Circulation. Arrhythmia and electrophysiology最新文献

{"title":"Long-Term Risk Assessment in Athletes With Complex Ventricular Arrhythmias.","authors":"Paolo Compagnucci, Michela Casella, Maria Lucia Narducci, Edoardo Conte, Michela Cammarano, Gemma Pelargonio, Daniele Andreini, Vincenzo Palmieri, Giulia Stronati, Gerardo Lo Russo, Matteo Brusamolino, Gianluca Pontone, Federico Guerra, Andrea Natale, Claudio Tondo, Filippo Crea, Paolo Zeppilli, Antonio Dello Russo","doi":"10.1161/CIRCEP.124.013480","DOIUrl":"https://doi.org/10.1161/CIRCEP.124.013480","url":null,"abstract":"<p><strong>Background: </strong>Ventricular arrhythmias (VAs) are a major concern in athletes. We sought to determine the prognostic role of noninvasive and invasive assessments in athletes with complex VAs.</p><p><strong>Methods: </strong>One-hundred-ninety athletes (82% male; 28 [19-43] years; 148 [78%] competitive athletes) with frequent or exercise-induced premature ventricular complexes or nonsustained ventricular tachycardia were included in a multicenter cohort study and categorized based on VA ECG morphology into common (n=99) and uncommon (n=91) VA groups. Each athlete underwent a comprehensive diagnostic workup, including cardiac magnetic resonance in 94% (n=178) and electrophysiology study/electroanatomical mapping in 87% (n=166). The primary end point was the occurrence of sudden death or sustained VAs during long-term follow-up.</p><p><strong>Results: </strong>Athletes with uncommon VA morphology had higher rates of abnormal findings at multimodality assessment and more final diagnoses of structural heart disease. Over a median follow-up of 6.2 (4.3-8.1) years, 7 (4%) athletes experienced a primary outcome event, including 1 sudden death. Interestingly, no events occurred in athletes with common morphology VAs. In univariable Cox models, factors associated with the primary end point included uncommon VA morphology (<i>P</i>=0.003), lack of VA suppression (<i>P</i>=0.049), and nonsustained ventricular tachycardia/ventricular tachycardia induction (<i>P</i>=0.010) during stress testing, late gadolinium enhancement (<i>P</i>=0.045), electroanatomical scar regions (<i>P</i>=0.022), and sustained VA inducibility by electrophysiology study (<i>P</i><0.001). Incorporating findings of invasive tests improved prediction of primary outcome events over clinical/noninvasive findings in isolation (log-likelihood ratio for nested models, <i>P</i>=0.004). A survival tree model based on VA morphology, late gadolinium enhancement, VA response to exercise testing, and electroanatomical mapping allowed risk stratification, identifying subgroups of athletes without primary outcome events during follow-up. Among 148 competitive athletes, 101 (68%) regained eligibility after 3 months of detraining, but only 42 (28%) continued long-term.</p><p><strong>Conclusions: </strong>A comprehensive diagnostic assessment integrating ECG, stress testing, and imaging findings, along with the selective use of invasive electrophysiology assessments, may help refine the prognostic evaluation of athletes with complex VAs.</p>","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":" ","pages":"e013480"},"PeriodicalIF":9.1,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144157159","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}

{"title":"Mechanisms Underlying Sinus Node Dysfunction in a Rat Model of Genetic Atrial Cardiomyopathy.","authors":"Edouard Marcoux, Martin Mackasey, Deanna Sosnowski, Patrice Naud, Louis Villeneuve, Martin G Sirois, Jean-Claude Tardif, T Alexander Quinn, Stanley Nattel","doi":"10.1161/CIRCEP.124.013180","DOIUrl":"10.1161/CIRCEP.124.013180","url":null,"abstract":"<p><strong>Background: </strong>Sinoatrial node (SAN) dysfunction is commonly associated with atrial dysrhythmia (tachy-brady syndrome) and is a particularly important feature of inherited atrial cardiomyopathies leading to artificial pacemaker implantation. Essential MYL4 (myosin light chain-4) is an atrial-selective protein that associates with the myosin light chain and participates importantly in cardiacmuscle contraction. <i>MYL4</i> gene variants encoding dysfunctional versions of MYL4 cause familial atrial cardiomyopathy with a high incidence of early SAN dysfunction (SND) and pacemaker requirement. In this study, we used a rat line, genetically modified to express an <i>E11K</i> gene mutation responsible for familial atrial cardiomyopathy, to address the mechanisms underlying SND.</p><p><strong>Methods: </strong>Cardiac structure and function were assessed by echocardiography and in vivo telemetry recording. SAN function was studied in vivo with intracardiac electrophysiology and ex vivo with optical mapping. Mechanisms underlying SND were interrogated in vitro with the use of voltage and current clamp with tight-seal patch-clamp and Ca²⁺ imaging of isolated SAN cardiomyocytes. Gene expression was assessed by quantitative polymerase chain reaction, and fibrosis was determined with Masson's trichrome stain.</p><p><strong>Results: </strong>Mutant <i>Myl4-p.E11K</i>^<i>+/+</i> rats exhibited worse SAN function compared with wild-type controls. In vivo, SND was demonstrated by ≈63% increase in sinus node recovery time compared with wild type. In vitro, SAN conduction velocity was reduced by ≈ 50% for <i>Myl4-p.E11K</i>^<i>+/+</i> compared with wild type. Isolated SAN cells showed ≈50% reduction in funny current and L-type Ca²⁺-current densities. Dysregulation of Ca²⁺ homeostasis was observed in <i>Myl4-p.E11K</i>^<i>+/+</i>, with ≈30% slower time to peak and Ca²⁺ decay. Masson's trichrome staining showed ≈45% increase in SAN region collagen deposition in <i>Myl4-p.E11K</i>^<i>+/+.</i></p><p><strong>Conclusions: </strong><i>Myl4-p.E11K</i>^<i>+/+</i> mutation causes progressive SND with aging, as a result of extensive abnormalities in the underlying determinants of SAN function, including ion-channel properties, Ca²⁺-homeostasis, and SAN structure. These observations provide new insights into the mechanisms of SAN abnormality in atrial cardiomyopathy.</p>","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":" ","pages":"e013180"},"PeriodicalIF":9.1,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149479","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}

{"title":"Fragmented QRS, Arrhythmic Causes, and Myocardial Fibrosis Burden by Autopsy Among Countywide Sudden Deaths.","authors":"Jakrin Kewcharoen, Kosuke Nakasuka, James W Salazar, Andrew J Connolly, Ellen Moffatt, Zian H Tseng","doi":"10.1161/CIRCEP.125.013809","DOIUrl":"https://doi.org/10.1161/CIRCEP.125.013809","url":null,"abstract":"","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":" ","pages":"e013809"},"PeriodicalIF":9.1,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109783","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}

{"title":"Validation of a Novel Risk Prediction Score for Sudden Cardiac Death in the Framingham Heart Study.","authors":"Thien Tan Tri Tai Truyen, Honghuang Lin, Marco Mathias, Harpriya Chugh, Kyndaron Reinier, Emelia J Benjamin, Sumeet S Chugh","doi":"10.1161/CIRCEP.124.013647","DOIUrl":"https://doi.org/10.1161/CIRCEP.124.013647","url":null,"abstract":"<p><strong>Background: </strong>We have previously reported a novel clinical risk score (risk prediction score for shockable sudden cardiac arrest [VFRisk]) for the prediction of shockable sudden cardiac arrest, discovered and validated in 2 US west coast communities. We hypothesized that VFRisk predicts sudden cardiac death (SCD) risk in the geographically distinct FHS (Framingham Heart Study).</p><p><strong>Methods: </strong>We performed a nested case-referents study in the FHS to test VFRisk. Cases were participants who experienced SCD among the original and offspring FHS cohorts. Referents were randomly selected from FHS participants frequency-matched (ratio of 1:3) to cases on age, sex, cohort, and exam. VFRisk was the sum of 12 risk factors, each multiplied by its respective points.</p><p><strong>Results: </strong>Among 312 cases and 935 referents, mean ages were 69.5 and 69.7 years with 70.8% male in both groups. SCD cases had significantly higher prevalence of diabetes, heart failure, stroke, atrial fibrillation, and myocardial infarction compared with the referents group. The VFRisk score was validated with good discrimination (C-statistic, 0.71 [95% CI, 0.66-0.77]) for SCD. Cases had higher VFRisk scores than referents (3.8±2.8 versus 1.8±1.7; <i>P</i><0.001). A 1-unit increase in VFRisk score was associated with a 48% increase in odds of SCD (odds ratio, 1.48 [95% CI, 1.34-1.64]). The highest VFRisk quartile had 7.8-fold higher odds of SCD than the lowest quartile.</p><p><strong>Conclusions: </strong>The VFRisk score successfully predicted SCD in the FHS. The differences in discrimination between the 2 studies could partially be explained by the inability to distinguish shockable versus nonshockable events in the FHS.</p>","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":" ","pages":"e013647"},"PeriodicalIF":9.1,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101368","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}

{"title":"STAR Locally Prolongs Effective Refractory Period and Increases Ventricular Tachycardia Cycle Length Without Short-Term Scar Formation or Functional Decline: Insights From a Translational Porcine Model Study.","authors":"Brian Zenger, Timothy W Smith, Stephanie Hicks, Sherwin Ng, Todd Pavek, Nels Knutson, Pamela Samson, Jie Zheng, Caleb Berberet, El-Sayed H Ibrahim, Vinay Jani, James Tabor, Leslie Wilson, Samuel D Jordan, Luke Marut, Aryan Kumar, Sneha Manikandan, Ali Javaheri, Carmen Bergom, Julie K Schwarz, Patrick M Boyle, Geoffrey D Hugo, Phillip Cuculich, Cliff Robinson, Christian Zemlin, Stacey L Rentschler","doi":"10.1161/CIRCEP.124.013684","DOIUrl":"https://doi.org/10.1161/CIRCEP.124.013684","url":null,"abstract":"<p><strong>Background: </strong>Stereotactic arrhythmia radiotherapy (STAR) has emerged as a potential therapy for treatment-refractory ventricular tachycardia (VT). However, the mechanisms underlying STAR efficacy, such as scar or other electromechanical changes, are still unclear. The goal of this study was to develop a translational porcine model of ischemic monomorphic VT treated with STAR to examine the physiological changes after a typical clinical STAR treatment.</p><p><strong>Methods: </strong>We treated a previously validated porcine model of monomorphic VT after myocardial infarction with a clinically derived STAR protocol. A dose of 25 Gy was prescribed to the planning target volume and 35 Gy to the clinical target volume (regions of scar), while controls underwent a sham STAR treatment. All investigators in the study were blinded except the treating investigator. The primary study outcome was VT inducibility at 6 weeks post-STAR. Animals underwent pre- and post-STAR cardiac magnetic resonance imaging to quantify myocardial scar and function, as well as body surface mapping. Six weeks post-STAR, animals underwent a VT induction study, and tissue was harvested for optical mapping and histological analysis.</p><p><strong>Results: </strong>Six animals completed the study, which ended before finishing enrollment because all animals had inducible VT. We found a significantly longer local effective refractory period in the left ventricular apex and longer VT cycle lengths in STAR-treated animals compared with controls (<i>P</i><0.05). We found no difference in myocardial scar burden, mechanical function, or body surface recordings when comparing pre- and post-STAR.</p><p><strong>Conclusions: </strong>Our data suggest a novel therapeutic mechanism of STAR driven by increasing the effective refractory period in locally treated areas, corresponding to increased tissue wavelength. Our results corroborate clinical case reports and anecdotal evidence that STAR increases VT cycle length. Importantly, these effects were not mediated by an increase in myocardial scar burden. However, our studies do not examine the long-term effects of STAR.</p>","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":" ","pages":"e013684"},"PeriodicalIF":9.1,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101366","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}

{"title":"Stroke Mortality in Patients With Atrial Fibrillation/Flutter: Overall Trends and Sex Differences in the United States.","authors":"Issam Motairek, Chadi Tabaja, Arwa Younis, Ayman A Hussein, Bryan Baranowski, Shady Nakhla, Pasquale Santangeli, Mina Chung, Walid I Saliba, Oussama M Wazni","doi":"10.1161/CIRCEP.124.013631","DOIUrl":"https://doi.org/10.1161/CIRCEP.124.013631","url":null,"abstract":"","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":" ","pages":"e013631"},"PeriodicalIF":9.1,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143953592","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}

{"title":"Exploring the Hidden Side of Ventricular Arrhythmias in Elite Athletes With Structural Normal Hearts.","authors":"Giuseppe Di Gioia, Maria Rosaria Squeo, Cosimo Damiano Daniello, Armando Ferrera, Viviana Maestrini, Sara Monosilio, Federica Mango, Giulia Paoletti, Andrea Serdoz, Antonio Pelliccia","doi":"10.1161/CIRCEP.125.013807","DOIUrl":"https://doi.org/10.1161/CIRCEP.125.013807","url":null,"abstract":"","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":" ","pages":"e013807"},"PeriodicalIF":9.1,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993267","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}

{"title":"Heart Rate Mystery Unveiled: Sex Differences in Human Sinoatrial Node Genes and Female Tachycardia.","authors":"Ning Li, Amy Webb, James Kennelly, Roshan Sharma, Bryan A Whitson, Peter J Mohler, John D Hummel, Jichao Zhao, Vadim V Fedorov","doi":"10.1161/CIRCEP.124.013534","DOIUrl":"10.1161/CIRCEP.124.013534","url":null,"abstract":"<p><strong>Background: </strong>Despite over a century of clinical electrocardiographic studies showing that women exhibit a faster resting heart rate (HR), the mechanisms underlying sex differences in HR remain unresolved. Moreover, inappropriate sinus tachycardia primarily affects women, whereas men are at a higher risk for conduction block and atrial fibrillation. We hypothesized that the sexual dimorphism of genes responsible for sinoatrial node (SAN) pacemaking and signaling pathways may contribute to the sex differences in HR and susceptibility to arrhythmias.</p><p><strong>Methods: </strong>Human SAN central pacemaker and right atrial tissue were isolated from nondiseased ex vivo donor hearts. Gene expressions were quantified and validated using the transcriptomic panel and quantitative polymerase chain reaction. Gene set enrichment analysis, Ingenuity Pathway Analysis, and human-specific SAN models were utilized to define regulatory mechanisms and functional impacts of sex-biased gene transcription.</p><p><strong>Results: </strong>We identified differentially expressed region- and sex-specific genes, with gene sets enriched in HR regulation (eg, <i>TBX3</i>, <i>HCN1</i>) and metabolism (eg, <i>ADIPOQ</i>, <i>LEP</i>) pathways in female SAN. In contrast, differential genes and gene sets involved in collagen biosynthetic processes, fibrogenesis (eg, <i>EGR1</i>), and immune response (eg, <i>IL6</i>, <i>CXCL8</i>) pathways were enriched in males SAN and right atrial. Ingenuity Pathway Analysis predicted significant roles for <i>TBX3</i> and estradiol in the sex-specific expression of genes involved in SAN function. Computational simulations showed that the sex-specific SAN differences in I_f (pacemaker current; <i>HCN1</i>) and I_Ca,L(L-type calcium current; <i>CACNA1D</i>) can explain the faster HR in female SAN, with female SAN having a lower threshold for inappropriate sinus tachycardia, whereas male SAN are more vulnerable to sinus arrest.</p><p><strong>Conclusions: </strong>The human SAN exhibits region-specific sexual dimorphism in pacemaking gene sets. Higher expression of <i>TBX3</i> and <i>HCN1</i> in female SAN may underlie faster HR and increased susceptibility to inappropriate sinus tachycardia in women, whereas enriched gene sets related to inflammation and collagen biosynthesis in men may predispose them to conduction impairments and atrial fibrillation risk.</p>","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":" ","pages":"e013534"},"PeriodicalIF":9.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143969836","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}

{"title":"Intermediate Monocytes and High Levels of Chemokine CCL3 Are Associated With Increased Risk of Atrial Fibrillation in the General Population.","authors":"Kari Anne Sveen, J Gustav Smith, Isabel Goncalves, Andreas Edsfeldt, Daniel Engelbertsen, Linda S Johnson, Olle Melander, Gunnar Engström, Jan Nilsson, Harry Björkbacka, Eva Bengtsson","doi":"10.1161/CIRCEP.124.013621","DOIUrl":"10.1161/CIRCEP.124.013621","url":null,"abstract":"","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":" ","pages":"e013621"},"PeriodicalIF":9.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094257/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143987471","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}

{"title":"ECGi QRS-T Subtraction Algorithm to Regionalize Nonpulmonary Vein Triggers of Atrial Fibrillation With Obscured P Waves.","authors":"Alireza Oraii, Munveer Thind, Qing Lou, Cory M Tschabrunn, Francis E Marchlinski","doi":"10.1161/CIRCEP.125.013725","DOIUrl":"10.1161/CIRCEP.125.013725","url":null,"abstract":"","PeriodicalId":10319,"journal":{"name":"Circulation. Arrhythmia and electrophysiology","volume":" ","pages":"e013725"},"PeriodicalIF":9.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985603","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}