Author
Tina Baykaner
Other affiliations: University of California, San Diego, Cardiovascular Institute of the South, Veterans Health Administration
Bio: Tina Baykaner is an academic researcher from Stanford University. The author has contributed to research in topics: Medicine & Atrial fibrillation. The author has an hindex of 14, co-authored 66 publications receiving 1009 citations. Previous affiliations of Tina Baykaner include University of California, San Diego & Cardiovascular Institute of the South.
Papers
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TL;DR: FIRM-guided ablation is more durable than conventional trigger-based ablation in preventing 3-year AF recurrence and future studies should investigate how ablation of patient-specific AF-sustaining rotors and focal sources alters the natural history of arrhythmia recurrence.
331 citations
TL;DR: In this article, the success of pulmonary vein isolation (PVI) for atrial fibrillation (AF) may be improved if stable AF sources identified by Focal Impulse and Rotor Mapping (FIRM) are also eliminated.
Abstract: Introduction
The success of pulmonary vein isolation (PVI) for atrial fibrillation (AF) may be improved if stable AF sources identified by Focal Impulse and Rotor Mapping (FIRM) are also eliminated. The long-term results of this approach are unclear outside the centers where FIRM was developed; thus, we assessed outcomes of FIRM-guided AF ablation in the first cases at 10 experienced centers.
175 citations
TL;DR: In this large prospective cohort of subjects with CHA2DS2-VASc scores ≥2, 22.4% were newly diagnosed with AF and the majority of these subjects were given OACs, suggesting a potential role of ICMs in AF screening.
79 citations
TL;DR: In this paper, a systematic literature review and meta-analysis was conducted to determine outcomes from ablation of AF drivers in addition to pulmonary vein isolation (PVI) or as a stand-alone procedure.
Abstract: Background: The outcomes from pulmonary vein isolation (PVI) for atrial fibrillation (AF) are suboptimal, but the benefits of additional lesion sets remain unproven. Recent studies propose ablation of AF drivers improves outcomes over PVI, yet with conflicting reports in the literature. We undertook a systematic literature review and meta-analysis to determine outcomes from ablation of AF drivers in addition to PVI or as a stand-alone procedure. Methods: Database search was done using the terms atrial fibrillation and ablation or catheter ablation and driver or rotor or focal impulse or FIRM (Focal Impulse and Rotor Modulation). We pooled data using random effects model and assessed heterogeneity with I 2 statistic. Results: Seventeen studies met inclusion criteria, in a cohort size of 3294 patients. Adding AF driver ablation to PVI reported freedom from AF of 72.5% (confidence interval [CI], 62.1%–81.8%; P P P =0.02) for freedom from AF and an odds ratio of 1.8 (CI, 1.2–2.7; P P Conclusions: In controlled studies, the addition of AF driver ablation to PVI supports the possible benefit of a combined approach of AF driver ablation and PVI in improving single-procedure freedom from all arrhythmias. However, most studies are uncontrolled and are limited by substantial heterogeneity in outcomes. Large multicenter randomized trials are needed to precisely define the benefits of adding driver ablation to PVI.
71 citations
TL;DR: Local activation mapping at sites of termination of persistent AF showed repetitive patterns of rotational or focal activity, and in computer simulations, complete rotational activation sequence was observed but was sensitive to assignment of activation timing particularly in segments of slow conduction.
Abstract: Background: The mechanisms by which persistent atrial fibrillation (AF) terminates via localized ablation are not well understood. To address the hypothesis that sites where localized ablation terminates persistent AF have characteristics identifiable with activation mapping during AF, we systematically examined activation patterns acquired only in cases of unequivocal termination by ablation. Methods and Results: We recruited 57 patients with persistent AF undergoing ablation, in whom localized ablation terminated AF to sinus rhythm or organized tachycardia. For each site, we performed an offline analysis of unprocessed unipolar electrograms collected during AF from multipolar basket catheters using the maximum –dV/dt assignment to construct isochronal activation maps for multiple cycles. Additional computational modeling and phase analysis were used to study mechanisms of map variability. At all sites of AF termination, localized repetitive activation patterns were observed. Partial rotational circuits were observed in 26 of 57 (46%) cases, focal patterns in 19 of 57 (33%), and complete rotational activity in 12 of 57 (21%) cases. In computer simulations, incomplete segments of partial rotations coincided with areas of slow conduction characterized by complex, multicomponent electrograms, and variations in assigning activation times at such sites substantially altered mapped mechanisms. Conclusions: Local activation mapping at sites of termination of persistent AF showed repetitive patterns of rotational or focal activity. In computer simulations, complete rotational activation sequence was observed but was sensitive to assignment of activation timing particularly in segments of slow conduction. The observed phenomena of repetitive localized activation and the mechanism by which local ablation terminates putative AF drivers require further investigation.
46 citations
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Leipzig University1, University of Belgrade2, Leiden University3, Uppsala University4, University of Modena and Reggio Emilia5, University of Barcelona6, Carol Davila University of Medicine and Pharmacy7, National and Kapodistrian University of Athens8, François Rabelais University9, Royal Melbourne Hospital10, University of Melbourne11, University of Lisbon12, University of Birmingham13, University of Groningen14, University Medical Center Groningen15, University of Central Lancashire16
TL;DR: The content of these European Society of Cardiology (ESC) Guidelines has been published for personal and educational use only and no commercial use is authorized.
Abstract: Supplementary Table 9, column 'Edoxaban', row 'eGFR category', '95 mL/min' (page 15). The cell should be coloured green instead of yellow. It should also read "60 mg"instead of "60 mg (use with caution in 'supranormal' renal function)."In the above-indicated cell, a footnote has also been added to state: "Edoxaban should be used in patients with high creatinine clearance only after a careful evaluation of the individual thromboembolic and bleeding risk."Supplementary Table 9, column 'Edoxaban', row 'Dose reduction in selected patients' (page 16). The cell should read "Edoxaban 60 mg reduced to 30 mg once daily if any of the following: creatinine clearance 15-50 mL/min, body weight <60 kg, concomitant use of dronedarone, erythromycin, ciclosporine or ketokonazole"instead of "Edoxaban 60 mg reduced to 30 mg once daily, and edoxaban 30 mg reduced to 15mg once daily, if any of the following: creatinine clearance of 30-50 mL/min, body weight <60 kg, concomitant us of verapamil or quinidine or dronedarone."
4,285 citations
Johns Hopkins University1, Leipzig University2, Korea University3, Yale University4, West Virginia University5, University of Barcelona6, St George's, University of London7, Indiana University8, National Yang-Ming University9, Cleveland Clinic10, Aarhus University11, University at Buffalo12, Imperial College London13, Primary Children's Hospital14, Erasmus University Rotterdam15, Yeshiva University16, Ghent University17, Baylor University18, Virginia Commonwealth University19, Harvard University20, Federal University of São Paulo21, University of California, San Francisco22, Beaumont Hospital23, Boston University24, University of Oklahoma25, Carlos III Health Institute26, University of Michigan27, University of Melbourne28, Saint Louis University29, Université de Montréal30, University of Pennsylvania31, McGill University32, Mayo Clinic33, Lahey Hospital & Medical Center34, Royal Adelaide Hospital35, University of Milan36, University of Toronto37, Loyola University Chicago38, Jikei University School of Medicine39
TL;DR: This 2017 Consensus Statement is to provide a state-of-the-art review of the field of catheter and surgical ablation of AF and to report the findings of a writing group, convened by these five international societies.
1,626 citations
TL;DR: Among patients with persistent atrial fibrillation, there was no reduction in the rate of recurrent atrialfibrillation when either linear ablation or ablation of complex fractionated electrograms was performed in addition to pulmonary-vein isolation.
Abstract: BackgroundCatheter ablation is less successful for persistent atrial fibrillation than for paroxysmal atrial fibrillation. Guidelines suggest that adjuvant substrate modification in addition to pulmonary-vein isolation is required in persistent atrial fibrillation. MethodsWe randomly assigned 589 patients with persistent atrial fibrillation in a 1:4:4 ratio to ablation with pulmonary-vein isolation alone (67 patients), pulmonary-vein isolation plus ablation of electrograms showing complex fractionated activity (263 patients), or pulmonary-vein isolation plus additional linear ablation across the left atrial roof and mitral valve isthmus (259 patients). The duration of follow-up was 18 months. The primary end point was freedom from any documented recurrence of atrial fibrillation lasting longer than 30 seconds after a single ablation procedure. ResultsProcedure time was significantly shorter for pulmonary-vein isolation alone than for the other two procedures (P<0.001). After 18 months, 59% of patients ass...
1,549 citations
TL;DR: This review is a comprehensive examination of the epidemiological data associating unmodifiable and modifiable risk factors for AF and of the pathophysiological evidence supporting the mechanistic link between each risk factor and AF genesis.
Abstract: The past 3 decades have been characterized by an exponential growth in knowledge and advances in the clinical treatment of atrial fibrillation (AF). It is now known that AF genesis requires a vulnerable atrial substrate and that the formation and composition of this substrate may vary depending on comorbid conditions, genetics, sex, and other factors. Population-based studies have identified numerous factors that modify the atrial substrate and increase AF susceptibility. To date, genetic studies have reported 17 independent signals for AF at 14 genomic regions. Studies have established that advanced age, male sex, and European ancestry are prominent AF risk factors. Other modifiable risk factors include sedentary lifestyle, smoking, obesity, diabetes mellitus, obstructive sleep apnea, and elevated blood pressure predispose to AF, and each factor has been shown to induce structural and electric remodeling of the atria. Both heart failure and myocardial infarction increase risk of AF and vice versa creating a feed-forward loop that increases mortality. Other cardiovascular outcomes attributed to AF, including stroke and thromboembolism, are well established, and epidemiology studies have championed therapeutics that mitigate these adverse outcomes. However, the role of anticoagulation for preventing dementia attributed to AF is less established. Our review is a comprehensive examination of the epidemiological data associating unmodifiable and modifiable risk factors for AF and of the pathophysiological evidence supporting the mechanistic link between each risk factor and AF genesis. Our review also critically examines the epidemiological data on clinical outcomes attributed to AF and summarizes current evidence linking each outcome with AF.
634 citations
Royal Melbourne Hospital1, Yale University2, European University3, Cedars-Sinai Medical Center4, University of Parma5, Icahn School of Medicine at Mount Sinai6, University of Duisburg-Essen7, Federal University of São Paulo8, Pennsylvania State University9, University of Paris10, Boston University11, Leipzig University12, Imperial College London13, University of Michigan14, Korea University Medical Center15, University of Birmingham16, University of California, San Francisco17, Vanderbilt University18, University of Tsukuba19, Royal Adelaide Hospital20, Cleveland Clinic21, McGill University22
TL;DR: The working group proposes the following working definition of atrial cardiomyopathy: ‘Any complex of structural, architectural, contractile or electrophysiological changes affecting the atria with the potential to produce clinically-relevant manifestations’ (Table 1).
530 citations