Pub Date : 2019-11-01DOI: 10.1161/CIRCEP.119.007382
M. Cacheux, B. Strauss, N. Raad, Zeki Ilkan, Jun Hu, L. Bénard, S. Feske, J. Hulot, F. Akar
Supplemental Digital Content is available in the text.
补充数字内容可在文本中找到。
{"title":"Cardiomyocyte-Specific STIM1 (Stromal Interaction Molecule 1) Depletion in the Adult Heart Promotes the Development of Arrhythmogenic Discordant Alternans","authors":"M. Cacheux, B. Strauss, N. Raad, Zeki Ilkan, Jun Hu, L. Bénard, S. Feske, J. Hulot, F. Akar","doi":"10.1161/CIRCEP.119.007382","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007382","url":null,"abstract":"Supplemental Digital Content is available in the text.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"571 1","pages":"e007382 - e007382"},"PeriodicalIF":0.0,"publicationDate":"2019-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78913687","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 : 2019-11-01DOI: 10.1161/CIRCEP.119.008034
Paul J. Wang
{"title":"Case Series and Reports 1.0: Team Science Meets Clinical Care?","authors":"Paul J. Wang","doi":"10.1161/CIRCEP.119.008034","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.008034","url":null,"abstract":"","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"57 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81489687","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 : 2019-10-30DOI: 10.1161/CIRCEP.119.007428
Seokhun Yang, S. Kwak, S. Kwon, Hyun-Jung Lee, Heesun Lee, Jun‐Bean Park, Seung‐Pyo Lee, Hoon Kim, Kyungdo Han, Yong‐Jin Kim, Hyung‐Kwan Kim
BACKGROUND The association of lifetime exposure to endogenous sex hormone with incident atrial fibrillation (AF) and subsequent ischemic stroke has never been studied. METHODS This study involved 4 638 299 natural postmenopausal waomen aged ≥40 years without prior history of AF and with national breast cancer check-up between January 1, 2009 and December 31, 2014. The primary end point was incident AF, and the secondary end point was subsequent ischemic stroke once AF has developed. Cox proportional hazard regression analysis was used to estimate the risk of end points. RESULTS During the mean follow-up of 6.3 years, shorter total reproductive years (<30 years) were associated with 7% increased risk of AF after adjusting for confounding variables (adjusted hazard ratio [aHR], 1.07 [95% CI, 1.05-1.09]). Risk of AF declined progressively with every 5-yearly increment in total reproductive years (P-for-trend <0.001). However, the prolonged (≥2 years) use of hormone replacement therapy after menopause was paradoxically associated with a 3% increase in AF risk (aHR, 1.03 [95% CI, 1.01-1.05]). For the secondary end point analysis, the risk of ischemic stroke after AF development significantly decreased with each 5-yearly increment in total reproductive years (with <30 years as reference; aHR, 0.93 [95% CI, 0.88-0.99] for 30-34 years; aHR, 0.84 [95% CI, 0.79-0.89] for 35-39 years; and aHR, 0.88 [95% CI, 0.80-0.97] for ≥40 years, P-for-trend <0.001). CONCLUSIONS In women with natural menopause, shorter lifetime exposure to endogenous sex hormone, that is, shorter total reproductive years, was significantly associated with a higher risk of AF and subsequent ischemic stroke. Paradoxically, prolonged exogenous hormone replacement therapy increased the risk of incident AF.
{"title":"Association of Total Reproductive Years With Incident Atrial Fibrillation, and Subsequent Ischemic Stroke in Women With Natural Menopause.","authors":"Seokhun Yang, S. Kwak, S. Kwon, Hyun-Jung Lee, Heesun Lee, Jun‐Bean Park, Seung‐Pyo Lee, Hoon Kim, Kyungdo Han, Yong‐Jin Kim, Hyung‐Kwan Kim","doi":"10.1161/CIRCEP.119.007428","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007428","url":null,"abstract":"BACKGROUND\u0000The association of lifetime exposure to endogenous sex hormone with incident atrial fibrillation (AF) and subsequent ischemic stroke has never been studied.\u0000\u0000\u0000METHODS\u0000This study involved 4 638 299 natural postmenopausal waomen aged ≥40 years without prior history of AF and with national breast cancer check-up between January 1, 2009 and December 31, 2014. The primary end point was incident AF, and the secondary end point was subsequent ischemic stroke once AF has developed. Cox proportional hazard regression analysis was used to estimate the risk of end points.\u0000\u0000\u0000RESULTS\u0000During the mean follow-up of 6.3 years, shorter total reproductive years (<30 years) were associated with 7% increased risk of AF after adjusting for confounding variables (adjusted hazard ratio [aHR], 1.07 [95% CI, 1.05-1.09]). Risk of AF declined progressively with every 5-yearly increment in total reproductive years (P-for-trend <0.001). However, the prolonged (≥2 years) use of hormone replacement therapy after menopause was paradoxically associated with a 3% increase in AF risk (aHR, 1.03 [95% CI, 1.01-1.05]). For the secondary end point analysis, the risk of ischemic stroke after AF development significantly decreased with each 5-yearly increment in total reproductive years (with <30 years as reference; aHR, 0.93 [95% CI, 0.88-0.99] for 30-34 years; aHR, 0.84 [95% CI, 0.79-0.89] for 35-39 years; and aHR, 0.88 [95% CI, 0.80-0.97] for ≥40 years, P-for-trend <0.001).\u0000\u0000\u0000CONCLUSIONS\u0000In women with natural menopause, shorter lifetime exposure to endogenous sex hormone, that is, shorter total reproductive years, was significantly associated with a higher risk of AF and subsequent ischemic stroke. Paradoxically, prolonged exogenous hormone replacement therapy increased the risk of incident AF.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"06 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80083128","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 : 2019-10-30DOI: 10.1161/CIRCEP.119.007312
Arvindh N Kanagasundram, R. John, W. Stevenson
As the population of patients with implanted defibrillators has grown, an increasing number of patients nonischemic cardiomyopathies are requiring therapy to reduce ventricular arrhythmias. Most of these arrhythmias are related to areas of ventricular scar. Although the pathophysiology of scar development is not well understood in these diseases, advances in cardiac imaging and mapping are better characterizing the scar locations that give rise to the arrhythmias. Here, we review the pathophysiologic and electrocardiographic correlations that inform ablation strategies for ventricular tachycardia in these diseases.
{"title":"Sustained Monomorphic Ventricular Tachycardia in Nonischemic Heart Disease: Arrhythmia-Substrate Correlations That Inform the Approach to Ablation.","authors":"Arvindh N Kanagasundram, R. John, W. Stevenson","doi":"10.1161/CIRCEP.119.007312","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007312","url":null,"abstract":"As the population of patients with implanted defibrillators has grown, an increasing number of patients nonischemic cardiomyopathies are requiring therapy to reduce ventricular arrhythmias. Most of these arrhythmias are related to areas of ventricular scar. Although the pathophysiology of scar development is not well understood in these diseases, advances in cardiac imaging and mapping are better characterizing the scar locations that give rise to the arrhythmias. Here, we review the pathophysiologic and electrocardiographic correlations that inform ablation strategies for ventricular tachycardia in these diseases.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"19 4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87579042","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 : 2019-10-01DOI: 10.1161/CIRCEP.119.007213
P. Platonov, S. McNitt, B. Polonsky, S. Rosero, W. Zareba
BACKGROUND Long QT syndrome (LQTS) is caused by the abnormal function of ion channels, which may also affect atrial electrophysiology and be associated with the risk of atrial fibrillation (AF). However, large-scale studies of AF risk among patients with LQTS and its relation to LQTS manifestations are lacking. We aimed to assess the risk of AF and its relationship to the LQTS genotype and the long-term prognosis in patients with LQTS. METHODS Genotype-positive patients with LQTS (784 LQT1, 746 LQT2, and 233 LQT3) were compared with 2043 genotype-negative family members. Information on the occurrence of AF was based on physician-reported ECG-verified events. Multivariate Cox proportional hazards regression analyses were performed for ages 0 to 60 and after 60 years (reflecting an early and late-onset of AF) to assess the risk of incident AF by genotype and the relationship of AF to the risk of cardiac events defined as syncope, documented torsades de pointes, and aborted cardiac arrest or sudden cardiac death. RESULTS In patients followed from birth to 60 years of age, patients with LQT3 had an increased risk of AF compared with genotype-negative family members (hazard ratio=6.62; 95% CI, 2.04-21.49; P<0.001), while neither LQT1 nor LQT2 demonstrated increased AF risk. After the age of 60 years, patients with LQT2 had significantly lower risk of AF compared with genotype-negative controls (hazard ratio=0.07; 95% CI, 0.01-0.53, P=0.011). AF was a significant predictor of cardiac events in patients with LQT3 through the age of 60 (hazard ratio=5.38; 95% CI, 1.17-24.82; P=0.031). CONCLUSIONS Our data demonstrate an increased risk of early age AF in patients with LQT3 and also indicate a protective effect of the LQT2 genotype in it's association with a decreased risk of AF after the age of 60.
{"title":"Atrial Fibrillation in Long QT Syndrome by Genotype.","authors":"P. Platonov, S. McNitt, B. Polonsky, S. Rosero, W. Zareba","doi":"10.1161/CIRCEP.119.007213","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007213","url":null,"abstract":"BACKGROUND\u0000Long QT syndrome (LQTS) is caused by the abnormal function of ion channels, which may also affect atrial electrophysiology and be associated with the risk of atrial fibrillation (AF). However, large-scale studies of AF risk among patients with LQTS and its relation to LQTS manifestations are lacking. We aimed to assess the risk of AF and its relationship to the LQTS genotype and the long-term prognosis in patients with LQTS.\u0000\u0000\u0000METHODS\u0000Genotype-positive patients with LQTS (784 LQT1, 746 LQT2, and 233 LQT3) were compared with 2043 genotype-negative family members. Information on the occurrence of AF was based on physician-reported ECG-verified events. Multivariate Cox proportional hazards regression analyses were performed for ages 0 to 60 and after 60 years (reflecting an early and late-onset of AF) to assess the risk of incident AF by genotype and the relationship of AF to the risk of cardiac events defined as syncope, documented torsades de pointes, and aborted cardiac arrest or sudden cardiac death.\u0000\u0000\u0000RESULTS\u0000In patients followed from birth to 60 years of age, patients with LQT3 had an increased risk of AF compared with genotype-negative family members (hazard ratio=6.62; 95% CI, 2.04-21.49; P<0.001), while neither LQT1 nor LQT2 demonstrated increased AF risk. After the age of 60 years, patients with LQT2 had significantly lower risk of AF compared with genotype-negative controls (hazard ratio=0.07; 95% CI, 0.01-0.53, P=0.011). AF was a significant predictor of cardiac events in patients with LQT3 through the age of 60 (hazard ratio=5.38; 95% CI, 1.17-24.82; P=0.031).\u0000\u0000\u0000CONCLUSIONS\u0000Our data demonstrate an increased risk of early age AF in patients with LQT3 and also indicate a protective effect of the LQT2 genotype in it's association with a decreased risk of AF after the age of 60.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"136 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82204344","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 : 2019-10-01DOI: 10.1161/CIRCEP.119.007711
M. Andreas, P. Arzl, A. Mitterbauer, Nicolás M Ballarini, F. Kainz, A. Kocher, G. Laufer, M. Wolzt
BACKGROUND Postoperative atrial fibrillation (POAF) occurs in up to 40% of patients undergoing cardiac surgery. Invasive stimulation of the vagal nerve previously demonstrated a reduced risk of POAF. Therefore, we examined the antiarrhythmic and anti-inflammatory effects of noninvasive low-level transcutaneous electrical stimulation (LLTS) of the greater auricular nerve in a pilot trial including patients undergoing cardiac surgery. METHODS Patients were randomized into a sham (n=20) or a treatment group (n=20) for LLTS. After cardiac surgery, electrodes were applied in the triangular fossa of the ear. Stimulation (amplitude 1 mA, frequency 1 Hz for 40 minutes, followed by a 20 minutes break) was performed for up to 2 weeks after cardiac surgery. Heart rhythm was recorded continuously using an ECG during the observation period. CRP (C-reactive protein) and IL (interleukin)-6 plasma concentrations were measured immediately after surgery as well as on day 2 and 7 postsurgery. RESULTS Patients receiving LLTS had a significantly reduced occurrence of POAF (4 of 20) when compared with controls (11 of 20, P=0.022) during a similar mean Holter recording period. The median duration of POAF was comparable between the treatment and the control group (878 [249; 1660] minutes versus 489 [148; 1775] minutes; P=0.661). No effect of LLTS on CRP or IL-6 levels was detectable. CONCLUSIONS LLTS of the greater auricular nerve may be a potential therapy for POAF. We demonstrated the feasibility to conduct a randomized trial of neurostimulation as an outlay for a multisite clinical trial.
{"title":"Electrical Stimulation of the Greater Auricular Nerve to Reduce Postoperative Atrial Fibrillation.","authors":"M. Andreas, P. Arzl, A. Mitterbauer, Nicolás M Ballarini, F. Kainz, A. Kocher, G. Laufer, M. Wolzt","doi":"10.1161/CIRCEP.119.007711","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007711","url":null,"abstract":"BACKGROUND\u0000Postoperative atrial fibrillation (POAF) occurs in up to 40% of patients undergoing cardiac surgery. Invasive stimulation of the vagal nerve previously demonstrated a reduced risk of POAF. Therefore, we examined the antiarrhythmic and anti-inflammatory effects of noninvasive low-level transcutaneous electrical stimulation (LLTS) of the greater auricular nerve in a pilot trial including patients undergoing cardiac surgery.\u0000\u0000\u0000METHODS\u0000Patients were randomized into a sham (n=20) or a treatment group (n=20) for LLTS. After cardiac surgery, electrodes were applied in the triangular fossa of the ear. Stimulation (amplitude 1 mA, frequency 1 Hz for 40 minutes, followed by a 20 minutes break) was performed for up to 2 weeks after cardiac surgery. Heart rhythm was recorded continuously using an ECG during the observation period. CRP (C-reactive protein) and IL (interleukin)-6 plasma concentrations were measured immediately after surgery as well as on day 2 and 7 postsurgery.\u0000\u0000\u0000RESULTS\u0000Patients receiving LLTS had a significantly reduced occurrence of POAF (4 of 20) when compared with controls (11 of 20, P=0.022) during a similar mean Holter recording period. The median duration of POAF was comparable between the treatment and the control group (878 [249; 1660] minutes versus 489 [148; 1775] minutes; P=0.661). No effect of LLTS on CRP or IL-6 levels was detectable.\u0000\u0000\u0000CONCLUSIONS\u0000LLTS of the greater auricular nerve may be a potential therapy for POAF. We demonstrated the feasibility to conduct a randomized trial of neurostimulation as an outlay for a multisite clinical trial.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"108 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91058905","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 : 2019-10-01DOI: 10.1161/CIRCEP.119.007865
J. Kron, Alex Y. Tan
Postoperative atrial fibrillation (POAF) occurs in up to 50% of patients undergoing open-heart surgery and is associated with worse outcomes, including stroke, mortality, increased length of hospital stay, and increased health care costs.1 AF typically occurs within one week after cardiac surgery and 70% of patients who have AF after coronary artery bypass surgery have episodes within the first 3 days.2 POAF is no longer considered a transient one-off event, as it highlights an increased long term vulnerability to the development of AF.3 Therefore, the consequences of POAF are more substantial and sustained than may first appear. The mechanism(s) of POAF (Figure) is a combination of postoperative pro-fibrillatory milieu consisting of pericarditis, atrial injury, heightened sympathetic tone, ischemia-reperfusion, hemodynamic and metabolic derangements, superimposed on preexisting electrophysiological and structural atrial abnormalities.4,5 An imbalance, specifically, overactivity in both sympathetic and parasympathetic activities of the cardiac autonomic nervous system (CANS), plays a crucial role in promoting AF, including postoperative AF.6–8 Current guidelines recommend medical therapy for AF after cardiac and thoracic surgery, but do not include any nonpharmacological interventions for treatment or prevention of AF.1 To treat postoperative AF, beta blockers are recommended as first-line therapy, followed by nondihydropyridine calcium channel blockers if adequate rate control is not achieved with beta blockers. For prevention of postoperative AF in high-risk patients undergoing cardiac surgery, preoperative amiodarone can be used to reduce the incidence of AF (Class IIA recommendation). There is also data to support using sotalol or colchicine to reduce the risk of postoperative AF (Class IIB recommendation). However, pharmacological preventative measures and treatments can be limited by medication side effects, including hypotension and bradycardia. In the current issue, Andreas et al9 present pilot data on the use of noninvasive low level transcutaneous electrical stimulation (LLTS) of the greater auricular nerve to reduce the risk of postoperative AF.9 Their hypothesis is that LLTS modulates activity of an imbalanced CANS triggered by the postoperative insult, leading to protection against POAF. In this single-center, randomized, double-blind study, 40 patients were randomized to LLTS treatment (n=20) or sham group (n=20). After cardiac surgery, patients in the treatment group received stimulation applied via electrodes in the triangular fossa of the ear for 40-minute increments followed by a 20-minute break for up to 2 weeks. All patients had continuous ECG monitoring as well as inflammatory markers including C-reactive protein and interleukin-6 measured immediately postsurgery and day 2 and 7 postsurgery. The key finding was that patients receiving LLTS had a significantly lower incidence of POAF EDITORIAL
{"title":"Preventing Postoperative Atrial Fibrillation: A Stimulating New Approach.","authors":"J. Kron, Alex Y. Tan","doi":"10.1161/CIRCEP.119.007865","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007865","url":null,"abstract":"Postoperative atrial fibrillation (POAF) occurs in up to 50% of patients undergoing open-heart surgery and is associated with worse outcomes, including stroke, mortality, increased length of hospital stay, and increased health care costs.1 AF typically occurs within one week after cardiac surgery and 70% of patients who have AF after coronary artery bypass surgery have episodes within the first 3 days.2 POAF is no longer considered a transient one-off event, as it highlights an increased long term vulnerability to the development of AF.3 Therefore, the consequences of POAF are more substantial and sustained than may first appear. The mechanism(s) of POAF (Figure) is a combination of postoperative pro-fibrillatory milieu consisting of pericarditis, atrial injury, heightened sympathetic tone, ischemia-reperfusion, hemodynamic and metabolic derangements, superimposed on preexisting electrophysiological and structural atrial abnormalities.4,5 An imbalance, specifically, overactivity in both sympathetic and parasympathetic activities of the cardiac autonomic nervous system (CANS), plays a crucial role in promoting AF, including postoperative AF.6–8 Current guidelines recommend medical therapy for AF after cardiac and thoracic surgery, but do not include any nonpharmacological interventions for treatment or prevention of AF.1 To treat postoperative AF, beta blockers are recommended as first-line therapy, followed by nondihydropyridine calcium channel blockers if adequate rate control is not achieved with beta blockers. For prevention of postoperative AF in high-risk patients undergoing cardiac surgery, preoperative amiodarone can be used to reduce the incidence of AF (Class IIA recommendation). There is also data to support using sotalol or colchicine to reduce the risk of postoperative AF (Class IIB recommendation). However, pharmacological preventative measures and treatments can be limited by medication side effects, including hypotension and bradycardia. In the current issue, Andreas et al9 present pilot data on the use of noninvasive low level transcutaneous electrical stimulation (LLTS) of the greater auricular nerve to reduce the risk of postoperative AF.9 Their hypothesis is that LLTS modulates activity of an imbalanced CANS triggered by the postoperative insult, leading to protection against POAF. In this single-center, randomized, double-blind study, 40 patients were randomized to LLTS treatment (n=20) or sham group (n=20). After cardiac surgery, patients in the treatment group received stimulation applied via electrodes in the triangular fossa of the ear for 40-minute increments followed by a 20-minute break for up to 2 weeks. All patients had continuous ECG monitoring as well as inflammatory markers including C-reactive protein and interleukin-6 measured immediately postsurgery and day 2 and 7 postsurgery. The key finding was that patients receiving LLTS had a significantly lower incidence of POAF EDITORIAL","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"57 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90530851","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 : 2019-10-01DOI: 10.1161/CIRCEP.119.007879
Markus Rottmann, A. Kleber, M. Barkagan, J. Sroubek, E. Leshem, Ayelet Shapira-Daniels, A. Buxton, E. Anter
BACKGROUND In infarct-related ventricular tachycardia (VT), the circuit often corresponds to a location characterized by activation slowing during sinus rhythm (SR). However, the relationship between activation slowing during SR and vulnerability for reentry and correlation to components of the VT circuit are unknown. This study examined the relationship between activation slowing during SR and vulnerability for reentry and correlated these areas with components of the circuit. METHODS In a porcine model of healed infarction, the spatial distribution of endocardial activation velocity was compared between SR and VT. Isthmus sites were defined using activation and entrainment mapping as areas exhibiting diastolic activity within the circuit while bystanders were defined as areas displaying diastolic activity outside the circuit. RESULTS Of 15 swine, 9 had inducible VT (5.2±3.0 per animal) while in 6 swine VT could not be induced despite stimulation from 4 RV and LV sites at 2 drive trains with 6 extra-stimuli down to refractoriness. Infarcts with VT had a greater magnitude of activation slowing during SR. A minimal endocardial activation velocity cutoff ≤0.1 m/s differentiated inducible from noninducible infarctions (P=0.015). Regions of maximal endocardial slowing during SR corresponded to the VT isthmus (area under curve=0.84 95% CI, 0.78-0.90) while bystander sites exhibited near-normal activation during SR. VT circuits were complex with 41.7% exhibiting discontinuous propagation with intramural bridges of slow conduction and delayed quasi-simultaneous endocardial activation. Regions forming the VT isthmus borders had faster activation during SR while regions forming the inner isthmus were activated faster during VT. CONCLUSIONS Endocardial activation slowing during SR may differentiate infarctions vulnerable for VT from those less vulnerable for VT. Sites of slow activation during SR correspond to sites forming the VT isthmus but not to bystander sites.
背景:在梗死相关性室性心动过速(VT)中，该电路通常对应于窦性心律(SR)期间激活减慢的位置。然而，SR期间的激活减慢与再入脆弱性之间的关系以及与VT电路组成的相关性尚不清楚。这项研究考察了SR期间的激活减慢和再入脆弱性之间的关系，并将这些区域与回路的组成部分联系起来。方法在猪梗死愈合模型中，比较SR和VT的心内膜激活速度的空间分布。使用激活和夹带映射将峡部定义为电路内显示舒张活动的区域，而将旁观者定义为电路外显示舒张活动的区域。结果15头猪中，9头猪可诱导VT(每头5.2±3.0)，6头猪在2个传动系的4个左室和左室部位进行6次额外刺激后仍不能诱导VT。伴有VT的梗死在sr期间具有更大程度的激活减慢。诱导性和非诱导性梗死的最小心内膜激活速度切断≤0.1 m/s (P=0.015)。SR期间最大心内膜减慢的区域对应于室速峡(曲线下面积=0.84 95% CI, 0.78-0.90)，而旁观者部位在SR期间表现出接近正常的激活。室速电路复杂，41.7%表现出不连续传播，伴有缓慢传导的壁内桥和延迟的准同步心内膜激活。结论静息期心肌激活减慢可能是区分易发生室性心动过速梗死和不易发生室性心动过速梗死的重要依据。静息期心肌激活减慢的部位与形成室性心动过速的部位相对应，而与旁观者部位不一致。
{"title":"Activation During Sinus Rhythm in Ventricles With Healed Infarction: Differentiation Between Arrhythmogenic and Nonarrhythmogenic Scar.","authors":"Markus Rottmann, A. Kleber, M. Barkagan, J. Sroubek, E. Leshem, Ayelet Shapira-Daniels, A. Buxton, E. Anter","doi":"10.1161/CIRCEP.119.007879","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007879","url":null,"abstract":"BACKGROUND\u0000In infarct-related ventricular tachycardia (VT), the circuit often corresponds to a location characterized by activation slowing during sinus rhythm (SR). However, the relationship between activation slowing during SR and vulnerability for reentry and correlation to components of the VT circuit are unknown. This study examined the relationship between activation slowing during SR and vulnerability for reentry and correlated these areas with components of the circuit.\u0000\u0000\u0000METHODS\u0000In a porcine model of healed infarction, the spatial distribution of endocardial activation velocity was compared between SR and VT. Isthmus sites were defined using activation and entrainment mapping as areas exhibiting diastolic activity within the circuit while bystanders were defined as areas displaying diastolic activity outside the circuit.\u0000\u0000\u0000RESULTS\u0000Of 15 swine, 9 had inducible VT (5.2±3.0 per animal) while in 6 swine VT could not be induced despite stimulation from 4 RV and LV sites at 2 drive trains with 6 extra-stimuli down to refractoriness. Infarcts with VT had a greater magnitude of activation slowing during SR. A minimal endocardial activation velocity cutoff ≤0.1 m/s differentiated inducible from noninducible infarctions (P=0.015). Regions of maximal endocardial slowing during SR corresponded to the VT isthmus (area under curve=0.84 95% CI, 0.78-0.90) while bystander sites exhibited near-normal activation during SR. VT circuits were complex with 41.7% exhibiting discontinuous propagation with intramural bridges of slow conduction and delayed quasi-simultaneous endocardial activation. Regions forming the VT isthmus borders had faster activation during SR while regions forming the inner isthmus were activated faster during VT.\u0000\u0000\u0000CONCLUSIONS\u0000Endocardial activation slowing during SR may differentiate infarctions vulnerable for VT from those less vulnerable for VT. Sites of slow activation during SR correspond to sites forming the VT isthmus but not to bystander sites.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"56 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80764860","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 : 2019-10-01DOI: 10.1161/CIRCEP.118.007281
Kazuki Iso, Y. Okumura, I. Watanabe, Koichi Nagashima, Keiko Takahashi, M. Arai, Ryuta Watanabe, Yuji Wakamatsu, Naoto Otsuka, S. Yagyu, Sayaka Kurokawa, T. Nakai, Kimie Ohkubo, A. Hirayama
BACKGROUND Ganglionated plexi (GPs) play an important role in both the initiation and maintenance of atrial fibrillation (AF). GPs can be located by using continuous high-frequency stimulation (HFS) to elicit a vagal response, but whether the vagal response phenomenon is common to patients without AF is unknown. METHODS HFS of the left atrial GPs was performed in 42 patients (aged 58.0±10.2 years) undergoing ablation for AF and 21 patients (aged 53.2±12.8 years) undergoing ablation for a left-sided accessory pathway. The HFS (20 Hz, 25 mA, 10-ms pulse duration) was applied for 5 seconds at 3 sites within the presumed anatomic area of each of the 5 major left atrial GPs (for a total of 15 sites per patient). We defined vagal response to HFS as prolongation of the R-R interval by >50% in comparison to the mean pre-HFS R-R interval averaged over 10 beats and active-GP areas as areas in which a vagal response was elicited. RESULTS Overall, more active-GP areas were found in the AF group patients than in the non-AF group patients, and at all 5 major GPs, the maximum R-R interval during HFS was significantly prolonged in the AF patients. After multivariate adjustment, association was established between the total number of vagal response sites and the presence of AF. Conclusions The significant increase in vagal responses elicited in patients with AF compared with responses in non-AF patients suggests that vagal responses to HFS reflect abnormally increased GP activity specific to AF substrates.
{"title":"Is Vagal Response During Left Atrial Ganglionated Plexi Stimulation a Normal Phenomenon?: Comparison Between Patients With and Without Atrial Fibrillation.","authors":"Kazuki Iso, Y. Okumura, I. Watanabe, Koichi Nagashima, Keiko Takahashi, M. Arai, Ryuta Watanabe, Yuji Wakamatsu, Naoto Otsuka, S. Yagyu, Sayaka Kurokawa, T. Nakai, Kimie Ohkubo, A. Hirayama","doi":"10.1161/CIRCEP.118.007281","DOIUrl":"https://doi.org/10.1161/CIRCEP.118.007281","url":null,"abstract":"BACKGROUND\u0000Ganglionated plexi (GPs) play an important role in both the initiation and maintenance of atrial fibrillation (AF). GPs can be located by using continuous high-frequency stimulation (HFS) to elicit a vagal response, but whether the vagal response phenomenon is common to patients without AF is unknown.\u0000\u0000\u0000METHODS\u0000HFS of the left atrial GPs was performed in 42 patients (aged 58.0±10.2 years) undergoing ablation for AF and 21 patients (aged 53.2±12.8 years) undergoing ablation for a left-sided accessory pathway. The HFS (20 Hz, 25 mA, 10-ms pulse duration) was applied for 5 seconds at 3 sites within the presumed anatomic area of each of the 5 major left atrial GPs (for a total of 15 sites per patient). We defined vagal response to HFS as prolongation of the R-R interval by >50% in comparison to the mean pre-HFS R-R interval averaged over 10 beats and active-GP areas as areas in which a vagal response was elicited.\u0000\u0000\u0000RESULTS\u0000Overall, more active-GP areas were found in the AF group patients than in the non-AF group patients, and at all 5 major GPs, the maximum R-R interval during HFS was significantly prolonged in the AF patients. After multivariate adjustment, association was established between the total number of vagal response sites and the presence of AF. Conclusions The significant increase in vagal responses elicited in patients with AF compared with responses in non-AF patients suggests that vagal responses to HFS reflect abnormally increased GP activity specific to AF substrates.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"112 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79671695","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 : 2019-10-01DOI: 10.1161/CIRCEP.119.007545
V. Essebag, J. Healey, J. Joza, P. Nery, E. Kalfon, T. Leiria, A. Verma, F. Ayala-Paredes, B. Coutu, G. Sumner, G. Becker, F. Philippon, J. Eikelboom, R. Sandhu, John Sapp, R. Leather, D. Yung, B. Thibault, C. Simpson, K. Ahmad, Satish C. Toal, M. Sturmer, K. Kavanagh, E. Crystal, G. Wells, A. Krahn, D. Birnie
BACKGROUND Oral anticoagulant use is common among patients undergoing pacemaker or defibrillator surgery. BRUISE CONTROL (Bridge or Continue Coumadin for Device Surgery Randomized Controlled Trial; NCT00800137) demonstrated that perioperative warfarin continuation reduced clinically significant hematomas (CSH) by 80% compared with heparin bridging (3.5% versus 16%). BRUISE-CONTROL-2 (NCT01675076) observed a similarly low risk of CSH when comparing continued versus interrupted direct oral anticoagulant (2.1% in both groups). Using patient level data from both trials, the current study aims to: (1) evaluate the effect of concomitant antiplatelet therapy on CSH, and (2) understand the relative risk of CSH in patients treated with direct oral anticoagulant versus continued warfarin. METHODS We analyzed 1343 patients included in BRUISE-CONTROL-1 and BRUISE-CONTROL-2. The primary outcome for both trials was CSH. There were 408 patients identified as having continued either a single or dual antiplatelet agent at the time of device surgery. RESULTS Antiplatelet use (versus nonuse) was associated with CSH in 9.8% versus 4.3% of patients (P<0.001), and remained a strong independent predictor after multivariable adjustment (odds ratio, 1.965; 95% CI, 1.202-3.213; P=0.0071). In multivariable analysis, adjusting for antiplatelet use, there was no significant difference in CSH observed between direct oral anticoagulant use compared with continued warfarin (odds ratio, 0.858; 95% CI, 0.375-1.963; P=0.717). CONCLUSIONS Concomitant antiplatelet therapy doubled the risk of CSH during device surgery. No difference in CSH was found between direct oral anticoagulant versus continued warfarin. In anticoagulated patients undergoing elective or semi-urgent device surgery, the patient specific benefit/risk of holding an antiplatelet should be carefully considered. CLINICAL TRIAL REGISTRATION URL: https://www.clinicaltrials.gov. Unique identifiers: NCT00800137, NCT01675076.
{"title":"Effect of Direct Oral Anticoagulants, Warfarin, and Antiplatelet Agents on Risk of Device Pocket Hematoma: Combined Analysis of BRUISE CONTROL 1 and 2.","authors":"V. Essebag, J. Healey, J. Joza, P. Nery, E. Kalfon, T. Leiria, A. Verma, F. Ayala-Paredes, B. Coutu, G. Sumner, G. Becker, F. Philippon, J. Eikelboom, R. Sandhu, John Sapp, R. Leather, D. Yung, B. Thibault, C. Simpson, K. Ahmad, Satish C. Toal, M. Sturmer, K. Kavanagh, E. Crystal, G. Wells, A. Krahn, D. Birnie","doi":"10.1161/CIRCEP.119.007545","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007545","url":null,"abstract":"BACKGROUND\u0000Oral anticoagulant use is common among patients undergoing pacemaker or defibrillator surgery. BRUISE CONTROL (Bridge or Continue Coumadin for Device Surgery Randomized Controlled Trial; NCT00800137) demonstrated that perioperative warfarin continuation reduced clinically significant hematomas (CSH) by 80% compared with heparin bridging (3.5% versus 16%). BRUISE-CONTROL-2 (NCT01675076) observed a similarly low risk of CSH when comparing continued versus interrupted direct oral anticoagulant (2.1% in both groups). Using patient level data from both trials, the current study aims to: (1) evaluate the effect of concomitant antiplatelet therapy on CSH, and (2) understand the relative risk of CSH in patients treated with direct oral anticoagulant versus continued warfarin.\u0000\u0000\u0000METHODS\u0000We analyzed 1343 patients included in BRUISE-CONTROL-1 and BRUISE-CONTROL-2. The primary outcome for both trials was CSH. There were 408 patients identified as having continued either a single or dual antiplatelet agent at the time of device surgery.\u0000\u0000\u0000RESULTS\u0000Antiplatelet use (versus nonuse) was associated with CSH in 9.8% versus 4.3% of patients (P<0.001), and remained a strong independent predictor after multivariable adjustment (odds ratio, 1.965; 95% CI, 1.202-3.213; P=0.0071). In multivariable analysis, adjusting for antiplatelet use, there was no significant difference in CSH observed between direct oral anticoagulant use compared with continued warfarin (odds ratio, 0.858; 95% CI, 0.375-1.963; P=0.717).\u0000\u0000\u0000CONCLUSIONS\u0000Concomitant antiplatelet therapy doubled the risk of CSH during device surgery. No difference in CSH was found between direct oral anticoagulant versus continued warfarin. In anticoagulated patients undergoing elective or semi-urgent device surgery, the patient specific benefit/risk of holding an antiplatelet should be carefully considered.\u0000\u0000\u0000CLINICAL TRIAL REGISTRATION\u0000URL: https://www.clinicaltrials.gov. Unique identifiers: NCT00800137, NCT01675076.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"11 1","pages":"e007545"},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81911888","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}
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