Dr. Narayan is Professor of Medicine and Cardiologist at Stanford University, and a biomedical engineer whose vision is to seamlessly integrate computational and analytic methods into clinical practice to improve patient outcomes. Dr. Narayan is Co-Founder and a Director of the Stanford Arrhythmia Center, whose mission is to develop world-leading therapy based on patient centered research for heart rhythm disorders. As Director of the Computational Arrhythmia Research Laboratory, Dr. Narayan has built an extramurally funded “bedside-to-bench-to-bedside” program focused on atrial and ventricular fibrillation, applying analytic methods, modeling and machine learning to define arrhythmia mechanisms and therapy. This work led to the discovery of rotational drivers (rotors) for human cardiac fibrillation, as confirmed by optical mapping in humans and independent clinical studies. Ablation of fibrillatory drivers (e.g. Focal Impulse and Rotor Modulation, FIRM) improves patient outcomes in reports from multiple centers, and understanding drivers of AF and VF has become a major clinical and research area.

Dr. Narayan is a passionate mentor, and has trained numerous graduate students in bioengineering, residents/fellows in training and medical students. A large number of these trainees have received extramural funding, have won research and clinical prizes and over 80% remain in academic medicine. Dr. Narayan has won teaching prizes for his clinical mentorship as well as research prizes and his mentorship program has been supported by the National Institutes of Health (K24 HL103800, 2010 to present).

Dr. Narayan was born in Aylesbury, Buckinghamshire, England, then his family moved to Birmingham where he trained in medicine (MB, ChB) then software engineering (MSc) with a concentration on neural networks. He gained membership (MRCP) then fellowship (FRCP) of the Royal College of Physicians of London. He moved to the renowned neuroimaging/computational laboratory of Arthur Toga, PhD at UCLA where his research in optical mapping/neuroscience led to his research doctorate (MD). He completed U.S. clinical training in Internal medicine at Harvard/Mount Auburn Hospital under Dr. Charles Hatem, and Cardiology/EP at Washington University in St. Louis under Drs Michael Cain and Bruce Lindsay. Dr. Narayan is board-certified in Cardiology and Clinical Cardiac Electrophysiology, and has been voted as a “Top Doctor". He is a devoted family man, and he and his wife have three children. Together, they enjoy swimming, biking, skiing, music and travel.

FINANCIAL DISCLOSURES: The Narayan laboratory is extremely grateful to its funding agencies. Fellows in Dr. Narayan's Laboratory have been funded by the Fulbright Foundation, American College of Cardiology, American Heart Association, Heart Rhythm Society and British Heart Foundation. Dr. Narayan's work has been supported by continuous grants over 2001-2020 from the NIH (HL70529, HL83359, HL103800, HL122384 and SBIR grants), the Doris Duke Charitable Foundation and American Heart Association. To further develop technology resulting from this research for wider clinical use, Dr. Narayan co-invented intellectual property from this research owned by the University of California Regents. This IP was licensed to a start-up Dr. Narayan co-founded (Topera), in which he held equity and which was acquired in 2014 by Abbott Laboratories. Dr. Narayan has received consulting income from Abbott Electrophysiology, Medtronic, St. Jude Medical, Uptodate and the American College of Cardiology

Clinical Focus

  • Clinical Cardiac Electrophysiology

Academic Appointments

Administrative Appointments

  • Co-Director, Stanford Arrhythmia Center (2016 - Present)
  • Director, Atrial Fibrillation Program, Stanford Medicine (2014 - Present)
  • Director, Electrophysiology Research, Stanford Medicine (2014 - Present)
  • Co-Director, Electrophysiology Program, University of California, San Diego (2008 - 2014)
  • Director, Clinical Cardiac Electrophysiology Fellowship Training Program, University of California, San Diego (2008 - 2012)
  • Director, Electrophysiology Program, Veterans Affairs San Diego Healthcare System (2001 - 2014)

Honors & Awards

  • Charter Member, ESTA Study Section, National Institutes of Health (2017 - present)
  • Mentor to Junaid Zaman, MD, Best Poster Award, European Society of Cardiology Meeting, Barcelona (2017)
  • Mentor to Rachita Navara, MD; 1st Prize 2017 Stanford General Internal Medicine Symposium, Stanford University (2017)
  • Mentor to Mallika Tomboli, BS (MD class of 2019); Stanford MedScholars Program, Stanford University (2016 - 2017)
  • Mentor to Rachita Navara, MD; 2016-7 Stanford Society of Physician Scholars research grant, Stanford University (2016 - 2017)
  • Mentor to Christopher Kowalewski; Clinical Prize 2016 Stanford-Karolinska Institute Symposium, Stanford University (2016)
  • Mentor to Tina Baykaner, MD, Recipient, Josephson and Wellens Fellowship, Heart Rhythm Society (2015-2016)
  • Mentor to Junaid Zaman, MD, Fulbright Scholar, Fulbright Foundation (2015 - 2016)
  • Mentor to Junaid Zaman, MD, Finalist Young Investigator Awards Competition, American Heart Association (2015)
  • Mentor to Tina Baykaner, MD, Awardee Postdoctoral Fellowship (declined for HRS fellowship), American Heart Association (2015)
  • Mentor to Junaid Zaman, MD, Recipient British Heart Foundation Grant 2014, British Heart Foundation (2014 - 2015)
  • Mentor to Amir Schricker, MD, Recipient 1st Prize HRS 2013 Young Investigator Awards, Heart Rhythm Society (2013)
  • Mentor to Amir Schricker, MD, Recipient, ACC-Merck Fellowship, American College of Cardiology Foundation (2012 - 2013)
  • Mentor to Amir Schricker, MD, HRS Max Schaldach Fellow (declined in favor of ACC-Merck), Heart Rhythm Society (2012)
  • Mentor to David Krummen, MD, Finalist, Samuel Levine Young Investigator Awards Competition, American Heart Association (2011)
  • Mentor to David E. Krummen, MD. AHA Beginning-Grant-In-Aid, American Heart Association (2010 - 2012)
  • Mentor to Antonio Moyeda, RCVT,1st Prize, Allied Professionals, Heart Rhythm Society (2010)
  • Ad Hoc Member, ESTA, CCIS, Other Study Section, National Institutes of Health (2008 - 2017)
  • Mentor to David Krummen, MD, Finalist Young Investigator Awards Competition, American College of Cardiology Foundation (2008)
  • Mentor to Han Bui, MD, Recipient of ACC-Merck Fellowship, American College of Cardiology Foundation (2005 - 2006)
  • Mentor to David Krummen, MD, Recipient, ACC-Merck Fellowship, American College of Cardiology Foundation (2003 - 2004)
  • Finalist, Astra-Zeneca Cardiovascular Young Investigator Awards Competition, Astra-Zeneca-Competition (2001)
  • Finalist, Samuel Levine Young Investigator Awards Competition, American Heart Association (1998)
  • Finalist, Young Investigator Awards Competition, North American Society for Pacing and Electrophysiology (NASPE/HRS) (1998)

Boards, Advisory Committees, Professional Organizations

  • Associate Editor, Journal of the American College of Cardiology (2006 - 2017)
  • Section Editor, Journal of the American College of Cardiology (2017 - Present)
  • Chair, Research Fellowship Committee, Heart Rhythm Society (2016 - Present)
  • Associate Editor, Journal of the American College Of Cardiology: Clinical Electrophysiology (2014 - Present)
  • Section Editor, Heart Rhythm Journal (2014 - 2014)
  • Member, Editorial Board, Journal of Interventional Cardiac Electrophysiology (2013 - Present)
  • Coordinator and Co-Coordinator, Electrophysiology Program, American College of Cardiology Scientific Sessions (2013 - 2015)
  • Member, Editorial Board, Journal of Cardiovascular Electrophysiology (2012 - Present)
  • Vice-Chair, Research Fellowship Committee, Heart Rhythm Society (2012 - 2016)
  • Scientific Program Committee, Member, American Heart Association Scientific Sessions (2010 - 2012)
  • Member, Editorial Board, Heart Rhythm Journal (2007 - Present)

Professional Education

  • Board Certification: Clinical Cardiac Electrophysiology, American Board of Internal Medicine (2001)
  • Fellowship:Washington University School of Medicine/Barnes Jewish Consortium (2001) MO
  • Board Certification: Cardiovascular Disease, American Board of Internal Medicine (2000)
  • Residency:Barnes and Allied Hospitals/Washington University School of Med (2000) MO
  • Internship:Mount Auburn / Harvard Medical School (1996) MA
  • MD (Neuroscience Doctorate), University of Birmingham, UK (1994)
  • Fellowship:UCLA - School of Medicine (1994) CA
  • Internship:University of Birmingham (1991) UK
  • MSc (Computer Science), University of Birmingham, UK (1990)
  • Medical Education:University of Birmingham (1987) United Kingdom


  • Carey R. Briggs, Sanjiv M. Narayan. "United States Patent 9,392,948 B2 System and Method for Identifying Sources for Biological Rhythms", University of California, Regents., Jul 19, 2016
  • Sanjiv Narayan, Ruchir Sehra. "United States Patent 8,868,169 B2 Method and System for Detection of Biological Rhythm Disorders", Regents of the University of California; Topera Inc; US Government represented by Dept of Veterans Affairs, Oct 21, 2014
  • Sanjiv M. Narayan, Wouter-Jan Rappel. "United States Patent 8,838,222 B2 Method for Treating Complex Rhythm Disorders", University of California Regents, Sep 16, 2014
  • Sanjiv M. Narayan, Wouter-Jan Rappel. "United States Patent 8,838,223 B2 Method for Analyzing Complex Rhythm Disorders.", University of California Regents, Sep 16, 2014
  • Sanjiv M. Narayan, Ruchir Sehra. "United States Patent 8,700,140 Methods, system and apparatus for the detection, diagnosis and treatment of biological rhythm disorders", Regents of the University of California; Topera Inc., US Department of Veterans Affairs, Apr 15, 2014
  • Sanjiv Narayan. "United States Patent 8,676,303 Machine and Process for Treating Heart Instability", University of California Regents, Mar 18, 2014
  • Carey R. Briggs, Sanjiv M. Narayan. "United States Patent 8,594,777 System And Method For Reconstructing Cardiac Activation Information", University of California Regents, Nov 26, 2013
  • Sanjiv M. Narayan, Wouter-Jan Rappel. "United States Patent 8,521,266 Methods for the Detection And/Or Diagnosis Of Biological Rhythm Disorders", University of California Regents, Aug 27, 2013
  • Carey R. Briggs, Sanjiv M. Narayan. "United States Patent 8,165,666 System And Method For Reconstructing Cardiac Activation Information", University of California Regents, Apr 24, 2012
  • Sanjiv Narayan, Valmik Bhargava. "United States Patent 7,123,954 Method and Apparatus for Classifying and Localizing Heart Arrhythmias", University of California Regents, Oct 17, 2006

Research & Scholarship

Current Research and Scholarly Interests

Dr. Narayan directs the Computational Arrhythmia Research Laboratory, whose goal is to define the mechanisms underlying complex human heart rhythm disorders, to develop bioengineering-focused solutions to improve therapy that will be tested in clinical trials. The laboratory has been funded continuously since 2001 by the National Institutes of Health, AHA and ACC, and interlinks a disease-focused group of clinicians, computational physicists, bioengineers and trialists.

Clinical Trials

  • The Dynamics of Human Atrial Fibrillation Not Recruiting

    The study is conducted in patients with atrial fibrillation undergoing clinically prescribed ablation. The study hypothesis is that ablation at specific sites that are identified to 'drive' the atrial fibrillation may improve the success of the ablation procedure.

    Stanford is currently not accepting patients for this trial. For more information, please contact Kathleen Mills, (858) 449-3252.

    View full details

  • Substrate Versus Trigger Ablation for Paroxysmal Atrial Fibrillation Not Recruiting

    This is a prospective randomized study to assess the safety and efficacy of FIRM (Focal Impulse and Rotor Modulation)-guided ablation for the treatment of symptomatic atrial fibrillation (AF). The study hypothesis is that the efficacy of AF elimination at 1 year will be higher by ablating patient-specific AF-sustaining rotors and focal sources by Focal Impulse and Rotor Modulation (FIRM) compared to conventional ablation alone (wide-area PV isolation).

    Stanford is currently not accepting patients for this trial.

    View full details

  • Ablation of Sources for Rapid Heart Rhythms Recruiting

    This study will test the hypothesis that many human heart rhythm disorders are caused by small localized sources, where brief ablation may successfully eliminate the heart rhythm disorder.

    View full details

  • The Maintenance of Human Atrial Fibrillation Recruiting

    Atrial fibrillation (AF) is the most prevalent heart rhythm disorder in the United States, affecting 2.5 million individuals in whom it may cause stroke, palpitations, heart failure, and even death. Unfortunately, therapy for AF is limited. Anti-arrhythmic or rate-controlling drugs are poorly tolerated, with frequent side effects and do not reduce stroke risk. Ablation is an emerging, minimally invasive therapy that has attracted considerable attention because it may eliminate AF. Unfortunately, AF ablation is technically challenging, with a success of only 50-70% (versus >90% for other arrhythmias) and serious risks. A major cause of these limitations is that the mechanisms for human AF are not known and thus ablation cannot be directed to them. As a result, AF ablation is empiric and results in extensive destruction of the atrium. This project will perform research to better understand AF and determine if abnormal activity in small regions or more widespread regions of the heart cause AF. By performing these studies in patients during clinical procedures, this project may lead to a paradigm shift in the understanding and treatment of AF.

    View full details


2017-18 Courses

Graduate and Fellowship Programs


All Publications

  • Multicentre safety of adding Focal Impulse and Rotor Modulation (FIRM) to conventional ablation for atrial fibrillation. Europace Krummen, D. E., Baykaner, T., Schricker, A. A., Kowalewski, C. A., Swarup, V., Miller, J. M., Tomassoni, G. F., Park, S., Viswanathan, M. N., Wang, P. J., Narayan, S. M. 2017; 19 (5): 769-774


    Focal Impulse and Rotor Modulation (FIRM) uses 64-electrode basket catheters to identify atrial fibrillation (AF)-sustaining sites for ablation, with promising results in many studies. Accordingly, new basket designs are being tested by several groups. We set out to determine the procedural safety of adding basket mapping and map-guided ablation to conventional pulmonary vein isolation (PVI).We collected 30 day procedural safety data in five US centres for consecutive patients undergoing FIRM plus PVI (FIRM-PVI) compared with contemporaneous controls undergoing PVI without FIRM. A total of 625 cases were included in this analysis: 325 FIRM-PVI and 300 PVI-controls. FIRM-PVI patients were more likely than PVI-controls to be male (83% vs. 66%, P < 0.001) and have long-standing persistent AF (26% vs. 13%, P < 0.001) reflecting patients referred for FIRM. Total ablation time was greater for FIRM-PVI (62 ± 22 min) vs. PVI-controls (52 ± 18 min, P = 0.03). The complication rate for FIRM-PVI procedures (4.3%) was similar to controls (4.0%, P = 1) for both major and minor complications; no deaths were reported. The rate of complications potentially attributable to the basket catheter was small and did not differ between basket types (Constellation 2.8% vs. FIRMap 1.8%, P = 0.7) or between cases in which basket catheters were and were not used (P = 0.5). Complication rates did not differ between centres (P = 0.6).Procedural complications from the use of the basket catheters for AF mapping are low, and thus procedural safety appears similar between FIRM-PVI and PVI-controls in a large multicentre cohort. Future studies are required to determine the optimal approach to maximize the efficacy of FIRM-guided ablation.

    View details for DOI 10.1093/europace/euw377

    View details for PubMedID 28339546

  • Spatial relationship of organized rotational and focal sources in human atrial fibrillation to autonomic ganglionated plexi. International journal of cardiology Baykaner, T., Zografos, T. A., Zaman, J. A., Pantos, I., Alhusseini, M., Navara, R., Krummen, D. E., Narayan, S. M., Katritsis, D. G. 2017


    One approach to improve ablation for atrial fibrillation (AF) is to focus on physiological targets including focal or rotational sources or ganglionic plexi (GP). However, the spatial relationship between these potential mechanisms has never been studied. We tested the hypothesis that rotors and focal sources for AF may co-localize with ganglionated plexi (GP).We prospectively identified locations of AF rotors and focal sources, and correlated these to GP sites in 97 consecutive patients (age 59.9±11.4, 73% persistent AF). AF was recorded with 64-pole catheters with activation/phase mapping, and related to anatomic GP sites on electroanatomic maps.AF sources arose in 96/97 (99%) patients for 2.6±1.4 sources per patient (left atrium: 1.7±0.9 right atrium: 1.1±0.8), each with an area of 2-3cm(2). On area analyses, the probability of an AF source randomly overlapping a GP area was 26%. Left atrial sources were seen in 94 (97%) patients, in whom ≥1 source co-localized with GP in 75 patients (80%; p<0.05). AF sources were more likely to colocalize with left vs right GPs (p<0.05), and colocalization was more likely in patients with higher CHADS2VASc scores (age>65, diabetes; p<0.05).This is the first study to demonstrate that clinically detected AF focal and rotational sources in the left atrium often colocalize with regions of autonomic innervation. Studies should define if the role of AF sources differs by their anatomical location.

    View details for DOI 10.1016/j.ijcard.2017.02.152

    View details for PubMedID 28433558

  • Determining conduction patterns on a sparse electrode grid: Implications for the analysis of clinical arrhythmias PHYSICAL REVIEW E Vidmar, D., Narayan, S. M., Krummen, D. E., Rappel, W. 2016; 94 (5)
  • Challenging the complementarity of different metrics of left atrial function: insight from a cardiomyopathy-based study. European heart journal cardiovascular Imaging Kobayashi, Y., Moneghetti, K. J., Boralkar, K., Amsallem, M., Tuzovic, M., Liang, D., Yang, P. C., Narayan, S., Kuznetsova, T., Wu, J. C., Schnittger, I., Haddad, F. 2016


    Left ventricular (LV) strain provides incremental values to LV ejection fraction (LVEF) in predicting outcome. We sought to investigate if similar relationship is observed between left atrial (LA) emptying fraction and LA strain.In this study, we selected 50 healthy subjects, 50 patients with dilated, 50 hypertrophic, and 50 infiltrative (light-chain (AL) amyloidosis) cardiomyopathy (CMP). Echocardiographic measures included LVEF and LA emptying fraction as well as LV and LA longitudinal strain (LVLS and LALS). After regression analysis, comparison of least square means of LA strain among aetiologies was performed. Intraclass correlation coefficient (ICC) and coefficient of variation (COV) were used in the assessment of variability and reproducibility of LV and LA metrics. The mean LVLS and all LA metrics were impaired in patients with all CMP compared with healthy subjects. In contrast to the moderate relationship between LVEF and LVLS (r = -0.51, P < 0.001), there was a strong linear relationship between LA emptying fraction and LA strain (r = 0.87, P < 0.001). In multiple regression analysis, total LA strain was associated with LVLS (β = -0.48, P < 0.001), lateral E/e' (β = -0.24, P < 0.001), age (β = -0.21, P < 0.001), and heart rate (β = -0.14, P = 0.02). The least square mean of LA strain adjusted for the parameters was not different among aetiologies (ANOVA P = 0.82). The ICC (>0.77) and COV (<13) were acceptable.In contrast to LV measures, there is a strong linear relationship between volumetric and longitudinal deformation indices of left atrium irrespective of CMP aetiology. Either LA emptying fraction or LA strain could be used as an important parameter in predictive models.

    View details for PubMedID 27638850

  • Mechanisms linking electrical alternans and clinical ventricular arrhythmia in human heart failure. Heart rhythm Bayer, J. D., Lalani, G. G., Vigmond, E. J., Narayan, S. M., Trayanova, N. A. 2016; 13 (9): 1922-1931


    Mechanisms of ventricular tachycardia (VT) and ventricular fibrillation (VF) in patients with heart failure (HF) are undefined.The purpose of this study was to elucidate VT/VF mechanisms in HF by using a computational-clinical approach.In 53 patients with HF and 18 control patients, we established the relationship between low-amplitude action potential voltage alternans (APV-ALT) during ventricular pacing at near-resting heart rates and VT/VF on long-term follow-up. Mechanisms underlying the transition of APV-ALT to VT/VF, which cannot be ascertained in patients, were dissected with multiscale human ventricular models based on human electrophysiological and magnetic resonance imaging data (control and HF).For patients with APV-ALT k-score >1.7, complex action potential duration (APD) oscillations (≥2.3% of mean APD), rather than APD alternans, most accurately predicted VT/VF during long-term follow-up (+82%; -90% predictive values). In the failing human ventricular models, abnormal sarcoplasmic reticulum (SR) calcium handling caused APV-ALT (>1 mV) during pacing with a cycle length of 550 ms, which transitioned into large magnitude (>100 ms) discordant repolarization time alternans (RT-ALT) at faster rates. This initiated VT/VF (cycle length <400 ms) by steepening apicobasal repolarization (189 ms/mm) until unidirectional conduction block and reentry. Complex APD oscillations resulted from nonstationary discordant RT-ALT. Restoring SR calcium to control levels was antiarrhythmic by terminating electrical alternans.APV-ALT and complex APD oscillations at near-resting heart rates in patients with HF are linked to arrhythmogenic discordant RT-ALT. This may enable novel physiologically tailored, bioengineered indices to improve VT/VF risk stratification, where SR calcium handling and spatial apicobasal repolarization are potential therapeutic targets.

    View details for DOI 10.1016/j.hrthm.2016.05.017

    View details for PubMedID 27215536

    View details for PubMedCentralID PMC4996715

  • Can Cardiac Conduction System Disease Be Prevented? JAMA internal medicine Narayan, S. M., Baykaner, T., Maron, D. J. 2016; 176 (8): 1093-1094

    View details for DOI 10.1001/jamainternmed.2016.2863

    View details for PubMedID 27367299

  • Comparison of Detailed and Simplified Models of Human Atrial Myocytes to Recapitulate Patient Specific Properties. PLoS computational biology Lombardo, D. M., Fenton, F. H., Narayan, S. M., Rappel, W. 2016; 12 (8)


    Computer studies are often used to study mechanisms of cardiac arrhythmias, including atrial fibrillation (AF). A crucial component in these studies is the electrophysiological model that describes the membrane potential of myocytes. The models vary from detailed, describing numerous ion channels, to simplified, grouping ionic channels into a minimal set of variables. The parameters of these models, however, are determined across different experiments in varied species. Furthermore, a single set of parameters may not describe variations across patients, and models have rarely been shown to recapitulate critical features of AF in a given patient. In this study we develop physiologically accurate computational human atrial models by fitting parameters of a detailed and of a simplified model to clinical data for five patients undergoing ablation therapy. Parameters were simultaneously fitted to action potential (AP) morphology, action potential duration (APD) restitution and conduction velocity (CV) restitution curves in these patients. For both models, our fitting procedure generated parameter sets that accurately reproduced clinical data, but differed markedly from published sets and between patients, emphasizing the need for patient-specific adjustment. Both models produced two-dimensional spiral wave dynamics for that were similar for each patient. These results show that simplified, computationally efficient models are an attractive choice for simulations of human atrial electrophysiology in spatially extended domains. This study motivates the development and validation of patient-specific model-based mechanistic studies to target therapy.

    View details for DOI 10.1371/journal.pcbi.1005060

    View details for PubMedID 27494252

    View details for PubMedCentralID PMC4975409

  • Organized Sources Are Spatially Conserved in Recurrent Compared to Pre-Ablation Atrial Fibrillation: Further Evidence for Non-Random Electrical Substrates JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY Lalani, G. G., Coysh, T., Baykaner, T., Zaman, J., Hopper, K., Schricker, A. A., Trikha, R., Clopton, P., Krummen, D. E., Narayan, S. M. 2016; 27 (6): 661-669


    CONSERVED ROTORS IN RECURRENT AF.Recurrent atrial fibrillation (AF) after ablation is associated with reconnection of initially isolated pulmonary vein (PV) trigger sites. Substrates are often targeted in addition to PVI, but it is unclear how substrates progress over time. We studied if substrates in recurrent AF are conserved or have developed de novo from pre-ablation AF.Of 137 patients undergoing Focal Impulse and Rotor Mapping (FIRM) at their index procedure for AF, 29 consecutive patients (60±8 years, 79% persistent) recurred and were also mapped at repeat procedure (21±20 months later) using carefully placed 64-pole baskets and RhythmView(TM) (Topera, Menlo Park, CA) to identify AF sources and disorganized zones. Compared to index AF, recurrent AF had a longer cycle length (177±21 vs. 167±19ms, p = 0.01). All patients (100%) had one or more conserved AF rotors between procedures with surrounding disorganization. The number of sources was similar for recurrent AF post-PVI versus index AF (3.2±1.4 vs. 3.1±1.0, p = 0.79), but was lower for recurrent AF after FIRM+PVI versus index AF (4.4±1.4 vs. 2.9±1.7, p = 0.03). Overall, 81% (61/75) of AF sources lay in conserved regions, while 19% (14/75) were detected de novo.Electrical propagation patterns for recurrent AF after unsuccessful ablation are similar in individual patients to their index AF. These data support temporospatial stability of AF substrates over 1-2 years. Trials should determine the relative benefit of adding substrate-mapping and ablation to PVI for recurrent AF. This article is protected by copyright. All rights reserved.

    View details for DOI 10.1111/jce.12964

    View details for Web of Science ID 000378396900001

    View details for PubMedID 26918971

  • Intracoronary Gene Transfer of Adenylyl Cyclase 6 in Patients With Heart Failure: A Randomized Clinical Trial. JAMA cardiology Hammond, H. K., Penny, W. F., Traverse, J. H., Henry, T. D., Watkins, M. W., Yancy, C. W., Sweis, R. N., Adler, E. D., Patel, A. N., Murray, D. R., Ross, R. S., Bhargava, V., Maisel, A., Barnard, D. D., Lai, N. C., Dalton, N. D., Lee, M. L., Narayan, S. M., Blanchard, D. G., Gao, M. H. 2016; 1 (2): 163-171


    Gene transfer has rarely been tested in randomized clinical trials.To evaluate the safety and efficacy of intracoronary delivery of adenovirus 5 encoding adenylyl cyclase 6 (Ad5.hAC6) in heart failure.A randomized, double-blind, placebo-controlled, phase 2 clinical trial was conducted in US medical centers (randomization occurred from July 19, 2010, to October 30, 2014). Participants 18 to 80 years with symptomatic heart failure (ischemic and nonischemic) and an ejection fraction (EF) of 40% or less were screened; 86 individuals were enrolled, and 56 were randomized. Data analysis was of the intention-to-treat population. Participants underwent exercise testing and measurement of left ventricular EF (echocardiography) and then cardiac catheterization, where left ventricular pressure development (+dP/dt) and decline (-dP/dt) were recorded. Participants were randomized (3:1 ratio) to receive 1 of 5 doses of intracoronary Ad5.hAC6 or placebo. Participants underwent a second catheterization 4 weeks later for measurement of dP/dt. Exercise testing and EF were assessed 4 and 12 weeks after randomization.Intracoronary administration of Ad5.hAC6 (3.2 × 109 to 1012 virus particles) or placebo.Primary end points included exercise duration and EF before and 4 and 12 weeks after randomization and peak rates of +dP/dt and -dP/dt before and 4 weeks after randomization. Fourteen placebo participants were compared (intention to treat) with 24 Ad5.hAC6 participants receiving the highest 2 doses (D4 + 5).Fifty-six individuals were randomized and monitored for up to 1 year. Forty-two participants (75%) received Ad5.hAC6 (mean [SE] age, 63 [1] years; EF, 30% [1%]), and 14 individuals (25%) received placebo (age, 62 [1] years; EF, 30% [2%]). Exercise duration showed no significant group differences (4 weeks, P = .27; 12 weeks, P = .47, respectively). The D4 + 5 participants had increased EF at 4 weeks (+6.0 [1.7] EF units; n = 21; P < .004), but not 12 weeks (+3.0 [2.4] EF units; n = 21; P = .16). Placebo participants showed no increase in EF at 4 weeks or 12 weeks. Exercise duration showed no between-group differences (4-week change from baseline: placebo, 27 [36] seconds; D4 + 5, 44 [25] seconds; P = .27; 12-week change from baseline: placebo, 44 [28] seconds; D4 + 5, 58 [29 seconds, P = .47). AC6 gene transfer increased basal left ventricular peak -dP/dt (4-week change from baseline: placebo, +93 [51] mm Hg/s; D4 + 5, -39 [33] mm Hg/s; placebo [n = 21]; P < .03); AC6 did not increase arrhythmias. The admission rate for patients with heart failure was 9.5% (4 of 42) in the AC6 group and 28.6% (4 of 14) in the placebo group (relative risk, 0.33 [95% CI, 0.08-1.36]; P = .10).AC6 gene transfer safely increased LV function beyond standard heart failure therapy, attainable with one-time administration. Larger trials are Identifier: NCT00787059.

    View details for DOI 10.1001/jamacardio.2016.0008

    View details for PubMedID 27437887

  • Mechanistically based mapping of human cardiac fibrillation JOURNAL OF PHYSIOLOGY-LONDON Narayan, S. M., Zaman, J. A. 2016; 594 (9): 2399-2415


    The mechanisms underpinning human cardiac fibrillation remain elusive. In his 1913 treatise on 'Dynamic Equilibrium in the Heart', Mines proposed that an activation wave front could propagate repeatedly in a circle, initiated by a stimulus in the vulnerable period. While the dynamics of activation and recovery are central to cardiac fibrillation, these physiological data are rarely used in clinical mapping. Fibrillation is a rapid irregular rhythm with spatiotemporal disorder resulting from 2 fundamental mechanisms - sources in preferred cardiac regions or spatially diffuse self-sustaining activity, i.e. with no preferred source. On close inspection, however, this debate may also reflect mapping technique. Fibrillation is initiated from triggers by regional dispersion in repolarization, slow conduction and wavebreak, then sustained by non-uniform interactions of these mechanisms. Notably, optical mapping of action potentials in atrial fibrillation (AF) show spiral wave sources (rotors) in nearly all studies including humans, while most traditional electrogram analyses of AF do not. Techniques may diverge in fibrillation because electrograms summate non-coherent waves within an undefined field whereas optical maps define waves with a visually defined field. Also fibrillation operates at the limits of activation and recovery, that are well represented by action potentials while fibrillatory electrograms poorly represent repolarization. We conclude by suggesting areas for study that may be used, until such time as optical mapping is clinically feasible, to improve mechanistic understanding and therapy of human cardiac fibrillation. This article is protected by copyright. All rights reserved.

    View details for DOI 10.1113/JP270513

    View details for Web of Science ID 000375601400006

    View details for PubMedID 26607671

  • The precise timing of tachycardia entrainment is determined by the postpacing interval, the tachycardia cycle length, and the pacing rate: Theoretical insights and practical applications. Heart rhythm Kaiser, D. W., Hsia, H. H., Dubin, A. M., Liem, L. B., Viswanathan, M. N., Zei, P. C., Wang, P. J., Narayan, S. M., Turakhia, M. P. 2016; 13 (3): 695-703


    Previous observations have reported that the number of pacing stimuli required to entrain a tachycardia varies on the basis of arrhythmia type and location, but a quantitative formulation of the number needed to entrain (NNE) that unifies these observations has not been characterized.We sought to investigate the relationship between the number of pacing stimulations, the tachycardia cycle length (TCL), the overdrive pacing cycle length (PCL), and the postpacing interval (PPI) to accurately estimate the timing of tachycardia entrainment.First, we detailed a mathematical derivation unifying electrophysiological parameters with empirical confirmation in 2 patients undergoing catheter ablation of typical atrial flutter. Second, we validated our formula in 44 patients who underwent various catheter ablation procedures. For accuracy, we corrected for rate-related changes in conduction velocity.We derived the equations NNE = |(PPI - TCL)/(TCL - PCL)| + 1 and Tachycardia advancement = (NNE - 1) × (TCL - PCL) - (PPI - TCL), which state that the NNE and the amount of tachycardia advancement on the first resetting stimulation are determined using regularly measured intracardiac parameters. In the retrospective cohort, the observed PPI - TCL highly correlated with the predicted PPI - TCL (mean difference 5.8 ms; r = 0.97; P < .001), calculated as PPI - TCL = (NNE - 1) × (TCL - PCL) - tachycardia advancement.The number of pacing stimulations required to entrain a reentrant tachycardia is predictable at any PCL after correcting for cycle length-dependent changes in conduction velocity. This relationship unifies established empirically derived diagnostic and mapping criteria for supraventricular tachycardia and ventricular tachycardia. This relationship may help elucidate when antitachycardia pacing episodes are ineffective or proarrhythmic and could potentially serve as a theoretical basis to customize antitachycardia pacing settings for improved safety and effectiveness.

    View details for DOI 10.1016/j.hrthm.2015.11.032

    View details for PubMedID 26611239

    View details for PubMedCentralID PMC4770895

  • The precise timing of tachycardia entrainment is determined by the postpacing interval, the tachycardia cycle length, and the pacing rate: Theoretical insights and practical applications HEART RHYTHM Kaiser, D. W., Hsia, H. H., Dubin, A. M., Liem, L. B., Viswanathan, M. N., Zei, P. C., Wang, P. J., Narayan, S. M., Turakhia, M. P. 2016; 13 (3): 695-703
  • New Mechanism-based Approaches to Ablating Persistent AF: Will Drug Therapy Soon Be Obsolete? JOURNAL OF CARDIOVASCULAR PHARMACOLOGY Zaman, J. A., Baykaner, T., Narayan, S. M. 2016; 67 (1): 1-8
  • New Mechanism-based Approaches to Ablating Persistent AF: Will Drug Therapy Soon Be Obsolete? Journal of cardiovascular pharmacology Zaman, J. A., Baykaner, T., Narayan, S. M. 2016; 67 (1): 1-8


    Persistent atrial fibrillation (AF) represents a major public health and medical challenge. The progressive nature of the disease, high morbidity and increasing health-economic costs ensure it remains at the forefront of novel research into mechanisms and potential therapies. These are largely divided into pharmacological (drugs) and electrical (ablation), with patients often going from former to latter. AF ablation has improved sufficiently to be offered as first line for paroxysmal AF, but there is uncertainty on whether drug therapy will improve from its current role or be relegated to niche status. In this review we shall outline the progress in mechanistic understanding of AF that may allow results from ablation to diverge dramatically from drug therapy, to identify populations in whom drug therapy may become less relevant. We end by looking ahead to future developments which we hope will spur on therapeutic efficacy in both fields.

    View details for DOI 10.1097/FJC.0000000000000270

    View details for PubMedID 25923323

  • Phase synchrony reveals organization in human atrial fibrillation AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY Vidmar, D., Narayan, S. M., Rappel, W. 2015; 309 (12): H2118-H2126
  • Mechanisms for the Termination of Atrial Fibrillation by Localized Ablation Computational and Clinical Studies CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY Rappel, W., Zaman, J. A., Narayan, S. M. 2015; 8 (6): 1325-1333

    View details for DOI 10.1161/CIRCEP.115.002956

    View details for Web of Science ID 000366604600007

    View details for PubMedID 26359479

  • Mechanisms for the Termination of Atrial Fibrillation by Localized Ablation: Computational and Clinical Studies. Circulation. Arrhythmia and electrophysiology Rappel, W., Zaman, J. A., Narayan, S. M. 2015; 8 (6): 1325-1333


    -Human atrial fibrillation (AF) can terminate after ablating localized regions, that supports the existence of localized rotors (spiral waves) or focal drivers. However, it is unclear why ablation near a spiral wave tip would terminate AF and not anchor reentry. We addressed this question by analyzing competing mechanisms for AF termination in numerical simulations, referenced to clinical observations.-Spiral wave reentry was simulated in monodomain 2D myocyte sheets using clinically realistic rate-dependent values for repolarization and conduction. Heterogeneous models were created by introduction of parameterized variations in tissue excitability. Ablation lesions were applied as non-conducting circular regions. Computational models confirmed localized ablation may anchor spiral wave reentry, producing organized tachycardias. Several mechanisms also explained termination of AF to sinus rhythm. First, lesions may create an excitable gap vulnerable to invasion by fibrillatory waves. Second, ablation of rotors in regions of low-excitability (from remodeling) produced reentry in more excitable tissue allowing collision of wave-front and back. Conversely, ablation of rotors in high-excitability regions migrated spiral waves to less excitable tissue, where they detached to collide with non-conducting boundaries. Third, ablation may connect rotors to non-conducting anatomic orifices. Fourth, reentry through slow conducting channels may terminate if ablation closes these channels.-Limited ablation can terminate AF by several mechanisms. These data shed light on how clinical AF may be sustained in patients' atria, emphasizing heterogeneities in tissue excitability, slow-conducting channels and obstacles that are increasingly detectable in patients and should be the focus of future translational studies.

    View details for DOI 10.1161/CIRCEP.115.002956

    View details for PubMedID 26359479

  • Modifying Ventricular Fibrillation by Targeted Rotor Substrate Ablation: Proof-of-Concept from Experimental Studies to Clinical VF JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY Krummen, D. E., Hayase, J., Vampola, S. P., Ho, G., Schricker, A. A., Lalani, G. G., Baykaner, T., Coe, T. M., Clopton, P., Rappel, W., Omens, J. H., Narayan, S. M. 2015; 26 (10): 1117-1126

    View details for DOI 10.1111/jce.12753

    View details for Web of Science ID 000363211600018

    View details for PubMedID 26179310

  • Ablation of atrial fibrillation TRENDS IN CARDIOVASCULAR MEDICINE Wright, M., Narayan, S. M. 2015; 25 (5): 409-419
  • Ablating Atrial Fibrillation: Customizing Lesion Sets Guided by Rotor Mapping. Methodist DeBakey cardiovascular journal Zaman, J. A., Narayan, S. M. 2015; 11 (2): 76-81


    Ablation occupies an increasing role in the contemporary management of atrial fibrillation (AF), but results are suboptimal, particularly for persistent AF. While an anatomic approach to ablation is a highly efficacious and safe method to isolate pulmonary vein (PV) triggers, recurrence of AF is not always associated with PV reconnection, and there is compelling evidence that non-PV sites sustain AF after it is triggered. Recent developments in wide-area mapping and signal processing now identify rotors in the vast majority of AF patients that sustain AF and whose elimination improves long-term freedom from AF in multicenter studies. Investigators have now demonstrated rotor and focal sources for AF that show many analogous properties between approaches: they lie in spatially reproducible regions temporally over hours to days, and they are amenable to targeted ablation. This review outlines the rationale and technical developments supporting this mechanistic paradigm for human AF, and discusses how rotor mapping may be implemented for individual patient customization of lesion sets. Mechanistic studies are required to explain why rotor elimination (or other ablation approaches) producing long-term elimination of AF may not always terminate AF acutely, how AF correlates with structural changes on magnetic resonance imaging, and how these findings can be integrated clinically with current ablation strategies to improve patient outcomes.

    View details for DOI 10.14797/mdcj-11-2-76

    View details for PubMedID 26306123

  • The role of rotors in atrial fibrillation. Journal of thoracic disease Krummen, D. E., Swarup, V., Narayan, S. M. 2015; 7 (2): 142-151


    Despite significant advances in our understanding of atrial fibrillation (AF) mechanisms in the last 15 years, ablation outcomes remain suboptimal. A potential reason is that many ablation techniques focus on anatomic, rather than patient-specific functional targets for ablation. Panoramic contact mapping, incorporating phase analysis, repolarization and conduction dynamics, and oscillations in AF rate, overcomes many prior difficulties with mapping AF. This approach provides evidence that the mechanisms sustaining human AF are deterministic, largely due to stable electrical rotors and focal sources in either atrium. Ablation of such sources (Focal Impulse and Rotor Modulation: FIRM ablation) has been shown to improve ablation outcome compared with conventional ablation alone; independent laboratories directly targeting stable rotors have shown similar results. Clinical trials examining the role of stand-alone FIRM ablation are in progress. Looking forward, translating insights from patient-specific mapping to evidence-based guidelines and clinical practice is the next challenge in improving patient outcomes in AF management.

    View details for DOI 10.3978/j.issn.2072-1439.2014.11.15

    View details for PubMedID 25713729

  • Rotor mapping and ablation to treat atrial fibrillation CURRENT OPINION IN CARDIOLOGY Zaman, J. A., Peters, N. S., Narayan, S. M. 2015; 30 (1): 24-32


    Rotors have long been postulated to drive atrial fibrillation, but evidence has been limited to animal models. This changed recently with the demonstration using focal impulse and rotor modulation (FIRM) mapping that rotors act as human atrial fibrillation sources. This mechanistic approach to diagnosing the causes of atrial fibrillation in individual patients has been supported by substantially improved outcomes from FIRM-guided ablation, resulting in increased attention to rotors as therapeutic targets.In this review, we outline the pathophysiology of rotors in animal and in-silico studies of fibrillation, and how this motivated FIRM mapping in humans. We highlight the characteristics of rotors in human atrial fibrillation, now validated by several techniques, with discussion on similar and discrepant findings between techniques. The interventional approaches to eliminate atrial fibrillation rotors are explained and the ablation results in latest studies using FIRM are discussed.We propose that mapping localized sources for human atrial fibrillation, specifically rotors, is moving the field towards a unifying hypothesis that explains several otherwise contradictory observations in atrial fibrillation management. We conclude by suggesting areas of potential research that may reveal more about these critical sites and how these may lead to better and novel treatments for atrial fibrillation.

    View details for DOI 10.1097/HCO.0000000000000123

    View details for Web of Science ID 000346157200004

    View details for PubMedID 25389649

  • Progress toward the prevention and treatment of atrial fibrillation: A summary of the Heart Rhythm Society Research Forum on the Treatment and Prevention of Atrial Fibrillation, Washington, DC, December 9-10, 2013. Heart rhythm Van Wagoner, D. R., Piccini, J. P., Albert, C. M., Anderson, M. E., Benjamin, E. J., Brundel, B., Califf, R. M., Calkins, H., Chen, P., Chiamvimonvat, N., Darbar, D., Eckhardt, L. L., Ellinor, P. T., Exner, D. V., Fogel, R. I., Gillis, A. M., Healey, J., Hohnloser, S. H., Kamel, H., Lathrop, D. A., Lip, G. Y., Mehra, R., Narayan, S. M., Olgin, J., Packer, D., Peters, N. S., Roden, D. M., Ross, H. M., Sheldon, R., Wehrens, X. H. 2015; 12 (1): e5-e29

    View details for DOI 10.1016/j.hrthm.2014.11.011

    View details for PubMedID 25460864

  • Stability of Rotors and Focal Sources for Human Atrial Fibrillation: Focal Impulse and Rotor Mapping (FIRM) of AF Sources and Fibrillatory Conduction JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY Swarup, V., Baykaner, T., Rostamian, A., Daubert, J. P., Hummel, J., Krummen, D. E., Trikha, R., Miller, J. M., Tomassoni, G. F., Narayan, S. M. 2014; 25 (12): 1284-1292


    Several groups report electrical rotors or focal sources that sustain atrial fibrillation (AF) after it has been triggered. However, it is difficult to separate stable from unstable activity in prior studies that examined only seconds of AF. We applied phase-based focal impulse and rotor mapping (FIRM) to study the dynamics of rotors/sources in human AF over prolonged periods of time.We prospectively mapped AF in 260 patients (169 persistent, 61 ± 12 years) at 6 centers in the FIRM registry, using baskets with 64 contact electrodes per atrium. AF was phase mapped (RhythmView, Topera, Menlo Park, CA, USA). AF propagation movies were interpreted by each operator to assess the source stability/dynamics over tens of minutes before ablation.Sources were identified in 258 of 260 of patients (99%), for 2.8 ± 1.4 sources/patient (1.8 ± 1.1 in left, 1.1 ± 0.8 in right atria). While AF sources precessed in stable regions, emanating activity including spiral waves varied from collision/fusion (fibrillatory conduction). Each source lay in stable atrial regions for 4,196 ± 6,360 cycles, with no differences between paroxysmal versus persistent AF (4,290 ± 5,847 vs. 4,150 ± 6,604; P = 0.78), or right versus left atrial sources (P = 0.26).Rotors and focal sources for human AF mapped by FIRM over prolonged time periods precess ("wobble") but remain within stable regions for thousands of cycles. Conversely, emanating activity such as spiral waves disorganize and collide with the fibrillatory milieu, explaining difficulties in using activation mapping or signal processing analyses at fixed electrodes to detect AF rotors. These results provide a rationale for targeted ablation at AF sources rather than fibrillatory spiral waves.

    View details for DOI 10.1111/jce.12559

    View details for Web of Science ID 000346020800004

    View details for PubMedID 25263408

  • Rotors and Focal Sources for Human Atrial Fibrillation - Mechanistic Paradigm With Direct Clinical Relevance CIRCULATION JOURNAL Lalani, G. G., Trikha, R., Krummen, D. E., Narayan, S. M. 2014; 78 (10): 2357-2366
  • Human Atrial Fibrillation Initiates via Organized Rather Than Disorganized Mechanisms CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY Schricker, A. A., Lalani, G. G., Krummen, D. E., Rappel, W., Narayan, S. M. 2014; 7 (5): 816-U94
  • Mapping and ablating stable sources for atrial fibrillation: summary of the literature on Focal Impulse and Rotor Modulation (FIRM) JOURNAL OF INTERVENTIONAL CARDIAC ELECTROPHYSIOLOGY Baykaner, T., Lalani, G. G., Schricker, A., Krummen, D. E., Narayan, S. M. 2014; 40 (3): 237-244


    Atrial fibrillation (AF) is the most common sustained arrhythmia and the most common indication for catheter ablation. However, despite substantial technical advances in mapping and energy delivery, ablation outcomes remain suboptimal. A major limitation to AF ablation is that the areas targeted for ablation are rarely of proven mechanistic importance, in sharp contrast to other arrhythmias in which ablation targets demonstrated mechanisms in each patient. Focal impulse and rotor modulation (FIRM) is a new approach to demonstrate the mechanisms that sustain AF ("substrates") in each patient that can be used to guide ablation then confirm elimination of each mechanism. FIRM mapping reveals that AF is sustained by 2-3 rotors and focal sources, with a greater number in patients with persistent than paroxysmal AF, lying within spatially reproducible 2.2 ± 1.4-cm(2) areas in diverse locations. This temporospatial reproducibility, now confirmed by several groups using various methods, changes the concepts regarding AF-sustaining mechanisms, enabling localized rather than widespread ablation. Mechanistically, the role of rotors and focal sources in sustaining AF has been demonstrated by the acute and chronic success of source (FIRM) ablation alone. Clinically, adding FIRM to conventional ablation substantially improves arrhythmia freedom compared with conventional ablation alone, and ongoing randomized trials are comparing FIRM-ablation with and without conventional ablation to conventional ablation alone. In conclusion, ablation of patient-specific AF-sustaining mechanisms (substrates), as exemplified by FIRM, may be central to substantially improving AF ablation outcomes.

    View details for DOI 10.1007/s10840-014-9889-8

    View details for Web of Science ID 000341693100006

    View details for PubMedID 24647673

  • Initial Independent Outcomes from Focal Impulse and Rotor Modulation Ablation for Atrial Fibrillation: Multicenter FIRM Registry JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY Miller, J. M., Kowal, R. C., Swarup, V., Daubert, J. P., Daoud, E. G., Day, J. D., Ellenbogen, K. A., Hummel, J. D., Baykaner, T., Krummen, D. E., Narayan, S. M., Reddy, V. Y., Shivkumar, K., Steinberg, J. S., Wheelan, K. R. 2014; 25 (9): 921-929


    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.We prospectively enrolled n = 78 consecutive patients (61 ± 10 years) undergoing FIRM guided ablation for persistent (n = 48), longstanding persistent (n = 7), or paroxysmal (n = 23) AF. AF recordings from both atria with a 64-pole basket catheter were analyzed using a novel mapping system (Rhythm View(TM) ; Topera Inc., CA, USA). Identified rotors/focal sources were ablated, followed by PVI.Each institution recruited a median of 6 patients, each of whom showed 2.3 ± 0.9 AF rotors/focal sources in diverse locations. 25.3% of all sources were right atrial (RA), and 50.0% of patients had ≥1 RA source. Ablation of all sources required a total of 16.6 ± 11.7 minutes, followed by PVI. On >1 year follow-up with a 3-month blanking period, 1 patient lost to follow-up (median time to 1st recurrence: 245 days, IQR 145-354), single-procedure freedom from AF was 87.5% (patients without prior ablation; 35/40) and 80.5% (all patients; 62/77) and similar for persistent and paroxysmal AF (P = 0.89).Elimination of patient-specific AF rotors/focal sources produced freedom-from-AF of ≈80% at 1 year at centers new to FIRM. FIRM-guided ablation has a rapid learning curve, yielding similar results to original FIRM reports in each center's first cases.

    View details for DOI 10.1111/jce.12474

    View details for Web of Science ID 000341821200003

    View details for PubMedID 24948520

  • CrossTalk proposal: Rotors have been demonstrated to drive human atrial fibrillation JOURNAL OF PHYSIOLOGY-LONDON Narayan, S. M., Jalife, J. 2014; 592 (15): 3163-3166

    View details for DOI 10.1113/jphysiol.2014.271031

    View details for Web of Science ID 000340404100001

    View details for PubMedID 25085968

  • Defining Arrhythmic Risk and Defibrillator Therapy in ARVC Shocking Rhythm? JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY McGarry, T. J., Narayan, S. M. 2014; 64 (2): 126-128

    View details for DOI 10.1016/j.jacc.2014.05.010

    View details for Web of Science ID 000340238400002

    View details for PubMedID 25011715

  • Rotor Stability Separates Sustained Ventricular Fibrillation From Self-Terminating Episodes in Humans JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY Krummen, D. E., Hayase, J., Morris, D. J., Ho, J., Smetak, M. R., Clopton, P., Rappel, W., Narayan, S. M. 2014; 63 (24): 2712-2721


    This study mapped human ventricular fibrillation (VF) to define mechanistic differences between episodes requiring defibrillation versus those that spontaneously terminate.VF is a leading cause of mortality; yet, episodes may also self-terminate. We hypothesized that the initial maintenance of human VF is dependent upon the formation and stability of VF rotors.We enrolled 26 consecutive patients (age 64 ± 10 years, n = 13 with left ventricular dysfunction) during ablation procedures for ventricular arrhythmias, using 64-electrode basket catheters in both ventricles to map VF prior to prompt defibrillation per the institutional review board-approved protocol. A total of 52 inductions were attempted, and 36 VF episodes were observed. Phase analysis was applied to identify biventricular rotors in the first 10 s or until VF terminated, whichever came first (11.4 ± 2.9 s to defibrillator charging).Rotors were present in 16 of 19 patients with VF and in all patients with sustained VF. Sustained, but not self-limiting VF, was characterized by greater rotor stability: 1) rotors were present in 68 ± 17% of cycles in sustained VF versus 11 ± 18% of cycles in self-limiting VF (p < 0.001); and 2) maximum continuous rotations were greater in sustained (17 ± 11, range 7 to 48) versus self-limiting VF (1.1 ± 1.4, range 0 to 4, p < 0.001). Additionally, biventricular rotor locations in sustained VF were conserved across multiple inductions (7 of 7 patients, p = 0.025).In patients with and without structural heart disease, the formation of stable rotors identifies individuals whose VF requires defibrillation from those in whom VF spontaneously self-terminates. Future work should define the mechanisms that stabilize rotors and evaluate whether rotor modulation may reduce subsequent VF risk.

    View details for DOI 10.1016/j.jacc.2014.03.037

    View details for Web of Science ID 000337358800010

    View details for PubMedID 24794115

  • Ablation of Rotor and Focal Sources Reduces Late Recurrence of Atrial Fibrillation Compared With Trigger Ablation Alone Extended Follow-Up of the CONFIRM Trial (Conventional Ablation for Atrial Fibrillation With or Without Focal Impulse and Rotor Modulation) JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY Narayan, S. M., Baykaner, T., Clopton, P., Schricker, A., Lalani, G. G., Krummen, D. E., Shivkumar, K., Miller, J. M. 2014; 63 (17): 1761-1768


    The aim of this study was to determine if ablation that targets patient-specific atrial fibrillation (AF)-sustaining substrates (rotors or focal sources) is more durable than trigger ablation alone at preventing late AF recurrence.Late recurrence substantially limits the efficacy of pulmonary vein isolation for AF and is associated with pulmonary vein reconnection and the emergence of new triggers.Three-year follow-up was performed of the CONFIRM (Conventional Ablation for Atrial Fibrillation With or Without Focal Impulse and Rotor Modulation) trial, in which 92 consecutive patients with AF (70.7% persistent) underwent novel computational mapping. Ablation comprised source (focal impulse and rotor modulation [FIRM]) and then conventional ablation in 27 patients (FIRM guided) and conventional ablation alone in 65 patients (FIRM blinded). Patients were followed with implanted electrocardiographic monitors when possible (85.2% of FIRM-guided patients, 23.1% of FIRM-blinded patients).FIRM mapping revealed a median of 2 (interquartile range: 1 to 2) rotors or focal sources in 97.7% of patients during AF. During a median follow-up period of 890 days (interquartile range: 224 to 1,563 days), compared to FIRM-blinded therapy, patients receiving FIRM-guided ablation maintained higher freedom from AF after 1.2 ± 0.4 procedures (median 1; interquartile range: 1 to 1) (77.8% vs. 38.5%, p = 0.001) and a single procedure (p < 0.001) and higher freedom from all atrial arrhythmias (p = 0.003). Freedom from AF was higher when ablation directly or coincidentally passed through sources than when it missed sources (p < 0.001).FIRM-guided ablation is more durable than conventional trigger-based ablation in preventing 3-year AF recurrence. Future studies should investigate how ablation of patient-specific AF-sustaining rotors and focal sources alters the natural history of arrhythmia recurrence. (The Dynamics of Human Atrial Fibrillation; NCT01008722).

    View details for DOI 10.1016/j.jacc.2014.02.543

    View details for Web of Science ID 000335312200011

    View details for PubMedID 24632280

  • Lone Atrial Fibrillation Does it Exist? JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY Wyse, D. G., van Gelder, I. C., Ellinor, P. T., Go, A. S., Kalman, J. M., Narayan, S. M., Nattel, S., Schotten, U., Rienstra, M. 2014; 63 (17): 1715-1723


    The historical origin of the term "lone atrial fibrillation" (AF) predates by 60 years our current understanding of the pathophysiology of AF, the multitude of known etiologies for AF, and our ability to image and diagnose heart disease. The term was meant to indicate AF in patients for whom subsequent investigations could not demonstrate heart disease, but for many practitioners has become synonymous with "idiopathic AF." As the list of heart diseases has expanded and diagnostic techniques have improved, the prevalence of lone AF has fallen. The legacy of the intervening years is that definitions of lone AF in the literature are inconsistent so that studies of lone AF are not comparable. Guidelines provide a vague definition of lone AF but do not provide direction about how much or what kind of imaging and other testing are necessary to exclude heart disease. There has been an explosion in the understanding of the pathophysiology of AF in the last 20 years in particular. Nevertheless, there are no apparently unique mechanisms for AF in patients categorized as having lone AF. In addition, the term "lone AF" is not invariably useful in making treatment decisions, and other tools for doing so have been more thoroughly and carefully validated. It is, therefore, recommended that use of the term "lone AF" be avoided.

    View details for DOI 10.1016/j.jacc.2014.01.023

    View details for Web of Science ID 000335312200004

    View details for PubMedID 24530673

  • Intermittent Atrial Tachycardia Promotes Repolarization Alternans and Conduction Slowing During Rapid Rates, and Increases Susceptibility to Atrial Fibrillation in a Free-Behaving Sheep Model JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY Monigatti-Tenkorang, J., Jousset, F., Pascale, P., Vesin, J., Ruchat, P., Fromer, M., Narayan, S. M., Pruvot, E. 2014; 25 (4): 418-427


    Paroxysmal atrial fibrillation (AF) may be triggered by intermittent atrial tachycardia, and ultimately lead to persistent AF. However, the mechanisms by which intermittent atrial tachycardia promotes sustained AF are not well understood.Eight sheep were chronically implanted with 2 pacemakers for the recording of broadband right atrial unipolar electrograms, and for the delivery of electrophysiological stimulation protocols and intermittent right atrial tachycardia. Right atrial kinetics of activation recovery interval (ARI) as a surrogate for action potential duration, of conduction time and velocity, and of repolarization alternans were analyzed at incremental pacing rates during the remodeling process induced by weeks of intermittent atrial tachycardia until the development of sustained AF. Intermittent atrial tachycardia decreased ARI and blunted its rate adaptation, facilitated atrial capture, and slowed conduction at high rates, and increased susceptibility to pacing-induced AF. In spite of blunted ARI rate adaptation, right atrial repolarization alternans was maintained during remodeling, and further increased in magnitude just before rapid pacing-induced AF.This study suggests that weeks of intermittent right atrial tachycardia result in a gradual electrical remodeling favorable for wavebreaks and reentry that may facilitate fibrillation.

    View details for DOI 10.1111/jce.12353

    View details for Web of Science ID 000334165500013

    View details for PubMedID 24383960

  • Highlights of the Year in JACC 2013 JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY DeMaria, A. N., Adler, E. D., Bax, J. J., Ben-Yehuda, O., Feld, G. K., Greenberg, B. H., Hall, J. L., Hlatky, M. A., Lew, W. Y., Lima, J. A., Mahmud, E., Maisel, A. S., Narayan, S. M., Nissen, S. E., Sahn, D. J., Tsimikas, S. 2014; 63 (6): 570-602
  • Structural contributions to fibrillatory rotors in a patient-derived computational model of the atria. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology Gonzales, M. J., Vincent, K. P., Rappel, W. J., Narayan, S. M., McCulloch, A. D. 2014; 16 Suppl 4: iv3–iv10


    The aim of this study was to investigate structural contributions to the maintenance of rotors in human atrial fibrillation (AF) and possible mechanisms of termination.A three-dimensional human biatrial finite element model based on patient-derived computed tomography and arrhythmia observed at electrophysiology study was used to study AF. With normal physiological electrical conductivity and effective refractory periods (ERPs), wave break failed to sustain reentrant activity or electrical rotors. With depressed excitability, decreased conduction anisotropy, and shorter ERP characteristic of AF, reentrant rotors were readily maintained. Rotors were transiently or permanently trapped by fibre discontinuities on the lateral wall of the right atrium near the tricuspid valve orifice and adjacent to the crista terminalis, both known sites of right atrial arrhythmias. Modelling inexcitable regions near the rotor tip to simulate fibrosis anchored the rotors, converting the arrhythmia to macro-reentry. Accordingly, increasing the spatial core of inexcitable tissue decreased the frequency of rotation, widened the excitable gap, and enabled an external wave to impinge on the rotor core and displace the source.These model findings highlight the importance of structural features in rotor dynamics and suggest that regions of fibrosis may anchor fibrillatory rotors. Increasing extent of fibrosis and scar may eventually convert fibrillation to excitable gap reentry. Such macro-reentry can then be eliminated by extending the obstacle or by external stimuli that penetrate the excitable gap.

    View details for DOI 10.1093/europace/euu251

    View details for PubMedID 25362167

  • Human Atrial Fibrillation Initiates via Organized Rather Than Disorganized Mechanisms. Circulation. Arrhythmia and electrophysiology Schricker, A. A., Lalani, G. G., Krummen, D. E., Rappel, W. J., Narayan, S. M. 2014; 7 (5): 816–24


    It is unknown how atrial fibrillation (AF) is actually initiated by triggers. Based on consistencies in atrial structure and function in individual patients between episodes of AF, we hypothesized that human AF initiates when triggers interact with deterministic properties of the atria and may engage organized mechanisms.In 31 patients with AF, we mapped AF initiation after spontaneous triggers or programmed stimulation. We used 64-pole basket catheters to measure regional dynamic conduction slowing and to create biatrial activation maps during transitions to AF. Sixty-two AF initiations were recorded (spontaneous, n=28; induced, n=34). Notably, AF did not initiate by disorganized mechanisms, but by either a dominant reentrant spiral wave (76%) or a repetitive focal driver. Both mechanisms were located 21±17 mm from their triggers. AF-initiating spirals formed at the site showing the greatest rate-dependent slowing in each patient. Accordingly, in 10 of 12 patients with multiple observed AF episodes, AF initiated using spatially conserved mechanisms despite diverse triggers.Human AF initiates from triggers by organized rather than disorganized mechanisms, either via spiral wave re-entry at sites of dynamic conduction slowing or via repetitive focal drivers. The finding that diverse triggers initiate AF at predictable, spatially conserved functional sites in each individual provides a novel deterministic paradigm for AF with therapeutic implications.

    View details for DOI 10.1161/CIRCEP.113.001289

    View details for PubMedID 25217042

  • Rotors and focal sources for human atrial fibrillation: mechanistic paradigm with direct clinical relevance. Circulation journal : official journal of the Japanese Circulation Society Lalani, G. G., Trikha, R., Krummen, D. E., Narayan, S. M. 2014; 78 (10): 2357–66


    Outcomes for patients with atrial fibrillation (AF) have changed little despite many advances in technology. In large part, this reflects fundamental uncertainty about the mechanisms for AF in humans, which must reconcile diverse observations. Despite the complexity of AF, many electrophysiologists have witnessed modulation of 'chaotic' AF after the first few ablation lesions, or before lines are complete or trigger sites are isolated, and numerous analyses demonstrate temporospatial stability in AF. These common observations challenge the concept that AF is driven by spatially disorganized, widespread mechanisms. Using mathematical techniques applied to other complex systems, evidence is rapidly accumulating that human AF is largely sustained by localized rotors and focal sources. Elimination of sources by Focal Impulse and Rotor Modulation (FIRM)-guided ablation has been shown by independent laboratories to substantially improve success compared with pulmonary vein isolation alone. These data advance our mechanistic understanding of AF. Randomized trials are underway to verify the relative efficacy of ablation at AF sources (substrate) vs. conventional trigger ablation. The renewed focus on AF substrates is a paradigm shift, but also a re-alignment of concepts for AF towards those for other cardiac arrhythmias that are generally defined by sustaining mechanisms (substrates).

    View details for PubMedID 25213002

  • Rhythm control in heart failure patients with atrial fibrillation: contemporary challenges including the role of ablation. Journal of the American College of Cardiology Trulock, K. M., Narayan, S. M., Piccini, J. P. 2014; 64 (7): 710–21


    Because nonpharmacological interventions likely alter the risks and benefits associated with rhythm control, this paper reviews the role of current rhythm control strategies in atrial fibrillation. This report also focuses on the specific limitations of pharmacological interventions and the utility of percutaneous ablation in this growing population of patients with concomitant atrial fibrillation and heart failure.

    View details for DOI 10.1016/j.jacc.2014.06.1169

    View details for PubMedID 25125304

  • A case of a human ventricular fibrillation rotor localized to ablation sites for scar-mediated monomorphic ventricular tachycardia HEART RHYTHM Hayase, J., Tung, R., Narayan, S. M., Krummen, D. E. 2013; 10 (12): 1913-1916

    View details for DOI 10.1016/j.hrthm.2013.07.049

    View details for Web of Science ID 000327767600035

    View details for PubMedID 23911894

  • Frequency Analysis of Atrial Action Potential Alternans A Sensitive Clinical Index of Individual Propensity to Atrial Fibrillation CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY Lalani, G. G., Schricker, A. A., Clopton, P., Krummen, D. E., Narayan, S. M. 2013; 6 (5): 859-867


    Few clinical indices identify the propensity of patients to atrial fibrillation (AF) when not in AF. Repolarization alternans has been shown to indicate AF vulnerability, but is limited in its sensitivity to detect changes in action potential (AP) duration (APD), which may be subtle. We hypothesized that spectral analysis would be a more sensitive and robust marker of AP alternans and thus a better clinical index of individual propensity to AF than APD alternans.In 31 patients (12 persistent AF, 15 paroxysmal AF, 4 controls with no AF), we recorded left (n=27) and right (n=6) atrial monophasic APs during incremental pacing from cycle length 500 ms (120 beats per minute) to AF onset. Alternans was measured by APD and spectral analysis. At baseline pacing (median cycle length [1st, 3rd quartiles], 500 ms [500, 500]), APD alternans was detected in only 7 of 27 AF patients (no controls), whereas spectral AP alternans was detected in 18 of 27 AF patients (no controls; P=0.003); AP alternans was more prevalent in persistent than paroxysmal AF, and absent in controls (P=0.018 APD; P=0.042 spectral). Spectral AP alternans magnitude at baseline was highest in persistent AF, with modest rate-dependent amplification, followed by paroxysmal AF, with marked rate dependence, and undetectable in controls until just before induced AF.Spectral AP alternans near baseline rates can identify patients with, versus those without, clinical histories and pathophysiological substrates for AF. Future studies should examine whether the presence of spectral AP alternans during sinus rhythm may obviate the need to actually demonstrate AF, such as on ambulatory ECG monitoring.

    View details for DOI 10.1161/CIRCEP.113.000204

    View details for Web of Science ID 000329923700014

    View details for PubMedID 23995250

  • Targeted Ablation at Stable Atrial Fibrillation Sources Improves Success Over Conventional Ablation in High-Risk Patients: A Substudy of the CONFIRM Trial CANADIAN JOURNAL OF CARDIOLOGY Baykaner, T., Clopton, P., Lalani, G. G., Schricker, A. A., Krummen, D. E., Narayan, S. M. 2013; 29 (10): 1218-1226


    Pulmonary vein (PV) isolation has disappointing results in patients with obesity, heart failure, obstructive sleep apnea (OSA) and enlarged left atria (LA), for unclear reasons. We hypothesized that these comorbidities may cause higher numbers or non-PV locations of atrial fibrillation (AF) sources, where targeted source ablation (focal impulse and rotor modulation [FIRM]) should improve the single-procedure success of ablation.The Conventional Ablation of AF With or Without Focal Impulse and Rotor Modulation (CONFIRM) trial prospectively enrolled 92 patients at 107 AF ablation procedures, in whom computational mapping identified AF rotors or focal sources. Patients underwent FIRM plus conventional ablation (FIRM-guided), or conventional ablation only, and were evaluated for recurrent AF quarterly with rigourous, often implanted, monitoring. We report the n = 73 patients undergoing first ablation in whom demographic information was available (n = 52 conventional, n = 21 FIRM-guided).Stable sources for AF were found in 97.1% of patients. The numbers of concurrent sources per patient (2.1 ± 1.1) rose with LA diameter (P = 0.021), lower left ventricular ejection fraction (P = 0.039), and the presence of OSA (P = 0.002) or hypomagnesemia (P = 0.017). Right atrial sources were associated with obesity (body mass index ≥ 30; P = 0.015). In patients with obesity, hypertension, OSA, and LA diameter > 40 mm, single-procedure freedom from AF was > 80% when FIRM-guided was used vs. < 50% when conventional ablation was used (all; P < 0.05).Patients with "difficult to treat" AF exhibit more concurrent AF sources in more widespread biatrial distributions than other patients. These mechanisms explain the disappointing results of PV isolation, and how FIRM can identify patient-specific AF sources to enable successful ablation in this population.

    View details for DOI 10.1016/j.cjca.2013.07.672

    View details for Web of Science ID 000324858700011

    View details for PubMedID 23993247

  • Direct or Coincidental Elimination of Stable Rotors or Focal Sources May Explain Successful Atrial Fibrillation Ablation On-Treatment Analysis of the CONFIRM Trial (Conventional Ablation for AF With or Without Focal Impulse and Rotor Modulation) JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY Narayan, S. M., Krummen, D. E., Clopton, P., Shivkumar, K., Miller, J. M. 2013; 62 (2): 138-147


    This study sought to determine whether ablation of recently described stable atrial fibrillation (AF) sources, either directly by Focal Impulse and Rotor Modulation (FIRM) or coincidentally when anatomic ablation passes through AF sources, may explain long-term freedom from AF.It is unclear why conventional anatomic AF ablation can be effective in some patients yet ineffective in others with similar profiles.The CONFIRM (Conventional Ablation for AF With or Without Focal Impulse and Rotor Modulation) trial prospectively revealed stable AF rotors or focal sources in 98 of 101 subjects with AF at 107 consecutive ablation cases. In 1:2 fashion, subjects received targeted source ablation (FIRM) followed by conventional ablation, or conventional ablation alone. We determined whether ablation lesions on electroanatomic maps passed through AF sources on FIRM maps.Subjects who completed follow-up (n = 94; 71.2% with persistent AF) showed 2.3 ± 1.1 concurrent AF rotors or focal sources that lay near pulmonary veins (22.8%), left atrial roof (16.0%), and elsewhere in the left (28.2%) and right (33.0%) atria. AF sources were ablated directly in 100% of FIRM cases and coincidentally (e.g., left atrial roof) in 45% of conventional cases (p < 0.05). During a median (interquartile range) of 273 days (138 to 636 days) after one procedure, AF was absent in 80.3% of patients if sources were ablated but in only 18.2% of patients if sources were missed (p < 0.001). Freedom from AF was highest if all sources were ablated, intermediate if some sources were ablated, and lowest if no sources were ablated (p < 0.001).Elimination of stable AF rotors and focal sources may explain freedom from AF after diverse approaches to ablation. Patient-specific AF source distributions are consistent with the reported success of specific anatomic lesion sets and of widespread ablation. These results support targeting AF sources to reduce unnecessary ablation, and motivate studies on FIRM-only ablation.

    View details for DOI 10.1016/j.jacc.2013.03.021

    View details for Web of Science ID 000321338600010

    View details for PubMedID 23563126

  • Panoramic Electrophysiological Mapping but not Electrogram Morphology Identifies Stable Sources for Human Atrial Fibrillation Stable Atrial Fibrillation Rotors and Focal Sources Relate Poorly to Fractionated Electrograms CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY Narayan, S. M., Shivkumar, K., Krummen, D. E., Miller, J. M., Rappel, W. 2013; 6 (1): 58-67


    The foundation for successful arrhythmia ablation is the mapping of electric propagation to identify underlying mechanisms. In atrial fibrillation (AF), however, mapping is difficult so that ablation has often targeted electrogram features, with mixed results. We hypothesized that wide field-of-view (panoramic) mapping of both atria would identify causal mechanisms for AF and allow interpretation of local electrogram features, including complex fractionated atrial electrograms (CFAE).Contact mapping was performed using biatrial multipolar catheters in 36 AF subjects (29 persistent). Stable AF rotors (spiral waves) or focal sources were seen in 35 of 36 cases and targeted for ablation (focal impulse and rotor modulation) before pulmonary vein isolation. In 31 of 36 subjects (86.1%), AF acutely terminated (n=20; 16 to sinus rhythm) or organized (n=11; 19±8% slowing) with 2.5 minutes focal impulse and rotor modulation (interquartile range, 1.0-3.1) at one source, defined as the primary source. Subjects exhibited 2.1±1.0 concurrent AF sources of which the primary, by phase mapping, precessed in limited areas (persistent 2.5±1.7 versus paroxysmal 1.7±0.5 cm(2); P=0.30). Notably, source regions showed mixed electrogram amplitudes and CFAE grades that did not differ from surrounding atrium (P=NS). AF sources were not consistently surrounded by CFAE (P=0.67).Stable rotors and focal sources for human AF were revealed by contact panoramic mapping (focal impulse and rotor modulation mapping), but not by electrogram footprints. AF sources precessed within areas of ≈2 cm(2), with diverse voltage characteristics poorly correlated with CFAE. Most CFAE sites lie remote from AF sources and are not suitable targets for catheter ablation of AF.

    View details for DOI 10.1161/CIRCEP.111.977264

    View details for Web of Science ID 000320670700013

    View details for PubMedID 23392583

  • What Tissue Does Circumferential PV Isolation Actually Modulate? Journal of cardiovascular electrophysiology 2013

    View details for DOI 10.1111/jce.12310

    View details for PubMedID 24152088

  • HRS Policy Statement: Clinical Cardiac Electrophysiology Fellowship Curriculum: Update 2011 HEART RHYTHM Link, M. S., Exner, D. V., Anderson, M., Ackerman, M., Al-Ahmad, A., Knight, B. P., Markowitz, S. M., Kaufman, E. S., Haines, D., Asirvatham, S. J., Callans, D. J., Mounsey, J. P., Bogun, F., Narayan, S. M., Krahn, A. D., Mittal, S., Singh, J., Fisher, J. D., Chugh, S. S. 2011; 8 (8): 1340-1356

    View details for DOI 10.1016/j.hrthm.2011.06.008

    View details for Web of Science ID 000293013600033

    View details for PubMedID 21699868

  • Highlights of the Year in JACC 2010 JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY DeMaria, A. N., Bax, J. J., Ben-Yehuda, O., Feld, G. K., Greenberg, B. H., Hall, J., Hlatky, M., Lew, W. Y., Lima, J. A., Maisel, A. S., Narayan, S. M., Nissen, S., Sahn, D. J., Tsimikas, S. 2011; 57 (4): 480-514

    View details for DOI 10.1016/j.jacc.2010.12.007

    View details for Web of Science ID 000286376500015

    View details for PubMedID 21251590

  • Highlights of the Year in JACC 2009 JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY DeMaria, A. N., Bax, J. J., Ben-Yehuda, O., Feld, G. K., Greenberg, B. H., Hall, J., Hlatky, M., Lew, W. Y., Lima, J. A., Maisel, A. S., Narayan, S. M., Nissen, S., Sahn, D. J., Tsimikas, S. 2010; 55 (4): 380-407

    View details for DOI 10.1016/j.jacc.2009.12.007

    View details for Web of Science ID 000273802200023

    View details for PubMedID 20117446