCI. Circulating MIF levels were measured at admission, and major adverse cardiovascular and cerebrovascular events (MACCE) were monitored during the follow-up period of 4.9 (3.9–5.8) years. MACCE occurred in 92 patients (22.9%), which was significantly higher in MetS (69/255, 27.1%) than in the non-MS subgroup (23/146, 15.8%, P < 0.05). Patients with MetS developed MACCE had the highest admission MIF level. Kaplan-Meier survival analysis using the cutoff value of admission MIF (143 ng/ml) showed that patients with a higher MIF level had a greater incidence of MACCE than those with lower MIF levels in both the MetS ( P < 0.0001) and non-MetS groups ( P = 0.016). After adjustment for clinical variables, the value of MIF ≥ 143 ng/ml still had the predictive power for the MetS group [HR 9.56, 95% CI (5.397–16.944), P < 0.001]; nevertheless, it was not the case in the non-MetS group. Our findings indicated that MetS is a critical risk factor for adverse clinical outcomes in patients with STEMI, and a high admission MIF level has predictive power for the long-term MACCE, which is superior in STEMI patients with MetS and better than other traditional predictors.