Pub Date : 2024-10-01Epub Date: 2024-09-26DOI: 10.1161/CIRCEP.124.013354
Julia H Indik
{"title":"Pulsed Field Ablation: The Temptation for More While Keeping It Safe.","authors":"Julia H Indik","doi":"10.1161/CIRCEP.124.013354","DOIUrl":"10.1161/CIRCEP.124.013354","url":null,"abstract":"","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01Epub Date: 2024-09-26DOI: 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
{"title":"Incidence and Predictors of Pacing-Induced Right Ventricular Cardiomyopathy.","authors":"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","doi":"10.1161/CIRCEP.124.013070","DOIUrl":"10.1161/CIRCEP.124.013070","url":null,"abstract":"","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342747","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01Epub Date: 2024-09-27DOI: 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
{"title":"Oral Anticoagulation and Factor VIII Replacement Therapy in Patients With Hemophilia Undergoing Pulsed-Field or Radiofrequency Catheter Ablation for Atrial Fibrillation.","authors":"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","doi":"10.1161/CIRCEP.124.012921","DOIUrl":"10.1161/CIRCEP.124.012921","url":null,"abstract":"","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01Epub Date: 2024-10-02DOI: 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.
{"title":"Plasma Proteomic Insights for Identification of Novel Predictors and Potential Drug Targets in Atrial Fibrillation: A Prospective Cohort Study and Mendelian Randomization Analysis.","authors":"Xiaodong Peng, Yukun Li, Nian Liu, Shijun Xia, Xin Li, Yiwei Lai, Liu He, Caihua Sang, Jianzeng Dong, Changsheng Ma","doi":"10.1161/CIRCEP.124.013037","DOIUrl":"10.1161/CIRCEP.124.013037","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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 <i>International Classification of Diseases, Tenth Revision</i> 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 <i>cis</i>-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.</p><p><strong>Results: </strong>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 <i>P</i> values below 0.05.</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01Epub Date: 2024-08-30DOI: 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.
{"title":"Characterization and Clinical Significance of Hemolysis After Pulsed Field Ablation for Atrial Fibrillation: Results of a Multicenter Analysis.","authors":"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","doi":"10.1161/CIRCEP.124.012732","DOIUrl":"10.1161/CIRCEP.124.012732","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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 (<i>P</i><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 <i>P</i><0.001). Hemolysis correlated with the number of PFA deliveries (r=0.62 [95% CI, 0.33-0.80]; <i>P</i><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; <i>P</i>=0.010).</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01Epub Date: 2024-08-30DOI: 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.
{"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":null,"pages":null},"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}
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.
{"title":"Roles of Atrial Arrhythmias in Triggering Torsade de Pointes in Patients With Acquired Long QT Syndrome.","authors":"Nobuhiro Takasugi, Susumu Endo, Mieko Takasugi, Ryota Tochibora, Akihiro Yoshida, Takatomo Watanabe, Tomonori Kawaguchi, Yoshihisa Yamada, Hiromitsu Kanamori, Hiroaki Ushikoshi, Hiroyuki Okura","doi":"10.1161/CIRCEP.123.012675","DOIUrl":"10.1161/CIRCEP.123.012675","url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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 <i>U</i> test or Fisher exact test.</p><p><strong>Results: </strong>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, <i>P</i>=0.008). AAs-induced group exhibited macroscopic T-wave alternans more frequently than non-AAs-induced group (6 versus 0 event, <i>P</i>=0.02).</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142132030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01Epub Date: 2024-09-25DOI: 10.1161/CIRCEP.124.013340
Abdullah Sarkar, Olujimi A Ajijola
{"title":"Ablating the Limits: Catheter Ablation of Ventricular Tachycardia in Cardiac Amyloid Patients.","authors":"Abdullah Sarkar, Olujimi A Ajijola","doi":"10.1161/CIRCEP.124.013340","DOIUrl":"10.1161/CIRCEP.124.013340","url":null,"abstract":"","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-01Epub Date: 2024-08-21DOI: 10.1161/CIRCEP.123.012690
Anna Kwiatek-Wrzosek, Mirosław Kowalski, Elżbieta K Biernacka, Piotr Hoffman, Ewa Kowalik
{"title":"Enormous Burden of Atrial Fibrillation in Older Patients With Congenital Heart Disease: Do Only Age and Underlying Heart Defect Matter?","authors":"Anna Kwiatek-Wrzosek, Mirosław Kowalski, Elżbieta K Biernacka, Piotr Hoffman, Ewa Kowalik","doi":"10.1161/CIRCEP.123.012690","DOIUrl":"10.1161/CIRCEP.123.012690","url":null,"abstract":"","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":null,"pages":null},"PeriodicalIF":9.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}