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中华心血管病杂志最新文献

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[Research progress on pericoronary fat attenuation index]. [冠状动脉脂肪衰减指数的研究进展]。
Q3 Medicine Pub Date : 2025-11-24 DOI: 10.3760/cma.j.cn112148-20251001-00688
T H Zhang, Y Du, X L Gao, L Xu, Y J Zhou
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引用次数: 0
[Introduction and interpretation of "2025 focused update of the 2019 ESC/EAS Guidelines for the management of dyslipidaemias"]. [对“2019 ESC/EAS血脂异常管理指南2025年重点更新”的介绍和解释]。
Q3 Medicine Pub Date : 2025-11-24 DOI: 10.3760/cma.j.cn112148-20250916-00655
J J Li, D Zhao
{"title":"[Introduction and interpretation of \"2025 focused update of the 2019 ESC/EAS Guidelines for the management of dyslipidaemias\"].","authors":"J J Li, D Zhao","doi":"10.3760/cma.j.cn112148-20250916-00655","DOIUrl":"10.3760/cma.j.cn112148-20250916-00655","url":null,"abstract":"","PeriodicalId":38755,"journal":{"name":"中华心血管病杂志","volume":"53 11","pages":"1278-1281"},"PeriodicalIF":0.0,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145597689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Extracorporeal focused ultrasound targeted renal denervation]. [体外聚焦超声定向肾去神经]。
Q3 Medicine Pub Date : 2025-11-24 DOI: 10.3760/cma.j.cn112148-20250715-00508
J Huang, S K Rong, J Qian, B Xiong, Y Q Yao, J L Du, Q She
{"title":"[Extracorporeal focused ultrasound targeted renal denervation].","authors":"J Huang, S K Rong, J Qian, B Xiong, Y Q Yao, J L Du, Q She","doi":"10.3760/cma.j.cn112148-20250715-00508","DOIUrl":"10.3760/cma.j.cn112148-20250715-00508","url":null,"abstract":"","PeriodicalId":38755,"journal":{"name":"中华心血管病杂志","volume":"53 11","pages":"1212-1215"},"PeriodicalIF":0.0,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145597768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Research progress on the role and mechanism of silent information regulator 3 in the development of diabetic cardiomyopathy]. 【沉默信息调控因子3在糖尿病性心肌病发生发展中的作用及机制研究进展】。
Q3 Medicine Pub Date : 2025-11-24 DOI: 10.3760/cma.j.cn112148-20250730-00537
L Zhang, J X Shen, R X Wang
{"title":"[Research progress on the role and mechanism of silent information regulator 3 in the development of diabetic cardiomyopathy].","authors":"L Zhang, J X Shen, R X Wang","doi":"10.3760/cma.j.cn112148-20250730-00537","DOIUrl":"https://doi.org/10.3760/cma.j.cn112148-20250730-00537","url":null,"abstract":"","PeriodicalId":38755,"journal":{"name":"中华心血管病杂志","volume":"53 11","pages":"1300-1305"},"PeriodicalIF":0.0,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145597692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Clinical applications of therapeutic ultrasound in cardiovascular diseases]. 【超声治疗在心血管疾病中的临床应用】。
Q3 Medicine Pub Date : 2025-11-24 DOI: 10.3760/cma.j.cn112148-20250820-00592
P F Zhang, Y Zhang
{"title":"[Clinical applications of therapeutic ultrasound in cardiovascular diseases].","authors":"P F Zhang, Y Zhang","doi":"10.3760/cma.j.cn112148-20250820-00592","DOIUrl":"10.3760/cma.j.cn112148-20250820-00592","url":null,"abstract":"","PeriodicalId":38755,"journal":{"name":"中华心血管病杂志","volume":"53 11","pages":"1201-1208"},"PeriodicalIF":0.0,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145597702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Construction and validation of acute pulmonary embolism diagnostic model based on clinical and laboratory indicators]. [基于临床和实验室指标的急性肺栓塞诊断模型的构建与验证]。
Q3 Medicine Pub Date : 2025-11-24 DOI: 10.3760/cma.j.cn112148-20250924-00677
M Li, M L Wang, Y R Li, H Y Zhang, X Q Jia, T T Huang

Objective: To establish and validate the diagnostic model of acute pulmonary embolism (APE) based on clinical and laboratory variables. Methods: This retrospective analysis was conducted on patients with suspected APE who underwent CT pulmonary angiography at the First Affiliated Hospital of Henan University of Chinese Medicine between February 2015 and December 2023. The patients were randomly divided into a training set and a validation set at a ratio of 7∶3. Clinical and laboratory data of the enrolled patients were collected, and patients were divided into an APE group and a non-APE group according to CT pulmonary angiography results. In the training set, univariate and multivariate logistic regression as well as Lasso regression were used to identify risk factors for APE, and a diagnostic model was developed and validated. Receiver operating characteristic curves were plotted, and calibration and decision curves were used to assess the performance of the diagnostic model. The diagnostic efficacy of the model was compared with that of the Wells score and the revised Geneva score using the DeLong test. Results: A total of 752 patients were enrolled, aged (64±15) years, including 417 (55.5%) males. The training set included 526 patients and the validation set included 226 patients. The incidence of APE in this cohort was 48.7% (366/752), with 366 cases in the APE group and 386 in the non-APE group. Multivariable logistic regression analysis showed that cyanosis (OR=8.88, 95%CI 2.04-49.11), elevated neutrophil count (OR=1.82, 95%CI 1.06-3.15), elevated creatine kinase isoenzyme (OR=3.45, 95%CI 1.76-6.91), decreased partial pressure of carbon dioxide (OR=12.88, 95%CI 7.64-22.34), elevated age-adjusted D-dimer (OR=2.53, 95%CI 1.10-6.20), prolonged thrombin time (OR=4.08, 95%CI 2.06-8.33), and positive lower limb venous ultrasound for thrombus (OR=4.39, 95%CI 2.59-7.58) were risk factors associated with APE. The area under the curve (AUC) of the diagnostic model was 0.92 (95%CI 0.90-0.94) in the training set and 0.92 (95%CI 0.89-0.95) in the validation set. The diagnostic efficacy of this model was superior to that of the Wells score (AUC: 0.92 vs. 0.63, P<0.01) and the revised Geneva score (AUC: 0.92 vs. 0.59, P<0.01). Conclusion: The diagnostic model for acute pulmonary embolism constructed based on clinical and laboratory parameters demonstrates excellent diagnostic performance and may facilitate rapid and accurate screening in clinical practice.

目的:建立并验证基于临床和实验室变量的急性肺栓塞(APE)诊断模型。方法:回顾性分析2015年2月至2023年12月在河南中医药大学第一附属医院行CT肺血管造影的疑似APE患者。患者按7∶3的比例随机分为训练组和验证组。收集入组患者的临床及实验室资料,根据CT肺血管造影结果将患者分为APE组和非APE组。在训练集中,采用单变量和多变量逻辑回归以及Lasso回归来识别APE的危险因素,并建立诊断模型并进行验证。绘制受试者工作特征曲线,并使用校准曲线和决策曲线来评估诊断模型的性能。采用DeLong检验将模型的诊断效果与Wells评分和修订后的Geneva评分进行比较。结果:共纳入752例患者,年龄(64±15)岁,其中男性417例(55.5%)。训练集包括526例患者,验证集包括226例患者。该队列中APE的发病率为48.7%(366/752),其中APE组366例,非APE组386例。多变量logistic回归分析显示:紫绀(OR=8.88, 95%CI 2.04-49.11)、中性粒细胞计数升高(OR=1.82, 95%CI 1.06-3.15)、肌酸激酶同功酶升高(OR=3.45, 95%CI 1.76-6.91)、二氧化碳分压降低(OR=12.88, 95%CI 7.64-22.34)、年龄调整d -二聚体升高(OR=2.53, 95%CI 1.10-6.20)、凝血酶时间延长(OR=4.08, 95%CI 2.06-8.33)、下肢静脉血栓超声检查阳性(OR=4.39,95%CI 2.59 ~ 7.58)是与APE相关的危险因素。该诊断模型的曲线下面积(AUC)在训练集为0.92 (95%CI 0.90 ~ 0.94),在验证集为0.92 (95%CI 0.89 ~ 0.95)。该模型的诊断效果优于Wells评分(AUC: 0.92 vs. 0.63, pac: 0.92 vs. 0.59, p)。结论:基于临床和实验室参数构建的急性肺栓塞诊断模型具有良好的诊断性能,可在临床实践中进行快速准确的筛查。
{"title":"[Construction and validation of acute pulmonary embolism diagnostic model based on clinical and laboratory indicators].","authors":"M Li, M L Wang, Y R Li, H Y Zhang, X Q Jia, T T Huang","doi":"10.3760/cma.j.cn112148-20250924-00677","DOIUrl":"https://doi.org/10.3760/cma.j.cn112148-20250924-00677","url":null,"abstract":"<p><p><b>Objective:</b> To establish and validate the diagnostic model of acute pulmonary embolism (APE) based on clinical and laboratory variables. <b>Methods:</b> This retrospective analysis was conducted on patients with suspected APE who underwent CT pulmonary angiography at the First Affiliated Hospital of Henan University of Chinese Medicine between February 2015 and December 2023. The patients were randomly divided into a training set and a validation set at a ratio of 7∶3. Clinical and laboratory data of the enrolled patients were collected, and patients were divided into an APE group and a non-APE group according to CT pulmonary angiography results. In the training set, univariate and multivariate logistic regression as well as Lasso regression were used to identify risk factors for APE, and a diagnostic model was developed and validated. Receiver operating characteristic curves were plotted, and calibration and decision curves were used to assess the performance of the diagnostic model. The diagnostic efficacy of the model was compared with that of the Wells score and the revised Geneva score using the DeLong test. <b>Results:</b> A total of 752 patients were enrolled, aged (64±15) years, including 417 (55.5%) males. The training set included 526 patients and the validation set included 226 patients. The incidence of APE in this cohort was 48.7% (366/752), with 366 cases in the APE group and 386 in the non-APE group. Multivariable logistic regression analysis showed that cyanosis (<i>OR</i>=8.88, 95%<i>CI</i> 2.04-49.11), elevated neutrophil count (<i>OR</i>=1.82, 95%<i>CI</i> 1.06-3.15), elevated creatine kinase isoenzyme (<i>OR</i>=3.45, 95%<i>CI</i> 1.76-6.91), decreased partial pressure of carbon dioxide (<i>OR</i>=12.88, 95%<i>CI</i> 7.64-22.34), elevated age-adjusted D-dimer (<i>OR</i>=2.53, 95%<i>CI</i> 1.10-6.20), prolonged thrombin time (<i>OR</i>=4.08, 95%<i>CI</i> 2.06-8.33), and positive lower limb venous ultrasound for thrombus (<i>OR</i>=4.39, 95%<i>CI</i> 2.59-7.58) were risk factors associated with APE. The area under the curve (<i>AUC</i>) of the diagnostic model was 0.92 (95%<i>CI</i> 0.90-0.94) in the training set and 0.92 (95%<i>CI</i> 0.89-0.95) in the validation set. The diagnostic efficacy of this model was superior to that of the Wells score (<i>AUC</i>: 0.92 vs. 0.63, <i>P</i><0.01) and the revised Geneva score (<i>AUC</i>: 0.92 vs. 0.59, <i>P</i><0.01). <b>Conclusion:</b> The diagnostic model for acute pulmonary embolism constructed based on clinical and laboratory parameters demonstrates excellent diagnostic performance and may facilitate rapid and accurate screening in clinical practice.</p>","PeriodicalId":38755,"journal":{"name":"中华心血管病杂志","volume":"53 11","pages":"1254-1262"},"PeriodicalIF":0.0,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145597727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Targeting the root causes of hypertension: bridging mechanistic insights and clinical translation]. [针对高血压的根本原因:架桥机制见解和临床翻译]。
Q3 Medicine Pub Date : 2025-11-24 DOI: 10.3760/cma.j.cn112148-20250807-00556
J Y Sun, X Q Kong
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引用次数: 0
[A case of light-chain amyloidosis with strongly positive 99mTc-pyrophosphate myocardial scintigraphy]. 【轻链淀粉样变性伴99mtc焦磷酸盐心肌显像强阳性1例】。
Q3 Medicine Pub Date : 2025-11-24 DOI: 10.3760/cma.j.cn112148-20250310-00175
J Y Li, S Y Wang, Z Tian
{"title":"[A case of light-chain amyloidosis with strongly positive <sup>99m</sup>Tc-pyrophosphate myocardial scintigraphy].","authors":"J Y Li, S Y Wang, Z Tian","doi":"10.3760/cma.j.cn112148-20250310-00175","DOIUrl":"https://doi.org/10.3760/cma.j.cn112148-20250310-00175","url":null,"abstract":"","PeriodicalId":38755,"journal":{"name":"中华心血管病杂志","volume":"53 11","pages":"1275-1277"},"PeriodicalIF":0.0,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145597732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Inhibition of NLRP3 inflammasome by sonodynamic therapy mediates CACNA1C upregulation to reduce atrial fibrillation susceptibility]. [通过声动力疗法抑制NLRP3炎性体介导CACNA1C上调以降低房颤易感性]。
Q3 Medicine Pub Date : 2025-11-24 DOI: 10.3760/cma.j.cn112148-20250717-00517
W Wang, Y M Wang, H W Cui, H Z Yang, S Y Guo, C Y Zhang, Y Wang, Q P Zhou, Y F Tian, D C Yin, Y Tian
<p><p><b>Objective:</b> To investigate the effect and underlying mechanism of sonodynamic therapy (SDT) on inflammation-related atrial fibrillation (AF) susceptibility. <b>Methods:</b> Lipopolysaccharide (LPS)-stimulated mouse and HL-1 mouse atrial myocyte models were used. (1) In vivo study: experimental groups included control, LPS, LPS+SDT, and SDT groups, with 20 mice in each group. Atrial fibrillation inducibility and duration were assessed by electrical stimulation. Western blot was used to analyze atrial expression of NOD-like receptor family pyrin domain-containing protein 3 (NLRP3), interleukin (IL)-1β, and IL-18. Immunohistochemistry was used to detect calcium voltage-gated channel subunit alpha1 C (CACNA1C) expression. (2) In vitro study: cell counting kit-8 (CCK-8) and Western blot were used to determine the optimal and safe LPS concentration. The safe incubation condition for the sonosensitizer sinoporphyrin sodium was determined by CCK-8 and fluorometry. An LPS-induced inflammatory model in HL-1 atrial myocytes was used, with experimental groups including control, LPS, LPS+SDT, LPS+sinoporphyrin sodium, and LPS+ultrasound groups. NLRP3 was overexpressed using plasmid transfection, with experimental groups including control, NLRP3 plasmid, negative control plasmid, and NLRP3 plasmid+SDT groups. SDT was applied to LPS-stimulated or NLRP3-overexpressing HL-1 cells. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to measure mRNA and protein levels of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), Cleaved Caspase-1, IL-1β, IL-18, and CACNA1C. The NLRP3 inhibitor MCC950 was used to validate the relationship of NLRP3 and CACNA1C. The experimental groups included control, LPS, LPS+MCC950, and MCC950 groups. Intracellular reactive oxygen species (ROS) levels were detected using the probe DCFH-DA, and the ROS scavenger N-acetyl-L-cysteine (NAC) was used to test if the effects of SDT was ROS-dependent. <b>Results:</b> (1) In vivo: The LPS+SDT group exhibited a lower incidence of atrial fibrillation induction and a shorter duration of atrial fibrillation compared to the LPS group(both <i>P</i><0.05). Protein expression levels of NLRP3 and IL-1β were lower than those in the LPS group (all <i>P</i><0.05), while the expression of CACNA1C subunit tended to increase relative to the LPS group (<i>P</i>>0.05). (2) In vitro: The safe concentration of LPS for administration was ≤20 μg/ml, with an optimal pro-inflammatory concentration of 4 μg/ml. The safe concentration of sinoporphyrin sodium for administration was 0.4 μmol/L, with an optimal incubation time of 4 hours. Compared to the LPS group or NLRP3 plasmid group, the LPS+SDT group or NLRP3 plasmid+SDT group exhibited lower expression levels of NLRP3, ASC, Cleaved Caspase-1, IL-1β, and IL-18, and higher mRNA and protein levels of CACNA1C (all <i>P</i><0.05). The LPS+MCC950 group had higher CACNA1C protein expression than the LPS group (
目的:探讨声动力治疗(SDT)对炎症相关性心房颤动(AF)易感性的影响及其机制。方法:采用脂多糖刺激小鼠和HL-1小鼠心房肌细胞模型。(1)体内研究:实验组分为对照组、LPS组、LPS+SDT组、SDT组,每组20只。通过电刺激评估心房颤动的诱发性和持续时间。Western blot检测nod样受体家族pyrin - domain-containing protein 3 (NLRP3)、白细胞介素(IL)-1β、IL-18的心房表达。免疫组织化学检测钙电压门控通道亚单位α 1c (CACNA1C)的表达。(2)体外研究:采用细胞计数试剂盒-8 (CCK-8)和Western blot法确定LPS的最佳安全浓度。采用CCK-8法和荧光法测定声敏剂辛卟啉钠的安全孵育条件。采用LPS诱导的HL-1心房肌细胞炎症模型,实验组分为对照组、LPS组、LPS+SDT组、LPS+中卟啉钠组和LPS+超声组。用质粒转染NLRP3过表达,实验组分为对照组、NLRP3质粒组、阴性对照质粒组和NLRP3质粒+SDT组。SDT应用于lps刺激或nlrp3过表达的HL-1细胞。采用实时定量聚合酶链反应(qRT-PCR)和Western blot检测NLRP3、凋亡相关斑点样蛋白(ASC)、Cleaved Caspase-1、IL-1β、IL-18和CACNA1C的mRNA和蛋白水平。使用NLRP3抑制剂MCC950来验证NLRP3与CACNA1C的关系。实验组分为对照组、LPS组、LPS+MCC950组和MCC950组。使用探针DCFH-DA检测细胞内活性氧(ROS)水平,并使用ROS清除剂n -乙酰- l-半胱氨酸(NAC)检测SDT的作用是否依赖于ROS。结果:(1)体内:与LPS组相比,LPS+SDT组诱发房颤的发生率更低,房颤持续时间更短(PPP均为0.05)。(2)体外:LPS给药安全浓度≤20 μg/ml,促炎最佳浓度为4 μg/ml。氨基卟啉钠的安全给药浓度为0.4 μmol/L,最佳孵育时间为4 h。与LPS组或NLRP3质粒组相比,LPS+SDT组或NLRP3质粒+SDT组NLRP3、ASC、Cleaved Caspase-1、IL-1β和IL-18的表达水平较低,CACNA1C的mRNA和蛋白水平较高(均为ppc)。结论:SDT通过抑制心房心肌细胞NLRP3炎性体的激活,从而上调l型钙通道亚基CACNA1C,从而降低小鼠心房颤动易感性。
{"title":"[Inhibition of NLRP3 inflammasome by sonodynamic therapy mediates CACNA1C upregulation to reduce atrial fibrillation susceptibility].","authors":"W Wang, Y M Wang, H W Cui, H Z Yang, S Y Guo, C Y Zhang, Y Wang, Q P Zhou, Y F Tian, D C Yin, Y Tian","doi":"10.3760/cma.j.cn112148-20250717-00517","DOIUrl":"https://doi.org/10.3760/cma.j.cn112148-20250717-00517","url":null,"abstract":"&lt;p&gt;&lt;p&gt;&lt;b&gt;Objective:&lt;/b&gt; To investigate the effect and underlying mechanism of sonodynamic therapy (SDT) on inflammation-related atrial fibrillation (AF) susceptibility. &lt;b&gt;Methods:&lt;/b&gt; Lipopolysaccharide (LPS)-stimulated mouse and HL-1 mouse atrial myocyte models were used. (1) In vivo study: experimental groups included control, LPS, LPS+SDT, and SDT groups, with 20 mice in each group. Atrial fibrillation inducibility and duration were assessed by electrical stimulation. Western blot was used to analyze atrial expression of NOD-like receptor family pyrin domain-containing protein 3 (NLRP3), interleukin (IL)-1β, and IL-18. Immunohistochemistry was used to detect calcium voltage-gated channel subunit alpha1 C (CACNA1C) expression. (2) In vitro study: cell counting kit-8 (CCK-8) and Western blot were used to determine the optimal and safe LPS concentration. The safe incubation condition for the sonosensitizer sinoporphyrin sodium was determined by CCK-8 and fluorometry. An LPS-induced inflammatory model in HL-1 atrial myocytes was used, with experimental groups including control, LPS, LPS+SDT, LPS+sinoporphyrin sodium, and LPS+ultrasound groups. NLRP3 was overexpressed using plasmid transfection, with experimental groups including control, NLRP3 plasmid, negative control plasmid, and NLRP3 plasmid+SDT groups. SDT was applied to LPS-stimulated or NLRP3-overexpressing HL-1 cells. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to measure mRNA and protein levels of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), Cleaved Caspase-1, IL-1β, IL-18, and CACNA1C. The NLRP3 inhibitor MCC950 was used to validate the relationship of NLRP3 and CACNA1C. The experimental groups included control, LPS, LPS+MCC950, and MCC950 groups. Intracellular reactive oxygen species (ROS) levels were detected using the probe DCFH-DA, and the ROS scavenger N-acetyl-L-cysteine (NAC) was used to test if the effects of SDT was ROS-dependent. &lt;b&gt;Results:&lt;/b&gt; (1) In vivo: The LPS+SDT group exhibited a lower incidence of atrial fibrillation induction and a shorter duration of atrial fibrillation compared to the LPS group(both &lt;i&gt;P&lt;/i&gt;&lt;0.05). Protein expression levels of NLRP3 and IL-1β were lower than those in the LPS group (all &lt;i&gt;P&lt;/i&gt;&lt;0.05), while the expression of CACNA1C subunit tended to increase relative to the LPS group (&lt;i&gt;P&lt;/i&gt;&gt;0.05). (2) In vitro: The safe concentration of LPS for administration was ≤20 μg/ml, with an optimal pro-inflammatory concentration of 4 μg/ml. The safe concentration of sinoporphyrin sodium for administration was 0.4 μmol/L, with an optimal incubation time of 4 hours. Compared to the LPS group or NLRP3 plasmid group, the LPS+SDT group or NLRP3 plasmid+SDT group exhibited lower expression levels of NLRP3, ASC, Cleaved Caspase-1, IL-1β, and IL-18, and higher mRNA and protein levels of CACNA1C (all &lt;i&gt;P&lt;/i&gt;&lt;0.05). The LPS+MCC950 group had higher CACNA1C protein expression than the LPS group (","PeriodicalId":38755,"journal":{"name":"中华心血管病杂志","volume":"53 11","pages":"1231-1243"},"PeriodicalIF":0.0,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145597733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[The clinical characteristics and treatment of 20 cases of ventricular electrical storm]. [20例脑室电暴的临床特点及治疗]
Q3 Medicine Pub Date : 2025-11-24 DOI: 10.3760/cma.j.cn112148-20250908-00637
J Q Wang, M Y Sun, Z L Wang, M Liang

Objective: To analyze the clinical characteristics, diagnostic and therapeutic strategies, and clinical outcomes of ventricular electrical storm. Methods: This study was a descriptive cross-sectional analysis. Patients with ventricular electrical storm admitted to the Department of cardiology, General Hospital of Northern Theater command between July 1, 2022 and July 31, 2023 were enrolled. A retrospective analysis was conducted on their demographic data, clinical characteristics, etiology, diagnosis, treatment, and outcome. Results: A total of 20 patients with ventricular electrical storm were enrolled, aged (62.4±12.0) years, including 13 males. There were 11 cases of acute myocardial infarction (AMI), 1 case of previous myocardial infarction complicated with ischemic cardiomyopathy, 4 cases of dilated cardiomyopathy, and 4 cases of valvular disease. Electrocardiographic manifestations comprised monomorphic ventricular tachycardia in 3 cases, polymorphic ventricular tachycardia in 6 cases, ventricular fibrillation in 4 cases, and polymorphic ventricular tachycardia combined with ventricular fibrillation in 7 cases. Antiarrhythmic therapy primarily involved amiodarone, combined with β-blockers and adjunctive agents such as lidocaine and nifekalant, along with sedation, hypothermia, and anti-heart failure treatment. Ten out of 11 AMI patients underwent successful revascularization, while 1 received medical therapy due to small vessel size. Ten patients met indications for implantable cardioverter-defibrillator (ICD) therapy, with 9 receiving ICD implantation during hospitalization and 1 refusing. Three patients underwent radiofrequency ablation. Two in-hospital deaths occurred due to refractory malignant arrhythmias. During a follow-up of (7.36±2.74) months, 10 out of 11 AMI patients remained free from recurrent ventricular tachycardia and ICD discharges, while 1 was hospitalized twice for heart failure. Both ICD-treated patients with DCM had appropriate shocks for ventricular tachycardia and ventricular fibrillation confirmed by device interrogation. Two additional deaths occurred during follow-up: 1 AMI patient (who refused ICD implantation) died from arrhythmia, and 1 post-mitral valve replacement patient succumbed to heart failure. Conclusion: Ventricular electrical storm represents a life-threatening emergency with poor prognosis, requiring a comprehensive treatment strategy that includes identification and management of triggers, treatment of the underlying disease, standardized drug therapy, and when necessary, adjunctive interventions such as catheter ablation, ICD implantation, and extracorporeal membrane oxygenation may contribute to reduce mortality and improve prognosis.

目的:分析脑室电风暴的临床特点、诊治策略及临床转归。方法:本研究采用描述性横断面分析。选取2022年7月1日至2023年7月31日在北方战区总医院心内科收治的室性电风暴患者。回顾性分析患者的人口学资料、临床特征、病因、诊断、治疗及转归。结果:共纳入20例脑室电风暴患者,年龄(62.4±12.0)岁,其中男性13例。急性心肌梗死(AMI) 11例,既往心肌梗死合并缺血性心肌病1例,扩张型心肌病4例,瓣膜病4例。心电图表现为单形态性室性心动过速3例,多形态性室性心动过速6例,室颤4例,多形态性室性心动过速合并室颤7例。抗心律失常治疗主要包括胺碘酮,联合β受体阻滞剂和辅助药物,如利多卡因和尼非卡兰特,以及镇静、低温和抗心力衰竭治疗。11例AMI患者中有10例血管重建术成功,1例因血管小接受药物治疗。10例患者符合植入式心律转复除颤器(ICD)治疗指征,9例住院期间接受ICD植入,1例拒绝。3例患者行射频消融术。2例因难治性恶性心律失常住院死亡。在(7.36±2.74)个月的随访中,11例AMI患者中有10例没有复发性室性心动过速和ICD出院,而1例因心力衰竭住院两次。两例采用icd治疗的DCM患者均有适当的电击治疗室性心动过速和室性颤动。随访期间新增2例死亡:1例AMI患者(拒绝ICD植入)死于心律失常,1例二尖瓣置换术后患者死于心力衰竭。结论:室性电风暴是一种危及生命且预后不良的急症,需要综合的治疗策略,包括识别和管理触发因素、治疗基础疾病、标准化药物治疗,必要时进行导管消融、ICD植入和体外膜氧合等辅助干预可能有助于降低死亡率和改善预后。
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引用次数: 0
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中华心血管病杂志
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