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Incidental Premature Ventricular Contractions in Young Athletes: Shape and Size (of Premature Ventricular Contractions burden) Matter. 年轻运动员的偶发性室性早搏:室性早搏负担)的形状和大小很重要。
IF 9.1 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-09-20 DOI: 10.1161/CIRCEP.124.013345
Marius I Chukwurah, Eugene H Chung
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引用次数: 0
Pulsed Field Ablation: The Temptation for More While Keeping It Safe. 脉冲场消融:在保证安全的同时,诱惑更多。
IF 9.1 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-09-26 DOI: 10.1161/CIRCEP.124.013354
Julia H Indik
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引用次数: 0
Incidence and Predictors of Pacing-Induced Right Ventricular Cardiomyopathy. 起搏诱发右室心肌病的发病率和预测因素。
IF 9.1 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-09-26 DOI: 10.1161/CIRCEP.124.013070
Thomas A Boyle, Naga Venkata K Pothineni, Melissa Austin, Poojita Shivamurthy, Timothy Markman, Gustavo Guandalini, Matthew Hyman, Andres Enriquez, Michael G Fradley, Robert Schaller, Gregory Supple, Rajat Deo, Vincent Y See, Michael Riley, Fermin Garcia, Saman Nazarian, David Lin, Sanjay Dixit, Andrew E Epstein, David Callans, Francis E Marchlinski, David S Frankel
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引用次数: 0
Oral Anticoagulation and Factor VIII Replacement Therapy in Patients With Hemophilia Undergoing Pulsed-Field or Radiofrequency Catheter Ablation for Atrial Fibrillation. 接受脉冲场或射频导管消融术治疗心房颤动的血友病患者的口服抗凝剂和因子 VIII 替代疗法。
IF 9.1 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-09-27 DOI: 10.1161/CIRCEP.124.012921
Sanghamitra Mohanty, Michela Casella, Paolo Compagnucci, Prem Geeta Torlapati, Vincenzo Mirco La Fazia, Carola Gianni, Bryan MacDonald, Angel Quintero Mayedo, Domenico Giovanni Della Rocca, John Allison, Mohamed Bassiouny, G Joseph Gallinghouse, John D Burkhardt, Rodney Horton, Amin Al-Ahmad, Luigi Di Biase, Antonio Dello Russo, Andrea Natale
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引用次数: 0
Elimination of Epicardial Scar-Related Ventricular Tachycardia With Endocardial Pulsed Field Ablation: First Clinical Report. 心内膜脉冲场消融术消除心外膜瘢痕相关性室性心动过速:首例临床报告。
IF 9.1 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-08-28 DOI: 10.1161/CIRCEP.124.012992
Jose Aguilera, Edmond Obeng-Gyimah, Yuki Kuramochi, Roy Chung, Hubert Cochet, Megan Christie, Hiroshi Nakagawa, Jakub Sroubek, Oussama Wazni, Pasquale Santangeli
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引用次数: 0
Plasma Proteomic Insights for Identification of Novel Predictors and Potential Drug Targets in Atrial Fibrillation: A Prospective Cohort Study and Mendelian Randomization Analysis. 用于识别心房颤动新预测因子和潜在药物靶点的血浆蛋白质组学见解:前瞻性队列研究和孟德尔随机分析
IF 9.1 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-10-02 DOI: 10.1161/CIRCEP.124.013037
Xiaodong Peng, Yukun Li, Nian Liu, Shijun Xia, Xin Li, Yiwei Lai, Liu He, Caihua Sang, Jianzeng Dong, Changsheng Ma

Background: Currently, there are no reliable methods for predicting and preventing atrial fibrillation (AF) in its early stages. This study aimed to identify plasma proteins associated with AF to discover biomarkers and potential drug targets.

Methods: The UK Biobank Pharma Proteomics Project examined 2923 circulating proteins using the Olink platform, forming the basis of this prospective cohort study. The UK Biobank Pharma Proteomics Project included a randomly selected discovery cohort and the consortium-selected replication cohort. The study's end point was incident AF, identified using International Classification of Diseases, Tenth Revision codes. The association between plasma proteins and incident AF was evaluated using Cox proportional hazard models in both cohorts. Proteins present in both cohorts underwent Mendelian randomization analysis to delineate causal connections, utilizing cis-protein quantitative trait loci as genetic tools. The predictive efficacy of the identified proteins for AF was assessed using the area under the receiver operating characteristic curve, and their druggability was explored.

Results: Data from 38 784 participants were included in this study. Incident AF cases were identified in the discovery cohort (1894; 5.5%) within a median follow-up of 14.5 years and in the replication cohort (451; 10.6%) within a median follow-up of 14.4 years. Twenty-one proteins linked to AF were identified in both cohorts. Specifically, COL4A1 (collagen IV α-1; odds ratio, 1.11 [95% CI, 1.04-1.19]; false discovery rate, 0.016) and RET (proto-oncogene tyrosine-protein kinase receptor Ret; odds ratio, 0.96 [95% CI, 0.94-0.98]; false discovery rate, 0.013) demonstrated a causal link with AF, and RET is druggable. COL4A1 improved the short- and long-term predictive performance of established AF models, as evidenced by significant enhancements in the area under the receiver operating characteristic, integrated discrimination improvement, and net reclassification index, all with P values below 0.05.

Conclusions: COL4A1 and RET are associated with the development of AF. RET is identified as a potential drug target for AF prevention, while COL4A1 serves as a biomarker for AF prediction. Future studies are needed to evaluate the effectiveness of targeting these proteins to reduce AF risk.

背景:目前,还没有可靠的方法在早期预测和预防心房颤动(AF)。这项研究旨在鉴定与房颤相关的血浆蛋白,以发现生物标记物和潜在的药物靶点:英国生物库药物蛋白质组学项目利用 Olink 平台检测了 2923 种循环蛋白质,为这项前瞻性队列研究奠定了基础。英国生物库医药蛋白质组学项目包括随机挑选的发现队列和联盟挑选的复制队列。研究终点是使用《国际疾病分类》第十版代码确定的房颤事件。在两个队列中使用 Cox 比例危险模型评估了血浆蛋白与心房颤动发病率之间的关系。利用顺式蛋白质定量性状位点作为遗传工具,对两个队列中存在的蛋白质进行孟德尔随机分析,以确定因果关系。利用接收者操作特征曲线下面积评估了已识别蛋白质对房颤的预测功效,并探讨了其可药用性:结果:本研究纳入了 53 032 名参与者的数据。在中位随访 14.5 年的发现队列(1894 例;5.5%)和中位随访 14.4 年的复制队列(451 例;10.6%)中发现了房颤病例。两个队列中均发现了 21 种与房颤相关的蛋白质。具体来说,COL4A1(胶原蛋白 IV α-1;几率比为 1.11 [95% CI, 1.04-1.19];错误发现率为 0.016)和 RET(原癌基因酪氨酸蛋白激酶受体 Ret;几率比为 0.96 [95% CI, 0.94-0.98];错误发现率为 0.013)与心房颤动有因果关系,而 RET 是可以药物治疗的。COL4A1改善了已建立的房颤模型的短期和长期预测性能,这体现在接收者操作特征下面积、综合辨别改进和净再分类指数的显著提高,所有P值均低于0.05:COL4A1和RET与房颤的发生有关。结论:COL4A1和RET与心房颤动的发生有关,RET被认为是预防心房颤动的潜在药物靶点,而COL4A1则是预测心房颤动的生物标志物。未来的研究需要评估以这些蛋白为靶点降低房颤风险的有效性。
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引用次数: 0
Characterization and Clinical Significance of Hemolysis After Pulsed Field Ablation for Atrial Fibrillation: Results of a Multicenter Analysis. 脉冲场消融治疗心房颤动后溶血的特征和临床意义:多中心分析结果。
IF 9.1 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-08-30 DOI: 10.1161/CIRCEP.124.012732
Miruna A Popa, Sandrine Venier, Roberto Menè, Domenico Giovanni Della Rocca, Frédéric Sacher, Nicolas Derval, Mélèze Hocini, Stéphanie Dulucq, Guido Caluori, Stéphane Combes, Jean-Paul Albenque, Federica Saitta, Bernhard Haller, Gian-Battista Chierchia, Carlo de Asmundis, Pascal Defaye, Serge Boveda, Pierre Jaïs

Background: Pulsed field ablation (PFA) is increasingly used in clinical practice for the treatment of atrial fibrillation. While the susceptibility of erythrocytes to electroporation is well established, the effect of cardiac PFA technologies on hemolysis has remained underreported. The aim of this study was to investigate the incidence, severity, and clinical impact of PFA-induced hemolysis.

Methods: We included n=145 patients undergoing atrial fibrillation catheter ablation with a pentaspline PFA catheter (biphasic, bipolar pulses of 2 kV) and n=70 patients receiving radiofrequency ablation (40-90 W) at 4 high-volume European centers. The lesion set comprised pulmonary vein isolation for paroxysmal atrial fibrillation and pulmonary vein isolation±additional lesions for persistent atrial fibrillation. Hemolysis and renal function biomarkers were analyzed in blood samples at baseline, at the end of ablation, and 24 hours after the procedure.

Results: Baseline characteristics were well balanced between groups (overall mean 65.7±9.4 years; 69.3% men). The ablation procedures comprised a mean of 61.6±27.4 PFA deliveries and 26.3±15.0 minutes RF duration. Hemolysis was detected in 94.3% versus 6.8% of patients after PFA versus radiofrequency ablation (P<0.001): PFA was associated with significantly lower haptoglobin levels (0.5±0.4 versus 1.0±0.4 g/L), while free plasma hemoglobin (592.8±330.6 versus 147.8±183.0 mg/L), bilirubin (21.3±11.3 versus 14.8±8.8 µmol/L), and LDH (lactate dehydrogenase, 352.7±115.7 versus 253.2±56.5 U/L) were significantly higher after PFA compared with radiofrequency ablation (all P<0.001). Hemolysis correlated with the number of PFA deliveries (r=0.62 [95% CI, 0.33-0.80]; P<0.001), with the highest severity occurring ≥54 PFA deliveries. After PFA, hemoglobinuria occurred in 36.4%, while creatinine increase was higher in patients with baseline glomerular filtration rate <50 mL/min than with baseline glomerular filtration rate >50 mL/min (Δcrea, 27.0±103.1 versus -0.2±12.1 µmol/L; P=0.010).

Conclusions: Intravascular hemolysis is a frequent finding after PFA and increases with the number of PFA deliveries. Until the clinical impact of PFA-associated hemolysis is fully elucidated, a careful titration of PFA deliveries during the ablation procedure is warranted.

背景:脉冲场消融术(PFA)越来越多地应用于治疗心房颤动的临床实践中。虽然红细胞对电穿孔的易感性已得到公认,但心脏 PFA 技术对溶血的影响仍未得到充分报道。本研究旨在调查 PFA 诱导溶血的发生率、严重程度和临床影响:我们纳入了在欧洲 4 个高容量中心接受心房颤动导管消融术的 145 名患者和接受射频消融术(40-90 W)的 70 名患者。病变集包括阵发性心房颤动的肺静脉隔离术和持续性心房颤动的肺静脉隔离术(附加病变)。对基线、消融结束时和术后24小时的血液样本进行了溶血和肾功能生物标志物分析:各组的基线特征非常均衡(总平均年龄为 65.7±9.4 岁;69.3% 为男性)。消融手术的平均PFA分娩次数为61.6±27.4次,射频持续时间为26.3±15.0分钟。PFA与射频消融术后,94.3%的患者与6.8%的患者检测到溶血(PPP50 mL/min (Δcrea, 27.0±103.1 versus -0.2±12.1 µmol/L; P=0.010):结论:血管内溶血是PFA术后的常见现象,并随着PFA分娩次数的增加而增加。在完全阐明 PFA 相关溶血的临床影响之前,有必要在消融术中谨慎调整 PFA 输送量。
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引用次数: 0
c-Src Is Responsible for Mitochondria-Mediated Arrhythmic Risk in Ischemic Cardiomyopathy. c-Src 对缺血性心肌病线粒体介导的心律失常风险负责
IF 9.1 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-08-30 DOI: 10.1161/CIRCEP.124.013054
An Xie, Gyeoung-Jin Kang, Eun Ji Kim, Hong Liu, Feng Feng, Samuel C Dudley

Background: Increased mitochondrial Ca2+ uptake has been implicated in the QT prolongation and lethal arrhythmias associated with nonischemic cardiomyopathy. We attempted to define the role of mitochondria in ischemic arrhythmic risk and to identify upstream regulators.

Methods: Myocardial infarction (MI) was induced in wild-type FVB/NJ mice by ligation of the left anterior descending coronary artery. Western blot, immunoprecipitation, ECG telemetry, and patch-clamp techniques were used.

Results: After MI, c-Src (proto-oncogene tyrosine-protein kinase Src) and its active form (phosphorylated Src, p-Src) were increased. The activation of c-Src was associated with increased diastolic Ca2+ sparks, action potential duration prolongation, and arrhythmia in MI mice. c-Src upregulation and arrhythmia could be reversed by treatment of mice with the Src inhibitor PP1 but not with the inactive analogue PP3. Tyrosine phosphorylated mitochondrial Ca2+ uniporter (MCU) was upregulated in the heart tissues of MI mice and patients with ischemic cardiomyopathy. In a heterologous expression system, c-Src could bind MCU and phosphorylate MCU tyrosines. Overexpression of wild-type c-Src significantly increased the mitochondrial Ca2+ transient while overexpression of dominant-negative c-Src significantly decreased the mitochondrial Ca2+ transient. c-Src inhibition by PP1, MCU inhibition by Ru360, or MCU knockdown could reduce the action potential duration, Ca2+ sparks, and arrhythmia after MI. The human heart tissue showed that patients with ischemic cardiomyopathy had significantly increased c-Src active form associated with increased MCU tyrosine phosphorylation and ventricular arrhythmia.

Conclusions: MI leads to increased c-Src active form that results in MCU tyrosine phosphorylation, increased mitochondrial Ca2+ uptake, QT prolongation, and arrhythmia, suggesting c-Src or MCU may represent novel antiarrhythmic targets.

背景:线粒体 Ca2+ 摄取增加与非缺血性心肌病相关的 QT 延长和致命性心律失常有关。我们试图确定线粒体在缺血性心律失常风险中的作用,并找出上游调节因子:方法:通过结扎左前降支冠状动脉诱发野生型 FVB/NJ 小鼠心肌梗死(MI)。采用了 Western 印迹、免疫沉淀、心电图遥测和膜片钳技术:结果:心肌梗死后,c-Src(原癌基因酪氨酸蛋白激酶 Src)及其活性形式(p-Src Y416)增加。c-Src 的激活与心肌梗死小鼠舒张期 Ca2+ 火花增加、动作电位持续时间延长和心律失常有关。Src 抑制剂 PP1 可逆转小鼠的 c-Src 上调和心律失常,但非活性类似物 PP3 则无法逆转。在心肌梗死小鼠和缺血性心肌病患者的心脏组织中,酪氨酸磷酸化线粒体 Ca2+ uniporter(MCU)上调。在异源表达系统中,c-Src能与MCU结合并使MCU酪氨酸磷酸化。过表达野生型c-Src可显著增加线粒体Ca2+瞬时,而过表达显性阴性c-Src可显著降低线粒体Ca2+瞬时。通过PP1抑制c-Src、Ru360抑制MCU或敲除MCU可缩短心肌梗死后的动作电位持续时间、减少Ca2+火花和心律失常。人体心脏组织显示,缺血性心肌病患者的c-Src活性显著增加,与MCU酪氨酸磷酸化增加和室性心律失常有关:结论:心肌梗死导致 c-Src 活性形式增加,从而导致 MCU 酪氨酸磷酸化、线粒体 Ca2+ 摄取增加、QT 延长和心律失常,这表明 c-Src 或 MCU 可能是新的抗心律失常靶点。
{"title":"c-Src Is Responsible for Mitochondria-Mediated Arrhythmic Risk in Ischemic Cardiomyopathy.","authors":"An Xie, Gyeoung-Jin Kang, Eun Ji Kim, Hong Liu, Feng Feng, Samuel C Dudley","doi":"10.1161/CIRCEP.124.013054","DOIUrl":"10.1161/CIRCEP.124.013054","url":null,"abstract":"<p><strong>Background: </strong>Increased mitochondrial Ca<sup>2+</sup> uptake has been implicated in the QT prolongation and lethal arrhythmias associated with nonischemic cardiomyopathy. We attempted to define the role of mitochondria in ischemic arrhythmic risk and to identify upstream regulators.</p><p><strong>Methods: </strong>Myocardial infarction (MI) was induced in wild-type FVB/NJ mice by ligation of the left anterior descending coronary artery. Western blot, immunoprecipitation, ECG telemetry, and patch-clamp techniques were used.</p><p><strong>Results: </strong>After MI, c-Src (proto-oncogene tyrosine-protein kinase Src) and its active form (phosphorylated Src, p-Src) were increased. The activation of c-Src was associated with increased diastolic Ca<sup>2+</sup> sparks, action potential duration prolongation, and arrhythmia in MI mice. c-Src upregulation and arrhythmia could be reversed by treatment of mice with the Src inhibitor PP1 but not with the inactive analogue PP3. Tyrosine phosphorylated mitochondrial Ca<sup>2+</sup> uniporter (MCU) was upregulated in the heart tissues of MI mice and patients with ischemic cardiomyopathy. In a heterologous expression system, c-Src could bind MCU and phosphorylate MCU tyrosines. Overexpression of wild-type c-Src significantly increased the mitochondrial Ca<sup>2+</sup> transient while overexpression of dominant-negative c-Src significantly decreased the mitochondrial Ca<sup>2+</sup> transient. c-Src inhibition by PP1, MCU inhibition by Ru360, or MCU knockdown could reduce the action potential duration, Ca<sup>2+</sup> sparks, and arrhythmia after MI. The human heart tissue showed that patients with ischemic cardiomyopathy had significantly increased c-Src active form associated with increased MCU tyrosine phosphorylation and ventricular arrhythmia.</p><p><strong>Conclusions: </strong>MI leads to increased c-Src active form that results in MCU tyrosine phosphorylation, increased mitochondrial Ca<sup>2+</sup> uptake, QT prolongation, and arrhythmia, suggesting c-Src or MCU may represent novel antiarrhythmic targets.</p>","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":" ","pages":"e013054"},"PeriodicalIF":9.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11477858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Ablating the Limits: Catheter Ablation of Ventricular Tachycardia in Cardiac Amyloid Patients. 消融极限:心脏淀粉样变性患者室性心动过速的导管消融。
IF 9.1 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-09-25 DOI: 10.1161/CIRCEP.124.013340
Abdullah Sarkar, Olujimi A Ajijola
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引用次数: 0
Roles of Atrial Arrhythmias in Triggering Torsade de Pointes in Patients With Acquired Long QT Syndrome. 房性心律失常在诱发获得性长 QT 综合征患者 Torsade de Pointes 中的作用。
IF 9.1 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-10-01 Epub Date: 2024-09-05 DOI: 10.1161/CIRCEP.123.012675
Nobuhiro Takasugi, Susumu Endo, Mieko Takasugi, Ryota Tochibora, Akihiro Yoshida, Takatomo Watanabe, Tomonori Kawaguchi, Yoshihisa Yamada, Hiromitsu Kanamori, Hiroaki Ushikoshi, Hiroyuki Okura

Background: Little is known about the role of atrial arrhythmias (AAs) in triggering Torsade de Pointes (TdP) in patients with long QT syndrome (LQTS). The aim of this study was to examine the contribution of AAs to the development of TdP in acquired LQTS patients.

Methods: The initiation patterns of 81 episodes of TdP obtained from 34 consecutive acute acquired LQTS patients (14 men, median age, 69 years; median QTc, 645.5 ms) with documented TdP were analyzed. The initiation mode of TdP was divided into 3 categories: (1) preceding short-long sequence (SLS); (2) sudden R-on-T phenomenon without preceding SLS; and (3) increased atrial rate. The patients were divided into 2 groups based on the presence or absence of AAs-induced TdP; AAs-induced (n=18) and non-AAs-induced (n=16) groups. The association of clinical/ECG characteristics and TdP frequency after initiating conventional therapy with AAs-induced TdP was evaluated. The groups were compared using the Mann-Whitney U test or Fisher exact test.

Results: AAs-induced group comprised 52.9% (18/34) of the patients studied. TdP was preceded by AAs-initiated SLSs in 41.2% (14/34) of the patients and was directly induced by R-on-T AAs (AAs coincidentally encountered a vulnerable repolarizing region during the T wave) in 23.5% (8/34). AAs triggered 48 (59.3%) of the 81 TdP episodes. AAs initiated SLSs in 67.8% (40/59) of the SLS-induced TdP episodes. R-on-T AAs accounted for 23.5% (19/81) of the TdP episodes. AAs-induced group experienced TdP after initiating therapy more frequently than non-AAs-induced group (2.5 versus 1 event, P=0.008). AAs-induced group exhibited macroscopic T-wave alternans more frequently than non-AAs-induced group (6 versus 0 event, P=0.02).

Conclusions: AAs play a key role in triggering TdP in more than half of patients with acute acquired LQTS and can increase TdP frequency after initiating therapy. Thus, AAs are not benign but rather can be life-threatening in patients with acute acquired LQTS.

背景:人们对房性心律失常(AAs)在诱发长QT综合征(LQTS)患者的Torsade de Pointes(TdP)中的作用知之甚少。本研究旨在探讨 AAs 对获得性 LQTS 患者 TdP 发生的影响:方法:分析了连续 34 例急性获得性 LQTS 患者(14 例男性,中位年龄 69 岁,中位 QTc 645.5 毫秒)中有记录的 81 次 TdP 的起始模式。TdP 的起始模式分为 3 类:(1)先兆短长序列(SLS);(2)无先兆 SLS 的突发 R-on-T 现象;(3)心房率增快。根据有无AAs诱导的TdP将患者分为两组:AAs诱导组(18人)和非AAs诱导组(16人)。评估了临床/ECG 特征和开始常规治疗后的 TdP 频率与 AAs 诱导的 TdP 的相关性。各组间的比较采用 Mann-Whitney U 检验或 Fisher exact 检验:结果:AAs诱发组占研究患者的52.9%(18/34)。41.2%的患者(14/34)在TdP之前由AA引发SLS,23.5%的患者(8/34)由R-on-T AAs直接诱发(AAs在T波期间巧遇易受影响的再极化区域)。在 81 次 TdP 发作中,有 48 次(59.3%)由 AAs 触发。在 SLS 诱导的 TdP 发作中,67.8%(40/59)的 SLS 由 AA 引发。R-on-T配气占 TdP 发作的 23.5%(19/81)。与非 AAs 诱发组相比,AAs 诱发组在开始治疗后发生 TdP 的频率更高(2.5 次对 1 次,P=0.008)。AAs诱导组比非AAs诱导组更频繁地出现宏观T波交替(6对0,P=0.02):结论:AAs 在引发半数以上急性获得性 LQTS 患者的 TdP 中起着关键作用,并可在开始治疗后增加 TdP 频率。因此,在急性获得性 LQTS 患者中,AAs 并非良性,反而可能危及生命。
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引用次数: 0
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Circulation. Arrhythmia and electrophysiology
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