Pub Date : 2019-11-01Epub Date: 2019-11-08DOI: 10.1161/CIRCEP.119.007733
Michele Orini, Neil Srinivasan, Adam J Graham, Peter Taggart, Pier D Lambiase
{"title":"Further Evidence on How to Measure Local Repolarization Time Using Intracardiac Unipolar Electrograms in the Intact Human Heart.","authors":"Michele Orini, Neil Srinivasan, Adam J Graham, Peter Taggart, Pier D Lambiase","doi":"10.1161/CIRCEP.119.007733","DOIUrl":"10.1161/CIRCEP.119.007733","url":null,"abstract":"","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75764914","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}
BACKGROUND Atrial tachycardia (AT) with cycle length (CL) alternans is a rare phenomenon. We aimed to identify the characteristics and precise mechanism of this special category of ATs by using an ultrahigh density mapping system. METHODS We identified 7 ATs with alternating CL in a total of 478 ATs from 2 institutions mapped with an ultrahigh density mapping system. Activation maps were performed for long CL (289±35 ms; mapping points, 21 520±11 103) and short CL (251±18 ms; mapping points,17 594±8059) separately. RESULTS We classified ATs with CL alternans into 2 types. Type 1: There existed 2 potential loops with different routes. CL alternans resulted from an intermittently 2:1 conducting block within the channel of the smaller loop. Type 2: CL alternans resulted from different conduction velocity through 2 closely spaced gaps within preexisting linear lesions. Catheter ablation successfully terminated all the 7 ATs. CONCLUSIONS Ultrahigh density mapping provides an opportunity to delineate the precise mechanism of AT with CL alternans. Intermittent conduction block or slowing of a channel was essential for the maintenance of AT.
{"title":"Insight Into the Mechanism of Macroreentrant Atrial Tachycardia With Cycle Length Alternans Using Ultrahigh Density Mapping System.","authors":"Jin-lin Zhang, Liangrong Zheng, Dongchen Zhou, Anquan Zhao, Cheng Tang, Yong-hua Zhang, X. Su","doi":"10.1161/CIRCEP.119.007634","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007634","url":null,"abstract":"BACKGROUND\u0000Atrial tachycardia (AT) with cycle length (CL) alternans is a rare phenomenon. We aimed to identify the characteristics and precise mechanism of this special category of ATs by using an ultrahigh density mapping system.\u0000\u0000\u0000METHODS\u0000We identified 7 ATs with alternating CL in a total of 478 ATs from 2 institutions mapped with an ultrahigh density mapping system. Activation maps were performed for long CL (289±35 ms; mapping points, 21 520±11 103) and short CL (251±18 ms; mapping points,17 594±8059) separately.\u0000\u0000\u0000RESULTS\u0000We classified ATs with CL alternans into 2 types. Type 1: There existed 2 potential loops with different routes. CL alternans resulted from an intermittently 2:1 conducting block within the channel of the smaller loop. Type 2: CL alternans resulted from different conduction velocity through 2 closely spaced gaps within preexisting linear lesions. Catheter ablation successfully terminated all the 7 ATs.\u0000\u0000\u0000CONCLUSIONS\u0000Ultrahigh density mapping provides an opportunity to delineate the precise mechanism of AT with CL alternans. Intermittent conduction block or slowing of a channel was essential for the maintenance of AT.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80136002","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.119.007382
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":null,"pages":null},"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":null,"pages":null},"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 : 2019-11-01Epub Date: 2019-10-31DOI: 10.1161/CIRCEP.119.007573
Leroy C Joseph, Uma Mahesh R Avula, Elaine Y Wan, Michael V Reyes, Kundanika R Lakkadi, Prakash Subramanyam, Koki Nakanishi, Shunichi Homma, Antoine Muchir, Utpal B Pajvani, Edward B Thorp, Steven R Reiken, Andrew R Marks, Henry M Colecraft, John P Morrow
Background: Obesity and diets high in saturated fat increase the risk of arrhythmias and sudden cardiac death. However, the molecular mechanisms are not well understood. We hypothesized that an increase in dietary saturated fat could lead to abnormalities of calcium homeostasis and heart rhythm by a NOX2 (NADPH oxidase 2)-dependent mechanism.
Methods: We investigated this hypothesis by feeding mice high-fat diets. In vivo heart rhythm telemetry, optical mapping, and isolated cardiac myocyte imaging were used to quantify arrhythmias, repolarization, calcium transients, and intracellular calcium sparks.
Results: We found that saturated fat activates NOX (NADPH oxidase), whereas polyunsaturated fat does not. The high saturated fat diet increased repolarization heterogeneity and ventricular tachycardia inducibility in perfused hearts. Pharmacological inhibition or genetic deletion of NOX2 prevented arrhythmogenic abnormalities in vivo during high statured fat diet and resulted in less inducible ventricular tachycardia. High saturated fat diet activates CaMK (Ca2+/calmodulin-dependent protein kinase) in the heart, which contributes to abnormal calcium handling, promoting arrhythmia.
Conclusions: We conclude that NOX2 deletion or pharmacological inhibition prevents the arrhythmogenic effects of a high saturated fat diet, in part mediated by activation of CaMK. This work reveals a molecular mechanism linking cardiac metabolism to arrhythmia and suggests that NOX2 inhibitors could be a novel therapy for heart rhythm abnormalities caused by cardiac lipid overload.
{"title":"Dietary Saturated Fat Promotes Arrhythmia by Activating NOX2 (NADPH Oxidase 2).","authors":"Leroy C Joseph, Uma Mahesh R Avula, Elaine Y Wan, Michael V Reyes, Kundanika R Lakkadi, Prakash Subramanyam, Koki Nakanishi, Shunichi Homma, Antoine Muchir, Utpal B Pajvani, Edward B Thorp, Steven R Reiken, Andrew R Marks, Henry M Colecraft, John P Morrow","doi":"10.1161/CIRCEP.119.007573","DOIUrl":"10.1161/CIRCEP.119.007573","url":null,"abstract":"<p><strong>Background: </strong>Obesity and diets high in saturated fat increase the risk of arrhythmias and sudden cardiac death. However, the molecular mechanisms are not well understood. We hypothesized that an increase in dietary saturated fat could lead to abnormalities of calcium homeostasis and heart rhythm by a NOX2 (NADPH oxidase 2)-dependent mechanism.</p><p><strong>Methods: </strong>We investigated this hypothesis by feeding mice high-fat diets. In vivo heart rhythm telemetry, optical mapping, and isolated cardiac myocyte imaging were used to quantify arrhythmias, repolarization, calcium transients, and intracellular calcium sparks.</p><p><strong>Results: </strong>We found that saturated fat activates NOX (NADPH oxidase), whereas polyunsaturated fat does not. The high saturated fat diet increased repolarization heterogeneity and ventricular tachycardia inducibility in perfused hearts. Pharmacological inhibition or genetic deletion of NOX2 prevented arrhythmogenic abnormalities in vivo during high statured fat diet and resulted in less inducible ventricular tachycardia. High saturated fat diet activates CaMK (Ca<sup>2+</sup>/calmodulin-dependent protein kinase) in the heart, which contributes to abnormal calcium handling, promoting arrhythmia.</p><p><strong>Conclusions: </strong>We conclude that NOX2 deletion or pharmacological inhibition prevents the arrhythmogenic effects of a high saturated fat diet, in part mediated by activation of CaMK. This work reveals a molecular mechanism linking cardiac metabolism to arrhythmia and suggests that NOX2 inhibitors could be a novel therapy for heart rhythm abnormalities caused by cardiac lipid overload.</p>","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2019-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73397431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","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":null,"pages":null},"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":null,"pages":null},"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":null,"pages":null},"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":null,"pages":null},"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
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