Imperial College London

Dr Fu Siong Ng

Faculty of MedicineNational Heart & Lung Institute

Clinical Senior Lecturer in Cardiac Electrophysiology
 
 
 
//

Contact

 

+44 (0)20 7594 3614f.ng Website

 
 
//

Location

 

ICTEM buildingHammersmith Campus

//

Summary

 

Publications

Publication Type
Year
to

92 results found

Li X, Handa BS, Peters NS, Ng FSet al., 2020, Classification of fibrillation subtypes with single-channel surface electrocardiogram, UK Workshop on Computational Intelligence (UKCI), Publisher: Springer International Publishing, Pages: 472-479, ISSN: 2194-5357

Atrial fibrillation (AF) and ventricular fibrillation (VF) are complex heart rhythm disorders with increasing prevalence. Mechanisms sustaining these arrhythmias are different, and subsequently, the required treatments options differ. Although many algorithms have been developed for differentiating fibrillation from normal sinus rhythm, very few methods exist to differentiate between different forms of AF and VF from surface electrocardiogram (ECG). To address the issue, we propose a novel ECG classification method to differentiate fibrillation that is completely chaotic from forms where it is organized with key driving sites. Differentiating fibrillation organisation from ECGs may aid patient selection, and identify those who may benefit from targeted ablation treatment. Evaluation using real-world data sets based on rat VF model shows that the proposed method could recognise the correct Fibrillation subtype from the single-channel electrocardiogram with an accuracy of 88.89 % .

Conference paper

Li X, Roney C, Handa B, Chowdhury R, Niederer S, Peters N, Ng FSet al., 2019, Standardised framework for quantitative analysisof fibrillation dynamics, Scientific Reports, Vol: 9, ISSN: 2045-2322

The analysis of complex mechanisms underlying ventricular fibrillation (VF) and atrial fibrillation (AF) requires sophisticatedtools for studying spatio-temporal action potential (AP) propagation dynamics. However, fibrillation analysis tools are oftencustom-made or proprietary, and vary between research groups. With no optimal standardised framework for analysis, resultsfrom different studies have led to disparate findings. Given the technical gap, here we present a comprehensive framework andset of principles for quantifying properties of wavefront dynamics in phase-processed data recorded during myocardial fibrillationwith potentiometric dyes. Phase transformation of the fibrillatory data is particularly useful for identifying self-perpetuating spiralwaves or rotational drivers (RDs) rotating around a phase singularity (PS). RDs have been implicated in sustaining fibrillation,and thus accurate localisation and quantification of RDs is crucial for understanding specific fibrillatory mechanisms. In thiswork, we assess how variation of analysis parameters and thresholds in the tracking of PSs and quantification of RDs couldresult in different interpretations of the underlying fibrillation mechanism. These techniques have been described and appliedto experimental AF and VF data, and AF simulations, and examples are provided from each of these data sets to demonstratethe range of fibrillatory behaviours and adaptability of these tools. The presented methodologies are available as an opensource software and offer an off-the-shelf research toolkit for quantifying and analysing fibrillatory mechanisms.

Journal article

Qureshi N, Kim S, Cantwell C, Afonso V, Bai WJ, Ali R, Shun-Shin M, Louisa M-L, Luther V, Leong K, Lim E, Wright I, Nagy S, Hayat S, Ng FS, Koa-Wing M, Linton N, Lefroy D, Whinnett Z, Davies DW, Kanagaratnam P, Peters N, Lim PBet al., 2019, Voltage during atrial fibrillation is superior to voltage during sinus rhythm in localizing areas of delayed enhancement on magnetic resonance imaging: An assessment of the posterior left atrium in patients with persistent atrial fibrillation, Heart Rhythm, Vol: 16, Pages: 1357-1367, ISSN: 1547-5271

BackgroundBipolar electrogram voltage during sinus rhythm (VSR) has been used as a surrogate for atrial fibrosis in guiding catheter ablation of persistent AF, but the fixed rate and wavefront characteristics present during sinus rhythm may not accurately reflect underlying functional vulnerabilities responsible for AF maintenance.ObjectivesWe hypothesized that given adequate temporal sampling, the spatial distribution of mean AF voltage (VmAF) should better correlate with delayed-enhancement MRI (MRI-DE) detected atrial fibrosis than VSR.MethodsAF was mapped (8s) during index ablation for persistent AF (20 patients) using a 20-pole catheter (660±28 points/map). Following cardioversion, VSR was mapped (557±326 points/map). Electroanatomic and MRI-DE maps were co-registered in 14 patients.Results(i) The time course of VmAF was assessed from 1-40 AF-cycles (∼8s) at 1113 locations. VmAF stabilized with sampling >4s (mean voltage error=0.05mV). (ii) Paired point analysis of VmAF from segments acquired 30s apart (3,667-sites, 15-patients), showed strong correlation (r=0.95, p<0.001). (iii) Delayed-enhancement (DE) was assessed across the posterior left atrial (LA) wall, occupying 33±13%. VmAF distributions (median[IQR]) were 0.21[0.14-0.35]mV in DE vs. 0.52[0.34-0.77]mV in Non-DE regions. VSR distributions were 1.34[0.65-2.48]mV in DE vs. 2.37[1.27-3.97]mV in Non-DE. A VmAF threshold of 0.35mV yielded sensitivity/specificity 75%/79% in detecting MRI-DE, compared with 63%/67% for VSR (1.8mV threshold).ConclusionThe correlation between low-voltage and posterior LA MRI-DE is significantly improved when acquired during AF vs. sinus rhythm. With adequate sampling, mean AF voltage is a reproducible marker reflecting the functional response to the underlying persistent AF substrate.

Journal article

Shun-Shin MJ, Leong KMW, Ng FS, Linton NWF, Whinnett ZI, Koa-Wing M, Qureshi N, Lefroy DC, Harding SE, Lim PB, Peters NS, Francis DP, Varnava AM, Kanagaratnam Pet al., 2019, Ventricular conduction stability test: a method to identify and quantify changes in whole heart activation patterns during physiological stress, EP-Europace, Vol: 21, Pages: 1422-1431, ISSN: 1099-5129

AIMS: Abnormal rate adaptation of the action potential is proarrhythmic but is difficult to measure with current electro-anatomical mapping techniques. We developed a method to rapidly quantify spatial discordance in whole heart activation in response to rate cycle length changes. We test the hypothesis that patients with underlying channelopathies or history of aborted sudden cardiac death (SCD) have a reduced capacity to maintain uniform activation following exercise. METHODS AND RESULTS: Electrocardiographical imaging (ECGI) reconstructs >1200 electrograms (EGMs) over the ventricles from a single beat, providing epicardial whole heart activation maps. Thirty-one individuals [11 SCD survivors; 10 Brugada syndrome (BrS) without SCD; and 10 controls] with structurally normal hearts underwent ECGI vest recordings following exercise treadmill. For each patient, we calculated the relative change in EGM local activation times (LATs) between a baseline and post-exertion phase using custom written software. A ventricular conduction stability (V-CoS) score calculated to indicate the percentage of ventricle that showed no significant change in relative LAT (<10 ms). A lower score reflected greater conduction heterogeneity. Mean variability (standard deviation) of V-CoS score over 10 consecutive beats was small (0.9 ± 0.5%), with good inter-operator reproducibility of V-CoS scores. Sudden cardiac death survivors, compared to BrS and controls, had the lowest V-CoS scores post-exertion (P = 0.011) but were no different at baseline (P = 0.50). CONCLUSION: We present a method to rapidly quantify changes in global activation which provides a measure of conduction heterogeneity and proof of concept by demonstrating SCD survivors have a reduced capacity to maintain uniform activation following exercise.

Journal article

Keene D, Shun-Shin M, Arnold A, Howard J, Lefroy D, Davies W, Lim PB, Ng FS, Koa-Wing M, Qureshi N, Linton N, Shah J, Peters N, Kanagaratnam P, Francis D, Whinnett Zet al., 2019, Quantification of Electromechanical Coupling to Prevent Inappropriate Implantable Cardioverter-Defibrillator Shocks, JACC: Clinical Electrophysiology, Vol: 5, Pages: 705-715, ISSN: 2405-500X

Objective To test specialised processing of laser Doppler signals for discriminating ventricular fibrillation(VF) from common causes of inappropriate therapies.BackgroundInappropriate ICD therapies remain a clinically important problem associated with morbidity and mortality.Tissue perfusion biomarkers, to assist automated diagnosis of VF, suffer the vulnerability of sometimes mistaking artefact and random noise for perfusion, which could lead to shocks being inappropriately withheld. MethodsWe developed a novel processing algorithm that combines electrogram data and laser Doppler perfusion monitoring, as a method for assessing circulatory status. We recruited 50 patients undergoing VF induction during ICD implantation. We recorded non-invasive laser Doppler and continuous electrograms, during both sinus-rhythm and VF. For each patient we simulated two additional scenarios that may lead to inappropriate shocks: ventricular-lead fracture and T-wave oversensing. We analysed the laser Doppler using three methods for reducing noise: (i)Running Mean, (ii)Oscillatory Height, (iii)a novel quantification of Electro-Mechanical coupling which gates laser Doppler against electrograms. We additionally tested the algorithm during exercise induced sinus tachycardia.ResultsOnly the Electro-mechanical coupling algorithm found a clear perfusion cut-off between sinus rhythm and VF (sensitivity and specificity 100%). Sensitivity and specificity remained 100% during simulated lead fracture and electrogram oversensing. (AUC: Running Mean 0.91, Oscillatory Height 0.86, Electro-Mechanical Coupling 1.00). Sinus tachycardia did not cause false positives.ConclusionsQuantifying the coupling between electrical and perfusion signals increases reliability of discrimination between VF and artefacts that ICDs may interpret as VF. Incorporating such methods into future ICDs may safely permit reductions of inappropriate shocks.

Journal article

Handa B, Li X, Mansfield C, Jabbour RJ, Pitcher D, Chowdhury RA, Peters N, Ng FSet al., 2019, MYOCARDIAL FIBROSIS AND THE DEGREE OF GAP JUNCTION COUPLING DIRECTLY MODIFIES THE UNDERLYING MECHANISM OF FIBRILLATION, Annual Conference of the British-Cardiovascular-Society (BCS) - Digital Health Revolution, Publisher: BMJ PUBLISHING GROUP, Pages: A179-A180, ISSN: 1355-6037

Conference paper

Handa B, Lawal S, Wright IJ, Li X, Cabello Garcia J, Mansfield C, Chowdhury R, Peters N, Ng FSet al., 2019, Interventricular differences in action potential duration restitution contribute to dissimilar ventricular rhythms in ex vivo perfused hearts, Frontiers in Cardiovascular Medicine, Vol: 6, ISSN: 2297-055X

Background: Dissimilar ventricular rhythms refer to the occurrence of different ventricular tachyarrhythmias in the right and left ventricles or different rates of the same tachyarrhythmia in the two ventricles.Objective: We investigated the inducibility of dissimilar ventricular rhythms, their underlying mechanisms, and the impact of anti-arrhythmic drugs (lidocaine and amiodarone) on their occurrence.Methods: Ventricular tachyarrhythmias were induced with burst pacing in 28 Langendorff-perfused Sprague Dawley rat hearts (14 control, 8 lidocaine, 6 amiodarone) and bipolar electrograms recorded from the right and left ventricles. Fourteen (6 control, 4 lidocaine, 4 amiodarone) further hearts underwent optical mapping of transmembrane voltage to study interventricular electrophysiological differences and mechanisms of dissimilar rhythms.Results: In control hearts, dissimilar ventricular rhythms developed in 8/14 hearts (57%). In lidocaine treated hearts, there was a lower cycle length threshold for developing dissimilar rhythms, with 8/8 (100%) hearts developing dissimilar rhythms in comparison to 0/6 in the amiodarone group. Dissimilar ventricular tachycardia (VT) rates occurred at longer cycle lengths with lidocaine vs. control (57.1 ± 7.9 vs. 36.6 ± 8.4 ms, p < 0.001). The ratio of LV:RV VT rate was greater in the lidocaine group than control (1.91 ± 0.30 vs. 1.76 ± 0.36, p < 0.001). The gradient of the action potential duration (APD) restitution curve was shallower in the RV compared with LV (Control - LV: 0.12 ± 0.03 vs RV: 0.002 ± 0.03, p = 0.015), leading to LV-to-RV conduction block during VT.Conclusion: Interventricular differences in APD restitution properties likely contribute to the occurrence of dissimilar rhythms. Sodium channel blockade with lidocaine increases the likelihood of dissimilar ventricular rhythms.

Journal article

Odening KE, Deiß S, Dilling-Boer D, Didenko M, Eriksson U, Nedios S, Ng FS, Roca Luque I, Sanchez Borque P, Vernooy K, Wijnmaalen AP, Yorgun Het al., 2019, Mechanisms of sex differences in atrial fibrillation: role of hormones and differences in electrophysiology, structure, function, and remodelling, EP-Europace, Vol: 21, Pages: 366-376, ISSN: 1099-5129

Atrial fibrillation (AF) is the clinically most prevalent rhythm disorder with large impact on quality of life and increased risk for hospitalizations and mortality in both men and women. In recent years, knowledge regarding epidemiology, risk factors, and patho-physiological mechanisms of AF has greatly increased. Sex differences have been identified in the prevalence, clinical presentation, associated comorbidities, and therapy outcomes of AF. Although it is known that age-related prevalence of AF is lower in women than in men, women have worse and often atypical symptoms and worse quality of life as well as a higher risk for adverse events such as stroke and death associated with AF. In this review, we evaluate what is known about sex differences in AF mechanisms-covering structural, electrophysiological, and hormonal factors-and underscore areas of knowledge gaps for future studies. Increasing our understanding of mechanisms accounting for these sex differences in AF is important both for prognostic purposes and the optimization of (targeted, mechanism-based, and sex-specific) therapeutic approaches.

Journal article

Leong KMW, Ng FS, Jones S, Chow J-J, Qureshi N, Koa-Wing M, Linton NWF, Whinnett ZI, Lefroy DC, Davies DW, Lim PB, Peters NS, Kanagaratnam P, Varnava AMet al., 2019, Prevalence of spontaneous type I ECG pattern, syncope, and other risk markers in sudden cardiac arrest survivors with Brugada syndrome, PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY, Vol: 42, Pages: 257-264, ISSN: 0147-8389

Journal article

Cantwell C, Mohamied Y, Tzortzis K, Garasto S, Houston C, Chowdhury R, Ng F, Bharath A, Peters Net al., 2019, Rethinking multiscale cardiac electrophysiology with machine learning and predictive modelling, Computers in Biology and Medicine, Vol: 104, Pages: 339-351, ISSN: 0010-4825

We review some of the latest approaches to analysing cardiac electrophysiology data using machine learning and predictive modelling. Cardiac arrhythmias, particularly atrial fibrillation, are a major global healthcare challenge. Treatment is often through catheter ablation, which involves the targeted localised destruction of regions of the myocardium responsible for initiating or perpetuating the arrhythmia. Ablation targets are either anatomically defined, or identified based on their functional properties as determined through the analysis of contact intracardiac electrograms acquired with increasing spatial density by modern electroanatomic mapping systems. While numerous quantitative approaches have been investigated over the past decades for identifying these critical curative sites, few have provided a reliable and reproducible advance in success rates. Machine learning techniques, including recent deep-learning approaches, offer a potential route to gaining new insight from this wealth of highly complex spatio-temporal information that existing methods struggle to analyse. Coupled with predictive modelling, these techniques offer exciting opportunities to advance the field and produce more accurate diagnoses and robust personalised treatment. We outline some of these methods and illustrate their use in making predictions from the contact electrogram and augmenting predictive modelling tools, both by more rapidly predicting future states of the system and by inferring the parameters of these models from experimental observations.

Journal article

Handa BS, Roney CH, Houston C, Qureshi N, Li X, Pitcher DS, Chowdhury RA, Lim PB, Dupont E, Niederer S, Cantwell C, Peters NS, Ng FSet al., 2018, Analytical approaches for myocardial fibrillation signals, Computers in Biology and Medicine, Vol: 102, Pages: 315-326, ISSN: 0010-4825

Atrial and ventricular fibrillation are complex arrhythmias, and their underlying mechanisms remain widely debated and incompletely understood. This is partly because the electrical signals recorded during myocardial fibrillation are themselves complex and difficult to interpret with simple analytical tools. There are currently a number of analytical approaches to handle fibrillation data. Some of these techniques focus on mapping putative drivers of myocardial fibrillation, such as dominant frequency, organizational index, Shannon entropy and phase mapping. Other techniques focus on mapping the underlying myocardial substrate sustaining fibrillation, such as voltage mapping and complex fractionated electrogram mapping. In this review, we discuss these techniques, their application and their limitations, with reference to our experimental and clinical data. We also describe novel tools including a new algorithm to map microreentrant circuits sustaining fibrillation.

Journal article

Roney C, Ng FS, Debney M, Eichhorn C, Nachiappan A, Chowdhury R, Qureshi N, Cantwell C, Tweedy J, Niederer S, Peters N, Vigmond Eet al., 2018, Determinants of new wavefront locations in cholinergic atrial fibrillation, EP-Europace, Vol: 20, Pages: iii3-iii15, ISSN: 1099-5129

AimsAtrial fibrillation (AF) wavefront dynamics are complex and difficult to interpret, contributing to uncertainty about the mechanisms that maintain AF. We aimed to investigate the interplay between rotors, wavelets, and focal sources during fibrillation.Methods and resultsArrhythmia wavefront dynamics were analysed for four optically mapped canine cholinergic AF preparations. A bilayer computer model was tuned to experimental preparations, and varied to have (i) fibrosis in both layers or the epicardium only, (ii) different spatial acetylcholine distributions, (iii) different intrinsic action potential duration between layers, and (iv) varied interlayer connectivity. Phase singularities (PSs) were identified and tracked over time to identify rotational drivers. New focal wavefronts were identified using phase contours. Phase singularity density and new wavefront locations were calculated during AF. There was a single dominant mechanism for sustaining AF in each of the preparations, either a rotational driver or repetitive new focal wavefronts. High-density PS sites existed preferentially around the pulmonary vein junctions. Three of the four preparations exhibited stable preferential sites of new wavefronts. Computational simulations predict that only a small number of connections are functionally important in sustaining AF, with new wavefront locations determined by the interplay between fibrosis distribution, acetylcholine concentration, and heterogeneity in repolarization within layers.ConclusionWe were able to identify preferential sites of new wavefront initiation and rotational activity, in order to determine the mechanisms sustaining AF. Electrical measurements should be interpreted differently according to whether they are endocardial or epicardial recordings.

Journal article

Sattler S, Ng FS, Panahi M, 2018, Immunopharmacology of post-myocardial infarction and heart failure medications, Journal of Clinical Medicine, Vol: 7, ISSN: 2077-0383

The immune system responds to acute tissue damage after myocardial infarction (MI) and orchestrates healing and recovery of the heart. However, excessive inflammation may lead to additional tissue damage and fibrosis and exacerbate subsequent functional impairment, leading to heart failure. The appreciation of the immune system as a crucial factor after MI has led to a surge of clinical trials investigating the potential benefits of immunomodulatory agents previously used in hyper-inflammatory conditions, such as autoimmune disease. While the major goal of routine post-MI pharmacotherapy is to support heart function by ensuring appropriate blood pressure and cardiac output to meet the demands of the body, several drug classes also affect a range of immunological pathways and modulate the post-MI immune response, which is crucial to take into account when designing future immunomodulatory trials. This review outlines how routine post-MI pharmacotherapy affects the immune response and may thus influence post-MI outcomes and development towards heart failure. Current key drug classes are discussed, including platelet inhibitors, statins, β-blockers, and renin–angiotensin–aldosterone inhibitors.

Journal article

Jabbour R, Kapnisi K, Mawad D, Handa B, Couch L, Mansfield C, Perbillini F, Terracciano C, Stevens M, Lyon A, Smith G, Peters N, Ng FS, Harding Set al., 2018, Conductive polymers affect myocardial conduction velocity but are not pro-arrhythmic, European-Society-of-Cardiology Congress, Publisher: OXFORD UNIV PRESS, Pages: 1205-1205, ISSN: 0195-668X

Conference paper

Luther V, Wright I, Lefroy D, Ng Fet al., 2018, A narrow complex tachycardia with variable R-R intervals: what is the mechanism?, Journal of Cardiovascular Electrophysiology, Vol: 29, Pages: 1174-1176, ISSN: 1045-3873

A 46-year-old man was referred for an invasive electrophysiological study with a view to ablation, for a history of classic sudden onset-offset palpitations. The patient’s son had recently survived an out of hospital cardiac arrest, and was found to have an accessory pathway (details unknown) at another institute, which was ablated. Our patient’s 12 lead electrocardiogram (ECG) showed sinus rhythm with no evidence of pre-excitation. Echocardiography revealed a structurally normal heart. An electrophysiological study was performed with a quadripolar catheter positioned at the high right atrium (HRA), a steerable decapolar catheter in the coronary sinus and quadripolar catheters along the His bundle and at the right ventricular apex. Baseline atrio-His (AH) and His-ventricular (HV) intervals measured 60ms and 40ms respectively. Programmed atrial extra-stimulus testing revealed decremental AH intervals, before tachycardia was reproducibly induced. Figure 1 shows the tachycardia on a 12-lead ECG. Figure 2 shows the induction of tachycardia with atrial pacing. Based on the findings within the figures, what is the mechanism of the tachycardia?

Journal article

Houston CPJ, Tzortzis KN, Roney C, Saglietto A, Pitcher DS, Cantwell C, Chowdhury RA, Ng FS, Peters NS, Dupont Eet al., 2018, Characterisation of re-entrant circuit (or rotational activity) in vitro using the HL1-6 myocyte cell line, Journal of Molecular and Cellular Cardiology, Vol: 119, Pages: 155-164, ISSN: 0022-2828

Fibrillation is the most common arrhythmia observed in clinical practice. Understanding of the mechanisms underlying its initiation and maintenance remains incomplete. Functional re-entries are potential drivers of the arrhythmia. Two main concepts are still debated, the “leading circle” and the “spiral wave or rotor” theories. The homogeneous subclone of the HL1 atrial-derived cardiomyocyte cell line, HL1-6, spontaneously exhibits re-entry on a microscopic scale due to its slow conduction velocity and the presence of triggers, making it possible to examine re-entry at the cellular level.We therefore investigated the re-entry cores in cell monolayers through the use of fluorescence optical mapping at high spatiotemporal resolution in order to obtain insights into the mechanisms of re-entry.Re-entries in HL1-6 myocytes required at least two triggers and a minimum colony area to initiate (3.5 to 6.4 mm2). After electrical activity was completely stopped and re-started by varying the extracellular K+ concentration, re-entries never returned to the same location while 35% of triggers re-appeared at the same position. A conduction delay algorithm also allows visualisation of the core of the re-entries. This work has revealed that the core of re-entries is conduction blocks constituted by lines and/or groups of cells rather than the round area assumed by the other concepts of functional re-entry. This highlights the importance of experimentation at the microscopic level in the study of re-entry mechanisms.

Journal article

Chowdhury RA, Tzortzis KN, Dupont E, Selvadurai S, Perbellini F, Cantwell C, Ng FS, Simon A, Terracciano C, Peters NSet al., 2018, Concurrent micro- to macro-cardiac electrophysiology in myocyte cultures and human heart slices, Scientific Reports, Vol: 8, ISSN: 2045-2322

The contact cardiac electrogram is derived from the extracellular manifestation of cellular action potentials and cell-to-cell communication. It is used to guide catheter based clinical procedures. Theoretically, the contact electrogram and the cellular action potential are directly related, and should change in conjunction with each other during arrhythmogenesis, however there is currently no methodology by which to concurrently record both electrograms and action potentials in the same preparation for direct validation of their relationships and their direct mechanistic links. We report a novel dual modality apparatus for concurrent electrogram and cellular action potential recording at a single cell level within multicellular preparations. We further demonstrate the capabilities of this system to validate the direct link between these two modalities of voltage recordings.

Journal article

Houston C, Ng FS, Dupont E, 2018, Letter by Houston et al regarding article, "Localized Optogenetic Targeting of Rotors in Atrial Cardiomyocyte Monolayers", Circulation: Arrhythmia and Electrophysiology, Vol: 11, Pages: e006118-e006118, ISSN: 1941-3084

Journal article

Luther V, Qureshi N, Lim PB, Koa-Wing M, Jamil-Copley S, Ng FS, Whinnett Z, Davies DW, Peters NS, Kanagaratnam P, Linton Net al., 2018, Isthmus sites identified by Ripple Mapping are usually anatomically stable: A novel method to guide atrial substrate ablation?, Journal of Cardiovascular Electrophysiology, Vol: 29, Pages: 404-411, ISSN: 1045-3873

BACKGROUND: Postablation reentrant ATs depend upon conducting isthmuses bordered by scar. Bipolar voltage maps highlight scar as sites of low voltage, but the voltage amplitude of an electrogram depends upon the myocardial activation sequence. Furthermore, a voltage threshold that defines atrial scar is unknown. We used Ripple Mapping (RM) to test whether these isthmuses were anatomically fixed between different activation vectors and atrial rates. METHODS: We studied post-AF ablation ATs where >1 rhythm was mapped. Multipolar catheters were used with CARTO Confidense for high-density mapping. RM visualized the pattern of activation, and the voltage threshold below which no activation was seen. Isthmuses were characterized at this threshold between maps for each patient. RESULTS: Ten patients were studied (Map 1 was AT1; Map 2: sinus 1/10, LA paced 2/10, AT2 with reverse CS activation 3/10; AT2 CL difference 50 ± 30 ms). Point density was similar between maps (Map 1: 2,589 ± 1,330; Map 2: 2,214 ± 1,384; P  =  0.31). RM activation threshold was 0.16 ± 0.08 mV. Thirty-one isthmuses were identified in Map 1 (median 3 per map; width 27 ± 15 mm; 7 anterior; 6 roof; 8 mitral; 9 septal; 1 posterior). Importantly, 7 of 31 (23%) isthmuses were unexpectedly identified within regions without prior ablation. AT1 was treated following ablation of 11/31 (35%) isthmuses. Of the remaining 20 isthmuses, 14 of 16 isthmuses (88%) were consistent between the two maps (four were inadequately mapped). Wavefront collision caused variation in low voltage distribution in 2 of 16 (12%). CONCLUSIONS: The distribution of isthmuses and nonconducting tissue within the ablated left atrium, as defined by RM, appear concordant between rhythms. This could guide a substrate ablative approach.

Journal article

Leong KMW, chow J-J, Ng FS, Falaschetti E, Qureshi N, Koa-Wing M, Linton N, Whinnett Z, Lefroy D, Davies DW, Lim PB, Peters N, Kanagaratnam P, Varnava Aet al., 2017, Comparison of the Prognostic Usefulness of the European Society of Cardiology and American Heart Association/American College of Cardiology Foundation Risk Stratification Systems for Patients With Hypertrophic Cardiomyopathy, American Journal of Cardiology, Vol: 121, Pages: 349-355, ISSN: 0002-9149

Implantable cardio-defibrillators (ICDs) have proven benefit in preventing sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HC), making risk stratification essential. Data on the predictive accuracy on the European Society of Cardiology (ESC) risk scoring system has been conflicting. We independently evaluated the ESC risk scoring system in our cohort of HC patients from a large tertiary centre and compared this to previous guidance by the American College of Cardiology Foundation and Heart Association (ACCF/AHA). Risk factor profiles, 5-year SCD risk estimates and ICD recommendations as defined by the ACCF/AHA and ESC guidelines, were retrospectively ascertained for 288 HC patients with and without SCD or equivalent events at our centre. In the SCD group (n=14), a significantly higher proportion of patients would not have met the criteria for an ICD implant using the ESC scoring algorithm than ACCF/AHA guidance (43%vs7%, p=0.029). In those without SCD events (n=274), a larger proportion of individuals not requiring an ICD was identified using the ESC risk score model compared to the ACCF/AHA model (82%vs57%; p<0.0001). Based on risk stratification criteria alone, 5 more individuals with a previously aborted SCD event would not have received an ICD with the ESC risk model than the ACCF/AHA risk model. In conclusion, we found that the current ESC scoring system potentially leaves more high-risk patients unprotected from sudden death in our cohort of patients.

Journal article

Leong KMW, Ng FS, Roney C, Cantwell C, Shun-Shin M, Linton N, Whinnett Z, Lefroy D, Davies DW, Harding S, Lim PB, Francis D, Peters N, Varnava A, Kanagaratnam Pet al., 2017, Repolarization abnormalities unmasked with exercise in sudden cardiac death survivors with structurally normal hearts, Journal of Cardiovascular Electrophysiology, Vol: 29, Pages: 115-126, ISSN: 1045-3873

BACKGROUND: Models of cardiac arrhythmogenesis predict that non-uniformity in repolarization and/or depolarization promotes ventricular fibrillation and is modulated by autonomic tone, but this is difficult to evaluate in patients. We hypothesize that such spatial heterogeneities would be detected by non-invasive ECG imaging (ECGi) in sudden cardiac death (SCD) survivors with structurally normal hearts under physiological stress. METHODS: ECGi was applied to 11 SCD survivors, 10 low-risk Brugada Syndrome patients (BrS) and 10 controls undergoing exercise treadmill testing. ECGi provides whole heart activation maps and > 1200 unipolar electrograms over the ventricular surface from which global dispersion of activation recovery interval (ARI) and regional delay in conduction were determined. These were used as surrogates for spatial heterogeneities in repolarization and depolarization. Surface ECG markers of dispersion (QT and Tpeak-end intervals) were also calculated for all patients for comparison. RESULTS: Following exertion, the SCD group demonstrated the largest increase in ARI dispersion compared to BrS and control groups (13±8 ms vs 4±7 ms vs 4±5 ms; p = 0.009), with baseline dispersion being similar in all groups. In comparison, surface ECG markers of dispersion of repolarisation were unable to discriminate between the groups at baseline or following exertion. Spatial heterogeneities in conduction were also present following exercise but were not significantly different between SCD survivors and the other groups. CONCLUSION: Increased dispersion of repolarization is apparent during physiological stress in SCD survivors and is detectable with ECGi but not with standard ECG parameters. The electrophysiological substrate revealed by ECGi could be the basis of alternative risk-stratification techniques. This article is protected by copyright. All rights reserved.

Journal article

Leong KMW, Ng FS, yao C, Roney C, Linton N, Whinnett Z, lefroy D, Davies DW, Lim PB, Harding S, Peters N, Kanagaratnam P, Varnava Aet al., 2017, ST-Elevation Magnitude Correlates With Right Ventricular Outflow Tract Conduction Delay in Type I Brugada ECG, Circulation: Arrhythmia and Electrophysiology, Vol: 10, ISSN: 1941-3084

Background: The substrate location and underlying electrophysiological mechanisms that contribute to the characteristic ECG pattern of Brugada syndrome (BrS) are still debated. Using noninvasive electrocardiographical imaging, we studied whole heart conduction and repolarization patterns during ajmaline challenge in BrS individuals.Methods and Results: A total of 13 participants (mean age, 44±12 years; 8 men), 11 concealed patients with type I BrS and 2 healthy controls, underwent an ajmaline infusion with electrocardiographical imaging and ECG recordings. Electrocardiographical imaging activation recovery intervals and activation timings across the right ventricle (RV) body, outflow tract (RVOT), and left ventricle were calculated and analyzed at baseline and when type I BrS pattern manifested after ajmaline infusion. Peak J-ST point elevation was calculated from the surface ECG and compared with the electrocardiographical imaging–derived parameters at the same time point. After ajmaline infusion, the RVOT had the greatest increase in conduction delay (5.4±2.8 versus 2.0±2.8 versus 1.1±1.6 ms; P=0.007) and activation recovery intervals prolongation (69±32 versus 39±29 versus 21±12 ms; P=0.0005) compared with RV or left ventricle. In controls, there was minimal change in J-ST point elevation, conduction delay, or activation recovery intervals at all sites with ajmaline. In patients with BrS, conduction delay in RVOT, but not RV or left ventricle, correlated to the degree of J-ST point elevation (Pearson R, 0.81; P<0.001). No correlation was found between J-ST point elevation and activation recovery intervals prolongation in the RVOT, RV, or left ventricle.Conclusions: Magnitude of ST (J point) elevation in the type I BrS pattern is attributed to degree of conduction delay in the RVOT and not prolongation in repolarization time.

Journal article

Mirza KB, Zuliani C, Hou B, Ng FS, Peters NS, Toumazou Cet al., 2017, Injection moulded microneedle sensor for real-time wireless pH monitoring, 39th Annual International Conference of the IEEE-Engineering-in-Medicine-and-Biology-Society (EMBC), Publisher: IEEE, Pages: 189-192, ISSN: 1094-687X

This paper describes the development of an array of individually addressable pH sensitive microneedles using injection moulding and their integration within a portable device for real-time wireless recording of pH distributions in biological samples. The fabricated microneedles are subjected to gold patterning followed by electrodeposition of iridium oxide to sensitize them to 0.07 units of pH change. Miniaturised electronics suitable for the sensors readout, analog-to-digital conversion and wireless transmission of the potentiometric data are embodied within the device, enabling it to measure real-time pH of soft biological samples such as muscles. In this paper, real-time recording of the cardiac pH distribution, during ischemia followed by reperfusion cycles in cardiac muscles of male Wistar rats has been demonstrated by using the microneedle array.

Conference paper

Leong KMW, Ng FS, Patil S, Lim PBet al., 2017, An electrocardiogram opinion from an National Health Service walk-in centre, Emergency Medicine Journal, Vol: 34, Pages: 631-632, ISSN: 1472-0205

Journal article

Roney CH, Cantwell CD, Bayer JD, Qureshi NA, Lim PB, Tweedy JH, Kanagaratnam P, Peters NS, Vigmond EJ, Ng Fet al., 2017, Spatial resolution requirements for accurate identification of drivers of atrial fibrillation, Circulation-Arrhythmia and Electrophysiology, Vol: 10, ISSN: 1941-3084

Background—Recent studies have demonstrated conflicting mechanisms underlying atrial fibrillation (AF), with the spatial resolution of data often cited as a potential reason for the disagreement. The purpose of this study was to investigate whether the variation in spatial resolution of mapping may lead to misinterpretation of the underlying mechanism in persistent AF.Methods and Results—Simulations of rotors and focal sources were performed to estimate the minimum number of recording points required to correctly identify the underlying AF mechanism. The effects of different data types (action potentials and unipolar or bipolar electrograms) and rotor stability on resolution requirements were investigated. We also determined the ability of clinically used endocardial catheters to identify AF mechanisms using clinically recorded and simulated data. The spatial resolution required for correct identification of rotors and focal sources is a linear function of spatial wavelength (the distance between wavefronts) of the arrhythmia. Rotor localization errors are larger for electrogram data than for action potential data. Stationary rotors are more reliably identified compared with meandering trajectories, for any given spatial resolution. All clinical high-resolution multipolar catheters are of sufficient resolution to accurately detect and track rotors when placed over the rotor core although the low-resolution basket catheter is prone to false detections and may incorrectly identify rotors that are not present.Conclusions—The spatial resolution of AF data can significantly affect the interpretation of the underlying AF mechanism. Therefore, the interpretation of human AF data must be taken in the context of the spatial resolution of the recordings.

Journal article

Luther V, Sikkel M, Bennett N, Guerrero F, Leong K, Qureshi N, Ng FS, Hayat SA, Sohaib SMA, Malcolme-Lawes L, Lim E, Wright I, Koa-Wing M, Lefroy DC, Linton NWF, Whinnett Z, Kanagaratnam P, Davies W, Peters NS, Lim PBet al., 2017, Visualizing Localized Reentry With Ultra-High Density Mapping in Iatrogenic Atrial Tachycardia Beware Pseudo-Reentry, CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY, Vol: 10, ISSN: 1941-3149

Background—The activation pattern of localized reentry (LR) in atrial tachycardia remains incompletely understood. We used the ultra–high density Rhythmia mapping system to study activation patterns in LR.Methods and Results—LR was suggested by small rotatory activations (carousels) containing the full spectrum of the color-coded map. Twenty-three left-sided atrial tachycardias were mapped in 15 patients (age: 64±11 years). 16 253±9192 points were displayed per map, collected over 26±14 minutes. A total of 50 carousels were identified (median 2; quartiles 1–3 per map), although this represented LR in only n=7 out of 50 (14%): here, rotation occurred around a small area of scar (<0.03 mV; 12±6 mm diameter). In LR, electrograms along the carousel encompassed the full tachycardia cycle length, and surrounding activation moved away from the carousel in all directions. Ablating fractionated electrograms (117±18 ms; 44±13% of tachycardia cycle length) within the carousel interrupted the tachycardia in every LR case. All remaining carousels were pseudo-reentrant (n=43/50 [86%]) occurring in areas of wavefront collision (n=21; median 0.5; quartiles 0–2 per map) or as artifact because of annotation of noise or interpolation in areas of incomplete mapping (n=22; median 1, quartiles 0–2 per map). Pseudo-reentrant carousels were incorrectly ablated in 5 cases having been misinterpreted as LR.Conclusions—The activation pattern of LR is of small stable rotational activations (carousels), and this drove 30% (7/23) of our postablation atrial tachycardias. However, this appearance is most often pseudo-reentrant and must be differentiated by interpretation of electrograms in the candidate circuit and activation in the wider surrounding region.

Journal article

Ng FS, Guerrero F, Luther V, Sikkel M, Lim PBet al., 2017, Microreentrant left atrial tachycardia circuit mapped with an ultra-high-density mapping system, HeartRhythm Case Reports, Vol: 3, Pages: 224-228, ISSN: 2214-0271

Micro-reentrant tachycardias are well described and are thought to be responsible for a small proportion of atrial tachycardias post-atrial fibrillation ablation. However, due to the small size of these re-entrant circuits and the poor spatial resolution of conventional mapping tools, they have not previously been mapped accurately in vivo in humans, and have therefore been difficult to distinguish from non-reentrant focal tachycardias. The newly-developed Rhythmia electroanatomical mapping system allows for the rapid creation of activation maps of ultra-high resolution. In this case report, we provide the first images of a micro-reentrant atrial tachycardia circuit in a post-atrial fibrillation setting, mapped with the high resolution Rhythmia mapping system.

Journal article

Sikkel MB, Luther V, Sau A, Guerrero F, Ng FS, Lim PBet al., 2017, High-Density Electroanatomical Mapping to Identify Point of Epicardial to Endocardial Breakthrough in Perimitral Flutter, JACC: Clinical Electrophysiology, Vol: 3, Pages: 637-639, ISSN: 2405-500X

Journal article

Rajkumar CA, Qureshi N, Ng F, Panoulas VF, Lim PBet al., 2017, Adenosine induced ventricular fibrillation in a structurally normal heart: a case report, Journal of Medical Case Reports, Vol: 11, ISSN: 1752-1947

BackgroundAdenosine is the first-line pharmacotherapy for termination of supraventricular tachycardia through its action on the atrioventricular node. However, pro-arrhythmic effects of adenosine are also recognised, most notably in the presence of pre-excited atrial fibrillation. In this case report, we describe the induction of ventricular fibrillation in a patient with no demonstrable accessory pathway, nor any other structural heart disease. This rare, idiosyncratic reaction has never previously been reported and is of relevance given the widespread and routine use of adenosine in clinical practice.Case presentationA 26-year-old woman of Cypriot origin presented to our emergency department with a sudden onset of palpitations and chest discomfort. She was healthy, with no previous medical history and no regular medications. An electrocardiogram demonstrated a narrow complex tachycardia with a rate of 194 beats per minute. Following failure of vagal maneuvers to terminate the tachycardia, the assessing physician administered a single intravenous dose of 6 mg adenosine. Our patient instantaneously developed coarse ventricular fibrillation and circulatory collapse. Cardiopulmonary resuscitation was initiated and our patient was rapidly defibrillated to sinus rhythm with a single 150 J direct current shock. A 900-mg loading dose of intravenous amiodarone was commenced and our patient was managed in the cardiac high dependency unit. No further arrhythmias were identified on continuous cardiac monitoring.On review, her presenting electrocardiogram had demonstrated rapidly conducted atrial fibrillation with no evidence of ventricular pre-excitation. Concordantly, her resting electrocardiogram was not suggestive of any accessory pathway. This was conclusively excluded on invasive electrophysiology study, with negative programmed ventricular stimulation up to three extrastimuli. Extensive laboratory investigations were unremarkable and failed to identify an underlying cau

Journal article

Roney CH, Cantwell CD, Qureshi NA, Chowdhury RA, Dupont E, Lim PB, Vigmond EJ, Tweedy JH, Ng FS, Peters NSet al., 2016, Rotor tracking using phase of electrograms recorded during atrial fibrillation, Annals of Biomedical Engineering, Vol: 45, Pages: 910-923, ISSN: 1573-9686

Extracellular electrograms recorded during atrial fibrillation (AF) are challenging to interpret due to the inherent beat-to-beat variability in amplitude and duration. Phase mapping represents these voltage signals in terms of relative position within the cycle, and has been widely applied to action potential and unipolar electrogram data of myocardial fibrillation. To date, however, it has not been applied to bipolar recordings, which are commonly acquired clinically. The purpose of this study is to present a novel algorithm for calculating phase from both unipolar and bipolar electrograms recorded during AF. A sequence of signal filters and processing steps are used to calculate phase from simulated, experimental, and clinical, unipolar and bipolar electrograms. The algorithm is validated against action potential phase using simulated data (trajectory centre error <0.8 mm); between experimental multi-electrode array unipolar and bipolar phase; and for wavefront identification in clinical atrial tachycardia. For clinical AF, similar rotational content (R (2) = 0.79) and propagation maps (median correlation 0.73) were measured using either unipolar or bipolar recordings. The algorithm is robust, uses standard signal processing techniques, and accurately quantifies AF wavefronts and sources. Identifying critical sources, such as rotors, in AF, may allow for more accurate targeting of ablation therapy and improved patient outcomes.

Journal article

This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.

Request URL: http://wlsprd.imperial.ac.uk:80/respub/WEB-INF/jsp/search-html.jsp Request URI: /respub/WEB-INF/jsp/search-html.jsp Query String: respub-action=search.html&id=00589520&limit=30&person=true