Heart rhythm最新文献

{"title":"Analysis of development trends in His bundle pacing research hotspots using bibliometrics","authors":"Zechuan Zhou MD , Bin Zheng MD","doi":"10.1016/j.hrthm.2024.11.007","DOIUrl":"10.1016/j.hrthm.2024.11.007","url":null,"abstract":"","PeriodicalId":12886,"journal":{"name":"Heart rhythm","volume":"22 10","pages":"Pages 2731-2732"},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142618779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prophylactic electrophysiologic interventions in congenital heart disease: New insights and fresh controversy","authors":"Jeremy P. Moore MD, MS, FHRS","doi":"10.1016/j.hrthm.2024.11.027","DOIUrl":"10.1016/j.hrthm.2024.11.027","url":null,"abstract":"","PeriodicalId":12886,"journal":{"name":"Heart rhythm","volume":"22 10","pages":"Pages e919-e920"},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prospective validation of a prespecified algorithm for the management of conduction disturbances after transcatheter aortic valve replacement: The PROMOTE study","authors":"Josep Rodés-Cabau MD, PhD ,&nbsp;Luis Nombela-Franco MD, PhD ,&nbsp;Guillem Muntané-Carol MD, PhD ,&nbsp;Gabriela Veiga MD, PhD ,&nbsp;Ander Regueiro MD, PhD ,&nbsp;Tamim Nazif MD ,&nbsp;Vicenç Serra MD ,&nbsp;Lluis Asmarats MD, PhD ,&nbsp;Henrique B. Ribeiro MD, PhD ,&nbsp;Azeem Latib MD ,&nbsp;Anthony Poulin MD ,&nbsp;Asim N. Cheema MD ,&nbsp;Pilar Jiménez-Quevedo MD, PhD ,&nbsp;Joan Antoni Gomez-Hospital MD, PhD ,&nbsp;Aritz Gil Ongay MD, PhD ,&nbsp;Rami Gabani MD ,&nbsp;Dabit Arzamendi MD ,&nbsp;Michael Brener MD ,&nbsp;Alvaro Calabuig MD ,&nbsp;Andrea Scotti MD ,&nbsp;François Philippon MD, FHRS","doi":"10.1016/j.hrthm.2024.12.019","DOIUrl":"10.1016/j.hrthm.2024.12.019","url":null,"abstract":"<div><h3>Background</h3><div><span>There is a large variability in the management of conduction disturbances (CDs) after </span>transcatheter aortic valve replacement (TAVR).</div></div><div><h3>Objective</h3><div>This study aimed to validate a prespecified algorithm for managing CDs in patients undergoing TAVR.</div></div><div><h3>Methods</h3><div><span>This was a prospective multicenter study including consecutive patients without prior pacemaker undergoing TAVR. Patients were stratified in different groups according to the presence of prior right bundle branch block (RBBB) and the occurrence of CDs during the procedure: no prior RBBB and no CDs (group NCD), prior RBBB and no CDs (group RBBB-NCD), and occurrence of CDs (group CD). A management algorithm was prespecified for each group. </span>Permanent pacemaker (PPM) and mortality (overall, sudden cardiac death) at 30 days were the primary end points.</div></div><div><h3>Results</h3><div>A total of 2110 TAVR recipients were included. Patients were distributed in NCD (32.0%), RBBB-NCD (5.1%), and CD (62.9%) groups. A total of 329 patients (15.6%) received a PPM at 30 days, with a PPM rate of 5.5%, 15.9%, and 20.7% in the NCD, RBBB-NCD, and CD groups, respectively (<em>P</em><span><span> &lt; .001). The PPM rate was 17.4% and 57.2% in patients with procedural new-onset left bundle branch block and high-degree atrioventricular block/complete heart block, respectively. There were no differences in 30-day all-cause mortality and </span>sudden cardiac death between groups (NCD group, 1.2% and 0.2%; RBBB-NCD group, 0% and 0%; CD group, 0.7% and 0.1%; </span><em>P</em> = .45 and <em>P</em><span> = .99 for all-cause mortality and sudden cardiac death, respectively).</span></div></div><div><h3>Conclusion</h3><div>A prespecified strategy for the management of CDs in contemporary TAVR recipients was feasible and safe, with no increased mortality and an extremely low rate of sudden cardiac death in patients with CDs. However, PPM rates remained high, and continued efforts for preventing the occurrence of CDs are warranted.</div></div>","PeriodicalId":12886,"journal":{"name":"Heart rhythm","volume":"22 10","pages":"Pages 2635-2643"},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exercise-induced dysregulation of the adrenergic response in a mouse model of PKP2-arrhythmogenic cardiomyopathy","authors":"Chantal J.M. van Opbergen PhD ,&nbsp;Lilian K. Gutierrez PhD ,&nbsp;Giorgia Bertoli PhD ,&nbsp;Mingliang Zhang PhD ,&nbsp;Sarah Boyce BSc ,&nbsp;Yan Deng MD, PhD ,&nbsp;Michael Cammer MFA, MAT ,&nbsp;Feng-Xia Liang PhD ,&nbsp;Mario Delmar MD, PhD","doi":"10.1016/j.hrthm.2025.05.015","DOIUrl":"10.1016/j.hrthm.2025.05.015","url":null,"abstract":"<div><h3>Background</h3><div><span>Plakophilin-2 (PKP2) is a component of the desmosome<span>. Pathogenic variants can lead to arrhythmogenic cardiomyopathy (PKP2-ACM). In patients with PKP2-ACM, exercise and </span></span>catecholamine<span> surges negatively impact arrhythmia incidence and severity.</span></div></div><div><h3>Objective</h3><div>The study aimed to characterize remodeling of the sympathetic input and adrenergic response in hearts of PKP2-deficient mice (PKP2cKO) subjected to endurance exercise.</div></div><div><h3>Methods</h3><div><span><span><span>We used expansion microscopy and structured illumination to characterize the abundance of beta 1-adrenergic receptors (β1-ARs) in the sarcolemma<span> in PKP2cKO-myocytes, sedentary or trained, and Cre-negative controls. We prevented endogenous catecholamine import by </span></span>short hairpin RNA<span> (shRNA)-mediated knockdown of its transporter [organic cation transporter 3 (OCT3)] and characterized differential effects of isoproterenol (membrane permeable) vs </span></span>norepinephrine (non-membrane permeable) on Ca</span>²⁺ transient dynamics. Separately, we evaluated the distribution of sympathetic terminals in PKP2cKO-trained hearts vs controls.</div></div><div><h3>Results</h3><div><span>Exercise led to “increased” abundance of sarcolemma β1-ARs in control, and “decreased” abundance in PKP2cKO-myocytes. OCT3 knockdown drastically reduced the response of trained PKP2cKO-myocytes to </span>norepinephrine<span> but not isoproterenol<span>, indicating preserved response to native catecholamines by intracellular (dyad-associated) receptors in the setting of a reduced sarcolemma pool. In tissue, we observed reduced abundance of sympathetic terminals and heterogeneous distribution across the myocardium.</span></span></div></div><div><h3>Conclusion</h3><div>Endurance exercise in PKP2-deficient myocytes leads to a reduced pool of functional β1-ARs in the sarcolemma and yet availability of intracellular receptors<span>, which can activate selected (and heterogeneous) routes of intracellular signaling cascades. We speculate that remodeling of nerve terminals affects sympathetic input distribution and hence, regional modulation of excitability and conduction. These changes can facilitate cell-generated triggered activity and heterogeneity of the underlying substrate, setting the stage for life-threatening arrhythmias.</span></div></div>","PeriodicalId":12886,"journal":{"name":"Heart rhythm","volume":"22 10","pages":"Pages e939-e950"},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Severe acute kidney injury from limited pulsed field ablation","authors":"Thomas A. Boyle MD,&nbsp;David S. Frankel MD, FHRS","doi":"10.1016/j.hrthm.2025.07.015","DOIUrl":"10.1016/j.hrthm.2025.07.015","url":null,"abstract":"","PeriodicalId":12886,"journal":{"name":"Heart rhythm","volume":"22 10","pages":"Page e1043"},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transatrial epicardial access: Advancing from experimental models to human feasibility","authors":"Muhieddine Omar Chokr MD, PhD,&nbsp;Mauricio Ibrahim Scanavacca MD, PhD","doi":"10.1016/j.hrthm.2025.06.052","DOIUrl":"10.1016/j.hrthm.2025.06.052","url":null,"abstract":"","PeriodicalId":12886,"journal":{"name":"Heart rhythm","volume":"22 10","pages":"Pages e1046-e1047"},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Table Of Content","authors":"","doi":"10.1016/S1547-5271(25)02871-1","DOIUrl":"10.1016/S1547-5271(25)02871-1","url":null,"abstract":"","PeriodicalId":12886,"journal":{"name":"Heart rhythm","volume":"22 10","pages":"Pages A7, A8, A9, A10, A11, A12, A13, A14, A15"},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145183822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SCD-HeFT","authors":"Jeanne E. Poole MD, FHRS ,&nbsp;Gust H. Bardy MD, FHRS","doi":"10.1016/j.hrthm.2025.07.023","DOIUrl":"10.1016/j.hrthm.2025.07.023","url":null,"abstract":"","PeriodicalId":12886,"journal":{"name":"Heart rhythm","volume":"22 10","pages":"Pages 2445-2446"},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145183823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Twin atrioventricular nodes and accessory pathways in congenital heart diseases with abnormal atrioventricular connections: Association with the developmental hierarchy of cardiac morphology","authors":"Mei-Hwan Wu MD, PhD,&nbsp;Sheunn-Nan Chiu MD, PhD,&nbsp;Chun-An Chen MD, PhD,&nbsp;Wei-Chieh Tseng MD,&nbsp;Chun-Wei Lu MD, PhD,&nbsp;Ming-Tai Lin MD, PhD,&nbsp;Jou-Kou Wang MD, PhD","doi":"10.1016/j.hrthm.2024.10.072","DOIUrl":"10.1016/j.hrthm.2024.10.072","url":null,"abstract":"<div><h3>Background</h3><div>Twin atrioventricular (AV) nodes (TWAVNs) are common in heterotaxy syndrome.</div></div><div><h3>Objective</h3><div>The purpose of this study was to investigate the presence and implications of TWAVNs and accessory pathways<span> in congenital heart diseases (CHDs) with abnormal AV connections.</span></div></div><div><h3>Methods</h3><div>A retrospective study of a 1980–2022 cohort with sufficient electrocardiographic (ECG) data for review was conducted.</div></div><div><h3>Results</h3><div><span><span><span>We enrolled 136 patients with heterotaxy syndrome, 70 with congenitally corrected transposition of the </span>great arteries (ccTGA) (4 with Ebstein anomaly), 47 with double-inlet ventricle (DIV), and 63 with isolated </span>AV canal defect. TWAVNs, detected in the same ECG (18%), in separate ECGs (70.8%), or after electrophysiological study (11.2%), were present in 43.4% of heterotaxy, 10.6% of DIV, 10% of ccTGA, and 1.6% of AV canal defect cases. Accessory pathways were noted in 11.4% of ccTGA and 4.4% of heterotaxy cases, but none of the DIV and AV canal cases. Actuarial incidence of supraventricular </span>tachycardia<span> (SVT) by age 10 was 0.354, 0.121, 0.022, and 0 in heterotaxy, ccTGA, DIV, and AV canal, respectively. In patients with TWAVNs, the risk of SVT varies according to the rate of TWAVNs in each CHD type, with risks of 65.5%, 58.3%, and 0% for TWAVNs rates &gt;50%, 10%–50%, and &lt;10%, respectively. Onset age of tachycardia did not differ between those with TWAVNs and those with accessory pathways.</span></div></div><div><h3>Conclusion</h3><div>In CHD with abnormal AV connections, evidence suggested a developmental hierarchy in the propensity to exhibit TWAVNs, but not for accessory pathways. The earlier cardiac developmental errors occur, the higher the likelihood of TWAVNs and the greater the chance of SVT.</div></div>","PeriodicalId":12886,"journal":{"name":"Heart rhythm","volume":"22 10","pages":"Pages 2678-2685"},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142618817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Accelerated biological aging and risk of atrial fibrillation: A cohort study","authors":"Meijia Yang PhD ,&nbsp;Ke Chao PhD ,&nbsp;Ziyang Wang MBBS ,&nbsp;Ruyue Xue PhD ,&nbsp;Xu Zhang PhD ,&nbsp;Dong Wang PhD","doi":"10.1016/j.hrthm.2024.11.017","DOIUrl":"10.1016/j.hrthm.2024.11.017","url":null,"abstract":"<div><h3>Background</h3><div>Even though aging has been demonstrated to be associated with a higher risk of atrial fibrillation (AF), it is unclear whether biological aging is associated with risk of incident AF.</div></div><div><h3>Objective</h3><div>This study aimed to investigate the association between biological aging and AF.</div></div><div><h3>Methods</h3><div>A total of 371,882 participants without AF at baseline from the UK Biobank<span> were included. The incident AF was ascertained through linkage to the UK National Health Services register. Biological age was evaluated from clinical traits by the Klemera-Doubal method–biological age (KDM-BA) and PhenoAge algorithms. The residual discrepancies between biological age and chronological age<span> were defined as the age accelerations (KDM-BA acceleration and PhenoAge acceleration). The Cox proportional hazards model was used to evaluate the effects of age accelerations with the risk of incident AF.</span></span></div></div><div><h3>Results</h3><div>During a mean follow-up of 13.04 years, a total of 28,076 new cases of AF were identified. Accelerated biological age was associated with an increased risk of AF, with a hazard ratio of 1.11 (95% confidence interval, 1.10–1.13) per standard deviation increase in KDM-BA acceleration (10.9 years) and 1.28 (95% confidence interval, 1.27–1.30) in PhenoAge acceleration (5.6 years).</div></div><div><h3>Conclusion</h3><div>Accelerated biological age quantified by clinical biomarkers is associated with increased risks of AF. Biological aging may represent a potential risk factor for incident AF in midlife and older adults and a potential target for risk assessment and intervention.</div></div>","PeriodicalId":12886,"journal":{"name":"Heart rhythm","volume":"22 10","pages":"Pages 2507-2514"},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}