Pub Date : 2025-11-24DOI: 10.3760/cma.j.cn112148-20251001-00688
T H Zhang, Y Du, X L Gao, L Xu, Y J Zhou
{"title":"[Research progress on pericoronary fat attenuation index].","authors":"T H Zhang, Y Du, X L Gao, L Xu, Y J Zhou","doi":"10.3760/cma.j.cn112148-20251001-00688","DOIUrl":"https://doi.org/10.3760/cma.j.cn112148-20251001-00688","url":null,"abstract":"","PeriodicalId":38755,"journal":{"name":"中华心血管病杂志","volume":"53 11","pages":"1282-1286"},"PeriodicalIF":0.0,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145597728","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}
Pub Date : 2025-11-24DOI: 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}
Pub Date : 2025-11-24DOI: 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}
Pub Date : 2025-11-24DOI: 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}
Pub Date : 2025-11-24DOI: 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}
Pub Date : 2025-11-24DOI: 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.
{"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}
Pub Date : 2025-11-24DOI: 10.3760/cma.j.cn112148-20250807-00556
J Y Sun, X Q Kong
{"title":"[Targeting the root causes of hypertension: bridging mechanistic insights and clinical translation].","authors":"J Y Sun, X Q Kong","doi":"10.3760/cma.j.cn112148-20250807-00556","DOIUrl":"https://doi.org/10.3760/cma.j.cn112148-20250807-00556","url":null,"abstract":"","PeriodicalId":38755,"journal":{"name":"中华心血管病杂志","volume":"53 11","pages":"1209-1211"},"PeriodicalIF":0.0,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145597813","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}
Pub Date : 2025-11-24DOI: 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}
Pub Date : 2025-11-24DOI: 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 (
{"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":"<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 (","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}
Pub Date : 2025-11-24DOI: 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.
{"title":"[The clinical characteristics and treatment of 20 cases of ventricular electrical storm].","authors":"J Q Wang, M Y Sun, Z L Wang, M Liang","doi":"10.3760/cma.j.cn112148-20250908-00637","DOIUrl":"https://doi.org/10.3760/cma.j.cn112148-20250908-00637","url":null,"abstract":"<p><p><b>Objective:</b> To analyze the clinical characteristics, diagnostic and therapeutic strategies, and clinical outcomes of ventricular electrical storm. <b>Methods:</b> 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. <b>Results:</b> 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. <b>Conclusion:</b> 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.</p>","PeriodicalId":38755,"journal":{"name":"中华心血管病杂志","volume":"53 11","pages":"1263-1270"},"PeriodicalIF":0.0,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145597841","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}