Pub Date : 2019-08-01DOI: 10.1161/CIRCEP.119.007683
S. Nazarian, F. Marchlinski
Beginning with initial reports of catheter ablation with high-energy direct current shocks for focal and simple arrhythmias in the early 1980s,1 catheter ablation technology and our understanding of arrhythmia mechanisms have rapidly evolved. The identification of left atrial muscular extensions in the pulmonary veins (PVs) by Haïssaguerre et al2 in 1998 opened the era of catheter ablation for suppression of atrial fibrillation (AF). The initial strategy of focal PV trigger ablation was limited by the variability in induction and mapping of the foci, as well as PV stenoses after ablation deep in the veins. To eliminate the need for identification and ablation of individual foci deep in the PVs, ostial isolation of the PV was pursued. Over time, this approach has evolved to an antral PV isolation technique resulting in wide-area circumferential ablation, which mitigates the likelihood of PV stenosis, includes more potential triggers within the isolation zone, and is more likely to modify periatrial autonomic inputs. With wide-area circumferential ablation, however, the ablation circumference has increased, thus increasing the potential for inadvertent gaps in ablation lesions. In addition, strategies such as linear ablation have been implemented in difficult cases, thus adding to the possibility that gaps may exist, and paths for initiation and maintenance of fixed reentry may be created after the procedure. The observation of reentrant atrial tachycardia (AT) after AF ablation is therefore not only related to the burden of de novo scar but also the presence of gaps in linear lesions or wide-area circumferential ablation. Approximately two thirds of post-AF ablation patients with an AT immediately after their ablation will have persistent AT after the healing period. Entrainment mapping strategies can be successfully applied to identify and target these circuits.3 Cardiac imaging with computed tomography or cardiac magnetic resonance (CMR) has long been implemented for creation of 3-dimensional segmentations for enhanced procedural guidance. Most commonly, this approach can be used to tailor lesion delivery to individual variations in left atrial geometry and PV anatomy. In 2007, a study from Peters et al4 suggested that late gadolinium enhancement (LGE) CMR could visualize left atrial lesions after PV isolation. LGE CMR was later championed by Marrouche et al5 to enhance the stratification of potential candidates for AF ablation. In this issue of Circulation: Arrhythmia and Electrophysiology, Fochler et al6 describe LGE CMR-based dechanneling as a strategy to treat reentrant AT after AF ablation. They report a retrospective analysis of 102 patients who underwent EP study and mapping after an initial AF ablation with CMR before each ablation. The authors confirm that a strategy of left atrial linear lesion sets at the index procedure associated with AT after ablation. Of 102 patients, 46 presented with AF only EDITORIAL
{"title":"Dechanneling Left Atrial Late Gadolinium Enhancement.","authors":"S. Nazarian, F. Marchlinski","doi":"10.1161/CIRCEP.119.007683","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007683","url":null,"abstract":"Beginning with initial reports of catheter ablation with high-energy direct current shocks for focal and simple arrhythmias in the early 1980s,1 catheter ablation technology and our understanding of arrhythmia mechanisms have rapidly evolved. The identification of left atrial muscular extensions in the pulmonary veins (PVs) by Haïssaguerre et al2 in 1998 opened the era of catheter ablation for suppression of atrial fibrillation (AF). The initial strategy of focal PV trigger ablation was limited by the variability in induction and mapping of the foci, as well as PV stenoses after ablation deep in the veins. To eliminate the need for identification and ablation of individual foci deep in the PVs, ostial isolation of the PV was pursued. Over time, this approach has evolved to an antral PV isolation technique resulting in wide-area circumferential ablation, which mitigates the likelihood of PV stenosis, includes more potential triggers within the isolation zone, and is more likely to modify periatrial autonomic inputs. With wide-area circumferential ablation, however, the ablation circumference has increased, thus increasing the potential for inadvertent gaps in ablation lesions. In addition, strategies such as linear ablation have been implemented in difficult cases, thus adding to the possibility that gaps may exist, and paths for initiation and maintenance of fixed reentry may be created after the procedure. The observation of reentrant atrial tachycardia (AT) after AF ablation is therefore not only related to the burden of de novo scar but also the presence of gaps in linear lesions or wide-area circumferential ablation. Approximately two thirds of post-AF ablation patients with an AT immediately after their ablation will have persistent AT after the healing period. Entrainment mapping strategies can be successfully applied to identify and target these circuits.3 Cardiac imaging with computed tomography or cardiac magnetic resonance (CMR) has long been implemented for creation of 3-dimensional segmentations for enhanced procedural guidance. Most commonly, this approach can be used to tailor lesion delivery to individual variations in left atrial geometry and PV anatomy. In 2007, a study from Peters et al4 suggested that late gadolinium enhancement (LGE) CMR could visualize left atrial lesions after PV isolation. LGE CMR was later championed by Marrouche et al5 to enhance the stratification of potential candidates for AF ablation. In this issue of Circulation: Arrhythmia and Electrophysiology, Fochler et al6 describe LGE CMR-based dechanneling as a strategy to treat reentrant AT after AF ablation. They report a retrospective analysis of 102 patients who underwent EP study and mapping after an initial AF ablation with CMR before each ablation. The authors confirm that a strategy of left atrial linear lesion sets at the index procedure associated with AT after ablation. Of 102 patients, 46 presented with AF only EDITORIAL","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"30 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74954738","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 : 2019-08-01DOI: 10.1161/CIRCEP.119.007691
K. Motonaga, H. Hsia
The left ventricular (LV) ostium or LV summit is the most superior aspect of the LV outflow tract (LVOT). Ventricular arrhythmias (VAs) arising from this region represent one of the most common sites of origin of idiopathic VAs.1 The LV summit is anatomically defined as the epicardial LV surface bounded by an arc from the left anterior descending coronary artery superior to the first septal perforating branch anterior to the left circumflex coronary artery laterally.2 The LV summit is transected laterally by the great cardiac vein (GCV) at its junction with the anterior interventricular vein, dividing the LV summit into what has traditionally been called the basal (inaccessible) and apical (accessible) segments.2–4 Not surprisingly, arrhythmias originating from the basal (inaccessible) LV summit have a significantly lower rate of ablation success (≈50%) compared with those originating from the apical (accessible) LV summit (≈100%).4 Catheter ablation in this region is challenging because of the complex and variable anatomy in close proximity to critical structures as well as intramural foci that are often encountered.5–7 To aid in determining the site of origin of VAs in the LV summit, several ECG and electrophysiological characteristics have been described, and various ablation strategies have been proposed.3,4,8,9 ECG findings are consistent with the more septal and superior location of the basal LV summit in relationship to the apical LV summit. Compared with the apical segment, arrhythmias originating from the basal segment typically have a left bundle branch block pattern, shorter QRS duration (≤175 ms), greater R-wave amplitude in the inferior leads, smaller R-wave ratio in III/II and Q wave ratio in aVL/aVR, and a later precordial transition.4 A direct ablation approach through the cardiac venous system is usually recommended when an early ventricular activation is recorded within the distal GCV.4,10 This approach can be problematic secondary to difficulty in passing the ablation catheter to the site of interest, inability to achieve adequate power, and proximity to coronary arteries. Alternatively, an anatomic approach from the adjacent endocardial site closest to the LV summit arrhythmia origin can be used, such as from the aortomitral continuity, LVOT, or coronary cusps.4 Predictors of successful ablation using an anatomic approach include a Q-wave ratio of <1.45 in leads aVL/aVR and a close anatomic distance <13.5 mm from the earliest activation site in the GCV.8 Importantly, anatomic proximity and not activation timing dictates the success of an anatomic approach.11 Finally, a percutaneous epicardial approach can be considered when a direct or anatomic ablation approach is unsuccessful. Unfortunately, this approach is only successful in a minority of patients (14%–17%), limited by proximity to major coronary arteries, the left atrial appendage, and poor energy delivery due to the presence of thick epicardial fat.3,4,9 EDITORIAL
{"title":"Road to the Summit May Follow an Eccentric Path.","authors":"K. Motonaga, H. Hsia","doi":"10.1161/CIRCEP.119.007691","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007691","url":null,"abstract":"The left ventricular (LV) ostium or LV summit is the most superior aspect of the LV outflow tract (LVOT). Ventricular arrhythmias (VAs) arising from this region represent one of the most common sites of origin of idiopathic VAs.1 The LV summit is anatomically defined as the epicardial LV surface bounded by an arc from the left anterior descending coronary artery superior to the first septal perforating branch anterior to the left circumflex coronary artery laterally.2 The LV summit is transected laterally by the great cardiac vein (GCV) at its junction with the anterior interventricular vein, dividing the LV summit into what has traditionally been called the basal (inaccessible) and apical (accessible) segments.2–4 Not surprisingly, arrhythmias originating from the basal (inaccessible) LV summit have a significantly lower rate of ablation success (≈50%) compared with those originating from the apical (accessible) LV summit (≈100%).4 Catheter ablation in this region is challenging because of the complex and variable anatomy in close proximity to critical structures as well as intramural foci that are often encountered.5–7 To aid in determining the site of origin of VAs in the LV summit, several ECG and electrophysiological characteristics have been described, and various ablation strategies have been proposed.3,4,8,9 ECG findings are consistent with the more septal and superior location of the basal LV summit in relationship to the apical LV summit. Compared with the apical segment, arrhythmias originating from the basal segment typically have a left bundle branch block pattern, shorter QRS duration (≤175 ms), greater R-wave amplitude in the inferior leads, smaller R-wave ratio in III/II and Q wave ratio in aVL/aVR, and a later precordial transition.4 A direct ablation approach through the cardiac venous system is usually recommended when an early ventricular activation is recorded within the distal GCV.4,10 This approach can be problematic secondary to difficulty in passing the ablation catheter to the site of interest, inability to achieve adequate power, and proximity to coronary arteries. Alternatively, an anatomic approach from the adjacent endocardial site closest to the LV summit arrhythmia origin can be used, such as from the aortomitral continuity, LVOT, or coronary cusps.4 Predictors of successful ablation using an anatomic approach include a Q-wave ratio of <1.45 in leads aVL/aVR and a close anatomic distance <13.5 mm from the earliest activation site in the GCV.8 Importantly, anatomic proximity and not activation timing dictates the success of an anatomic approach.11 Finally, a percutaneous epicardial approach can be considered when a direct or anatomic ablation approach is unsuccessful. Unfortunately, this approach is only successful in a minority of patients (14%–17%), limited by proximity to major coronary arteries, the left atrial appendage, and poor energy delivery due to the presence of thick epicardial fat.3,4,9 EDITORIAL","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84972786","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 : 2019-08-01DOI: 10.1161/CIRCEP.119.007710
A. Tseng, K. Kunze, S. Mulpuru
August 2019 1 Andrew S. Tseng, MD Katie L. Kunze, PhD Siva K. Mulpuru, MD In Response: We greatly appreciate the commentary by Zamani and Wininger in regard to our recent network meta-analysis on pharmacological and cardiac implantable electronic device therapies in heart failure with reduced ejection fraction.1 Their response to our article was meticulous and insightful, and we are privileged to be able to respond to their concerns. We agree with the commentators on the limitations of our design for Figure 6 and acknowledge errors in its construction. Figure 6 attempts to visually represent the temporal relationship between the number of pharmacological versus device studies and mean all-cause mortality incidence rates. We did not intend for Figure 6 to answer the question on overall comparative efficacy of medications versus devices in reducing all-cause mortality. The sole purpose of this supporting figure is to visually demonstrate the trend of all-cause mortality rates in heart failure trials over time. To more accurately represent the data and our intentions with this figure, we have revised the figure to be a bubbleplot, weighted by study sample size and study duration (in person-years). We also thank the commentators for mentioning the misattribution of the study years with the publication years, and we have rectified this in our new figure. Regrettably, Figure 6 had included additional studies from an older version of the data, and in the final publication, Figure 6 had not been updated to reflect only those studies included in the final analysis. All other figures and analyses in the article were derived from the final data. The revised figure is provided here and online (Figure). The raw data used to construct the figure have been provided online (https://drive.google.com/drive/folders/15YnklLuvORw 0oYSPLOcSYMk2WAuuAeGL?usp=sharing). Overall, our study is intended to assist clinicians and researchers generate hypotheses for the various roles of medications and devices in the treatment of heart failure with reduced ejection fraction. We thank the commentators for their thoughtful analysis and comments and believe that the revised figure more accurately represents the data and the intended scope of the figure.
1 Andrew S. Tseng医学博士Katie L. Kunze博士Siva K. Mulpuru医学博士回应:我们非常感谢Zamani和Wininger关于我们最近关于药物和心脏植入式电子设备治疗心力衰竭降低射血分数的网络荟萃分析的评论他们对我们文章的回应是细致而深刻的，我们很荣幸能够回应他们的担忧。我们同意评论者对图6设计的局限性的看法，并承认其构造中的错误。图6试图直观地表示药理学与器械研究数量与平均全因死亡率之间的时间关系。我们不打算用图6来回答关于药物与器械在降低全因死亡率方面的总体比较疗效的问题。这个支持数据的唯一目的是直观地展示心力衰竭试验中全因死亡率随时间的变化趋势。为了更准确地表示数据和我们的意图，我们将该图修改为气泡图，按研究样本量和研究持续时间(以人年为单位)加权。我们也感谢评论者提到的研究年份与出版年份的错误归属，我们已经在我们的新数据中纠正了这一点。遗憾的是，图6包含了来自旧版本数据的额外研究，并且在最终出版物中，图6没有更新以仅反映最终分析中包含的那些研究。文中其他所有的数据和分析均来源于最终数据。修改后的数字在这里和网上提供(图)。用于构建该图的原始数据已在网上提供(https://drive.google.com/drive/folders/15YnklLuvORw 0oYSPLOcSYMk2WAuuAeGL?usp=sharing)。总的来说，我们的研究旨在帮助临床医生和研究人员对药物和设备在治疗心力衰竭伴射血分数降低中的各种作用提出假设。我们感谢评论员们深思熟虑的分析和评论，并相信修订后的数字更准确地反映了数据和数字的预期范围。
{"title":"Response by Tseng et al to Letter Regarding Article, \"Efficacy of Pharmacologic and Cardiac Implantable Electronic Device Therapies in Patients With Heart Failure and Reduced Ejection Fraction: A Systematic Review and Network Meta-Analysis\".","authors":"A. Tseng, K. Kunze, S. Mulpuru","doi":"10.1161/CIRCEP.119.007710","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007710","url":null,"abstract":"August 2019 1 Andrew S. Tseng, MD Katie L. Kunze, PhD Siva K. Mulpuru, MD In Response: We greatly appreciate the commentary by Zamani and Wininger in regard to our recent network meta-analysis on pharmacological and cardiac implantable electronic device therapies in heart failure with reduced ejection fraction.1 Their response to our article was meticulous and insightful, and we are privileged to be able to respond to their concerns. We agree with the commentators on the limitations of our design for Figure 6 and acknowledge errors in its construction. Figure 6 attempts to visually represent the temporal relationship between the number of pharmacological versus device studies and mean all-cause mortality incidence rates. We did not intend for Figure 6 to answer the question on overall comparative efficacy of medications versus devices in reducing all-cause mortality. The sole purpose of this supporting figure is to visually demonstrate the trend of all-cause mortality rates in heart failure trials over time. To more accurately represent the data and our intentions with this figure, we have revised the figure to be a bubbleplot, weighted by study sample size and study duration (in person-years). We also thank the commentators for mentioning the misattribution of the study years with the publication years, and we have rectified this in our new figure. Regrettably, Figure 6 had included additional studies from an older version of the data, and in the final publication, Figure 6 had not been updated to reflect only those studies included in the final analysis. All other figures and analyses in the article were derived from the final data. The revised figure is provided here and online (Figure). The raw data used to construct the figure have been provided online (https://drive.google.com/drive/folders/15YnklLuvORw 0oYSPLOcSYMk2WAuuAeGL?usp=sharing). Overall, our study is intended to assist clinicians and researchers generate hypotheses for the various roles of medications and devices in the treatment of heart failure with reduced ejection fraction. We thank the commentators for their thoughtful analysis and comments and believe that the revised figure more accurately represents the data and the intended scope of the figure.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"84 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88500489","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 : 2019-07-29DOI: 10.1161/CIRCEP.118.006835
George Leef, F. Shenasa, N. Bhatia, A. Rogers, W. Sauer, John M. Miller, Mark Swerdlow, M. Tamboli, M. Alhusseini, E. Armenia, T. Baykaner, J. Brachmann, M. Turakhia, F. Atienza, W. Rappel, Paul J. Wang, S. Narayan
BACKGROUND Localized drivers are proposed mechanisms for persistent atrial fibrillation (AF) from optical mapping of human atria and clinical studies of AF, yet are controversial because drivers fluctuate and ablating them may not terminate AF. We used wavefront field mapping to test the hypothesis that AF drivers, if concurrent, may interact to produce fluctuating areas of control to explain their appearance/disappearance and acute impact of ablation. METHODS We recruited 54 patients from an international registry in whom persistent AF terminated by targeted ablation. Unipolar AF electrograms were analyzed from 64-pole baskets to reconstruct activation times, map propagation vectors each 20 ms, and create nonproprietary phase maps. RESULTS Each patient (63.6±8.5 years, 29.6% women) showed 4.0±2.1 spatially anchored rotational or focal sites in AF in 3 patterns. First, a single (type I; n=7) or, second, paired chiral-antichiral (type II; n=5) rotational drivers controlled most of the atrial area. Ablation of 1 to 2 large drivers terminated all cases of types I or II AF. Third, interaction of 3 to 5 drivers (type III; n=42) with changing areas of control. Targeted ablation at driver centers terminated AF and required more ablation in types III versus I (P=0.02 in left atrium). CONCLUSIONS Wavefront field mapping of persistent AF reveals a pathophysiologic network of a small number of spatially anchored rotational and focal sites, which interact, fluctuate, and control varying areas. Future work should define whether AF drivers that control larger atrial areas are attractive targets for ablation.
{"title":"Wavefront Field Mapping Reveals a Physiologic Network Between Drivers Where Ablation Terminates Atrial Fibrillation.","authors":"George Leef, F. Shenasa, N. Bhatia, A. Rogers, W. Sauer, John M. Miller, Mark Swerdlow, M. Tamboli, M. Alhusseini, E. Armenia, T. Baykaner, J. Brachmann, M. Turakhia, F. Atienza, W. Rappel, Paul J. Wang, S. Narayan","doi":"10.1161/CIRCEP.118.006835","DOIUrl":"https://doi.org/10.1161/CIRCEP.118.006835","url":null,"abstract":"BACKGROUND\u0000Localized drivers are proposed mechanisms for persistent atrial fibrillation (AF) from optical mapping of human atria and clinical studies of AF, yet are controversial because drivers fluctuate and ablating them may not terminate AF. We used wavefront field mapping to test the hypothesis that AF drivers, if concurrent, may interact to produce fluctuating areas of control to explain their appearance/disappearance and acute impact of ablation.\u0000\u0000\u0000METHODS\u0000We recruited 54 patients from an international registry in whom persistent AF terminated by targeted ablation. Unipolar AF electrograms were analyzed from 64-pole baskets to reconstruct activation times, map propagation vectors each 20 ms, and create nonproprietary phase maps.\u0000\u0000\u0000RESULTS\u0000Each patient (63.6±8.5 years, 29.6% women) showed 4.0±2.1 spatially anchored rotational or focal sites in AF in 3 patterns. First, a single (type I; n=7) or, second, paired chiral-antichiral (type II; n=5) rotational drivers controlled most of the atrial area. Ablation of 1 to 2 large drivers terminated all cases of types I or II AF. Third, interaction of 3 to 5 drivers (type III; n=42) with changing areas of control. Targeted ablation at driver centers terminated AF and required more ablation in types III versus I (P=0.02 in left atrium).\u0000\u0000\u0000CONCLUSIONS\u0000Wavefront field mapping of persistent AF reveals a pathophysiologic network of a small number of spatially anchored rotational and focal sites, which interact, fluctuate, and control varying areas. Future work should define whether AF drivers that control larger atrial areas are attractive targets for ablation.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"36 1","pages":"e006835"},"PeriodicalIF":0.0,"publicationDate":"2019-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88368571","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 : 2019-07-26DOI: 10.1161/CIRCEP.119.007320
Tadashi Hoshiyama, H. Fukushima, K. Noda, S. Oshima, K. Ashikaga, T. Ikeda, K. Sakamoto, K. Tsujita
{"title":"Effect of Contact Vector Direction on Achieving Pulmonary Vein Isolation.","authors":"Tadashi Hoshiyama, H. Fukushima, K. Noda, S. Oshima, K. Ashikaga, T. Ikeda, K. Sakamoto, K. Tsujita","doi":"10.1161/CIRCEP.119.007320","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007320","url":null,"abstract":"","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"49 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87470086","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 : 2019-07-26DOI: 10.1161/CIRCEP.119.007311
Koichiro Ejima, Ken-ichi Kato, Ayako Okada, O. Wakisaka, R. Kimura, Makoto Ishizawa, T. Imai, Yuko Toyama, M. Shoda, N. Hagiwara
BACKGROUND Both contact force monitoring (CFM) and unipolar signal modification (USM) are guides for ablation, which improve the efficacy of pulmonary vein isolation of atrial fibrillation. We sought to compare the outcomes of atrial fibrillation ablation guided by CFM or USM. METHODS A total of 136 patients with paroxysmal atrial fibrillation underwent a circumferential pulmonary vein isolation using CF sensing ablation catheters and were randomly assigned to undergo catheter ablation guided by either CFM (CFM-guided group: n=70) or USM (USM-guided group: n=66). In the USM-guided group, each radiofrequency application lasted until the development of completely positive unipolar electrograms. In the CFM-guided group, a CF of 20 g (range, 10-30 g) and minimum force-time integral of 400 g were the targets for each radiofrequency application. The primary end point was freedom from any atrial tachyarrhythmia recurrence without antiarrhythmic drugs at 12-months of follow-up. RESULTS The cumulative freedom from recurrences at 12-months was 85% in the USM-guided group and 70% in the CFM-guided group (P=0.031). The incidence of time-dependent and ATP-provoked early electrical reconnections between the left atrium and PVs, procedural time, fluoroscopic time, and average force-time integral, did not significantly differ between the 2 groups. The radiofrequency time for the pulmonary vein isolation was shorter in the USM-guided group than CFM-guided group but was not statistically significant (P=0.077). CONCLUSIONS USM was superior to CFM as an end point for radiofrequency energy deliveries during the pulmonary vein isolation in patients with paroxysmal atrial fibrillation in terms of the 12-month recurrence-free rate. CLINICAL TRIAL REGISTRATION URL: https://www.umin.ac.jp/ctr/index.htm. Unique identifier: UMIN000021127.
{"title":"Comparison Between Contact Force Monitoring and Unipolar Signal Modification as a Guide for Catheter Ablation of Atrial Fibrillation.","authors":"Koichiro Ejima, Ken-ichi Kato, Ayako Okada, O. Wakisaka, R. Kimura, Makoto Ishizawa, T. Imai, Yuko Toyama, M. Shoda, N. Hagiwara","doi":"10.1161/CIRCEP.119.007311","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007311","url":null,"abstract":"BACKGROUND\u0000Both contact force monitoring (CFM) and unipolar signal modification (USM) are guides for ablation, which improve the efficacy of pulmonary vein isolation of atrial fibrillation. We sought to compare the outcomes of atrial fibrillation ablation guided by CFM or USM.\u0000\u0000\u0000METHODS\u0000A total of 136 patients with paroxysmal atrial fibrillation underwent a circumferential pulmonary vein isolation using CF sensing ablation catheters and were randomly assigned to undergo catheter ablation guided by either CFM (CFM-guided group: n=70) or USM (USM-guided group: n=66). In the USM-guided group, each radiofrequency application lasted until the development of completely positive unipolar electrograms. In the CFM-guided group, a CF of 20 g (range, 10-30 g) and minimum force-time integral of 400 g were the targets for each radiofrequency application. The primary end point was freedom from any atrial tachyarrhythmia recurrence without antiarrhythmic drugs at 12-months of follow-up.\u0000\u0000\u0000RESULTS\u0000The cumulative freedom from recurrences at 12-months was 85% in the USM-guided group and 70% in the CFM-guided group (P=0.031). The incidence of time-dependent and ATP-provoked early electrical reconnections between the left atrium and PVs, procedural time, fluoroscopic time, and average force-time integral, did not significantly differ between the 2 groups. The radiofrequency time for the pulmonary vein isolation was shorter in the USM-guided group than CFM-guided group but was not statistically significant (P=0.077).\u0000\u0000\u0000CONCLUSIONS\u0000USM was superior to CFM as an end point for radiofrequency energy deliveries during the pulmonary vein isolation in patients with paroxysmal atrial fibrillation in terms of the 12-month recurrence-free rate.\u0000\u0000\u0000CLINICAL TRIAL REGISTRATION\u0000URL: https://www.umin.ac.jp/ctr/index.htm. Unique identifier: UMIN000021127.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"15 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89115311","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 : 2019-07-26DOI: 10.1161/CIRCEP.119.007387
B. Banavalikar, J. Shenthar, D. Padmanabhan, S. P. Valappil, S. Singha, A. Kottayan, M. Ghadei, Muzaffar Ali
BACKGROUND Incessant focal atrial tachycardia (FAT), if untreated, can lead to ventricular dysfunction and heart failure (tachycardia-induced cardiomyopathy). Drug therapy of FAT is often difficult and ineffective. The efficacy of ivabradine has not been systematically evaluated in the treatment of FAT. METHODS The study group consisted of patients with incessant FAT (lasting >24 hours) and structurally normal hearts. Patients with ventricular dysfunction as a consequence of FAT were not excluded. All antiarrhythmic drugs were discontinued at least 5 half-lives before the initiation of ivabradine. Oral ivabradine (adults, 10 mg twice 12 hours apart; pediatric patients: 0.28 mg/kg in 2 divided doses) was initiated in the intensive care unit under continuous electrocardiographic monitoring. A positive response was defined as the termination of tachycardia with the restoration of sinus rhythm or suppression of the tachycardia to <100 beats per minute without termination within 12 hours of initiating ivabradine. RESULTS Twenty-eight patients (mean age, 34.6±21.5 years; women, 60.7%) were included in the study. The most common symptom was palpitation (85.7%) followed by shortness of breath (25%). The mean atrial rate during tachycardia was 170±21 beats per minute, and the mean left ventricular ejection fraction was 54.7±14.3%. Overall, 18 (64.3%) patients responded within 6 hours of the first dose of ivabradine. Thirteen of 18 ivabradine responders subsequently underwent successful catheter ablation. FAT originating in the atrial appendages was a predictor of ivabradine response compared with those arising from other atrial sites (P=0.046). CONCLUSIONS Ivabradine-sensitive atrial tachycardia constitutes 64% of incessant FAT in patients without structural heart disease. Incessant FAT originating in the atrial appendages is more likely to respond to ivabradine than that arising from other atrial sites. Our findings implicate the funny current in the pathogenesis of FAT.
{"title":"Clinical and Electrophysiological Correlates of Incessant Ivabradine-Sensitive Atrial Tachycardia.","authors":"B. Banavalikar, J. Shenthar, D. Padmanabhan, S. P. Valappil, S. Singha, A. Kottayan, M. Ghadei, Muzaffar Ali","doi":"10.1161/CIRCEP.119.007387","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007387","url":null,"abstract":"BACKGROUND\u0000Incessant focal atrial tachycardia (FAT), if untreated, can lead to ventricular dysfunction and heart failure (tachycardia-induced cardiomyopathy). Drug therapy of FAT is often difficult and ineffective. The efficacy of ivabradine has not been systematically evaluated in the treatment of FAT.\u0000\u0000\u0000METHODS\u0000The study group consisted of patients with incessant FAT (lasting >24 hours) and structurally normal hearts. Patients with ventricular dysfunction as a consequence of FAT were not excluded. All antiarrhythmic drugs were discontinued at least 5 half-lives before the initiation of ivabradine. Oral ivabradine (adults, 10 mg twice 12 hours apart; pediatric patients: 0.28 mg/kg in 2 divided doses) was initiated in the intensive care unit under continuous electrocardiographic monitoring. A positive response was defined as the termination of tachycardia with the restoration of sinus rhythm or suppression of the tachycardia to <100 beats per minute without termination within 12 hours of initiating ivabradine.\u0000\u0000\u0000RESULTS\u0000Twenty-eight patients (mean age, 34.6±21.5 years; women, 60.7%) were included in the study. The most common symptom was palpitation (85.7%) followed by shortness of breath (25%). The mean atrial rate during tachycardia was 170±21 beats per minute, and the mean left ventricular ejection fraction was 54.7±14.3%. Overall, 18 (64.3%) patients responded within 6 hours of the first dose of ivabradine. Thirteen of 18 ivabradine responders subsequently underwent successful catheter ablation. FAT originating in the atrial appendages was a predictor of ivabradine response compared with those arising from other atrial sites (P=0.046).\u0000\u0000\u0000CONCLUSIONS\u0000Ivabradine-sensitive atrial tachycardia constitutes 64% of incessant FAT in patients without structural heart disease. Incessant FAT originating in the atrial appendages is more likely to respond to ivabradine than that arising from other atrial sites. Our findings implicate the funny current in the pathogenesis of FAT.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"121 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89470289","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 : 2019-07-01DOI: 10.1161/hae.0000000000000041
{"title":"Correction to: Machine Learning Prediction of Response to Cardiac Resynchronization Therapy: Improvement Versus Current Guidelines","authors":"","doi":"10.1161/hae.0000000000000041","DOIUrl":"https://doi.org/10.1161/hae.0000000000000041","url":null,"abstract":"","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"63 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88472894","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 : 2019-07-01DOI: 10.1161/CIRCEP.119.007197
M. Jin, Tae‐Hoon Kim, Ki-Woon Kang, H. Yu, J. Uhm, B. Joung, Moon‐Hyoung Lee, Eosu Kim, H. Pak
BACKGROUND Although atrial fibrillation (AF) has a risk of cognitive dysfunction, it is not clear whether AF catheter ablation improves or worsens cognitive function. This prospective case-control study sought to assess the 1-year serial changes in the cognitive function with or without AF catheter ablation. METHODS We evaluated the Montreal Cognitive Assessment score in 308 patients (71.4% male, 60.6±9.1 years of age, 34.1% persistent AF) who underwent AF ablation (ablation group) and 50 AF patients on medical therapy who met the same indication for AF ablation (control group), at baseline and 3 and 12 months after enrollment. Cognitive impairment was defined as a published cutoff score of <23 points. To exclude any learning effects, we used the practice-adjusted reliable change index for assessing the cognitive changes. RESULTS Preablation cognitive impairment was detected in 18.5% (57/308). The Montreal Cognitive Assessment score significantly improved 1 year after radiofrequency catheter ablation in both overall ablation group (24.9±2.9-26.4±2.5; P<0.001) and the propensity-matched ablation group (25.4±2.4-26.5±2.3; P<0.001), but not in the control group (25.4±2.5-24.8±2.5; P=0.012). Preablation cognitive impairment (odds ratio, 13.70; 95% CI, 4.83-38.87; P<0.001) was independently associated with an improvement in the 1-year post-ablation cognitive function. In the reliable change index analyses, 94.7% of propensity-matched ablation group showed an improved/stable cognitive function at the 1-year follow-up. CONCLUSIONS Catheter ablation of AF, at least, does not deteriorate the cognitive function, but rather improves the performance on 1-year follow-up neurocognitive tests, especially in patients with a preablation cognitive impairment.
{"title":"Atrial Fibrillation Catheter Ablation Improves 1-Year Follow-Up Cognitive Function, Especially in Patients With Impaired Cognitive Function.","authors":"M. Jin, Tae‐Hoon Kim, Ki-Woon Kang, H. Yu, J. Uhm, B. Joung, Moon‐Hyoung Lee, Eosu Kim, H. Pak","doi":"10.1161/CIRCEP.119.007197","DOIUrl":"https://doi.org/10.1161/CIRCEP.119.007197","url":null,"abstract":"BACKGROUND\u0000Although atrial fibrillation (AF) has a risk of cognitive dysfunction, it is not clear whether AF catheter ablation improves or worsens cognitive function. This prospective case-control study sought to assess the 1-year serial changes in the cognitive function with or without AF catheter ablation.\u0000\u0000\u0000METHODS\u0000We evaluated the Montreal Cognitive Assessment score in 308 patients (71.4% male, 60.6±9.1 years of age, 34.1% persistent AF) who underwent AF ablation (ablation group) and 50 AF patients on medical therapy who met the same indication for AF ablation (control group), at baseline and 3 and 12 months after enrollment. Cognitive impairment was defined as a published cutoff score of <23 points. To exclude any learning effects, we used the practice-adjusted reliable change index for assessing the cognitive changes.\u0000\u0000\u0000RESULTS\u0000Preablation cognitive impairment was detected in 18.5% (57/308). The Montreal Cognitive Assessment score significantly improved 1 year after radiofrequency catheter ablation in both overall ablation group (24.9±2.9-26.4±2.5; P<0.001) and the propensity-matched ablation group (25.4±2.4-26.5±2.3; P<0.001), but not in the control group (25.4±2.5-24.8±2.5; P=0.012). Preablation cognitive impairment (odds ratio, 13.70; 95% CI, 4.83-38.87; P<0.001) was independently associated with an improvement in the 1-year post-ablation cognitive function. In the reliable change index analyses, 94.7% of propensity-matched ablation group showed an improved/stable cognitive function at the 1-year follow-up.\u0000\u0000\u0000CONCLUSIONS\u0000Catheter ablation of AF, at least, does not deteriorate the cognitive function, but rather improves the performance on 1-year follow-up neurocognitive tests, especially in patients with a preablation cognitive impairment.","PeriodicalId":10167,"journal":{"name":"Circulation: Arrhythmia and Electrophysiology","volume":"70 1","pages":"e007197"},"PeriodicalIF":0.0,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82555749","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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