Imperial College London

Dr Fu Siong Ng

Faculty of MedicineNational Heart & Lung Institute

Reader in Cardiac Electrophysiology
 
 
 
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Contact

 

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

 
 
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Location

 

430ICTEM buildingHammersmith Campus

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Summary

 

Publications

Publication Type
Year
to

189 results found

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, Pages: 1-13, 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

Ng FS, Rashid M, Lim E, Lim PBet al., 2016, Mapping signatures of ventricular ectopy of endocavitary origin, JACC: Clinical Electrophysiology, Vol: 3, Pages: 186-188, ISSN: 2405-5018

A 53-year-old man with very frequent ventricular ectopic activity (39.4% burden) and a structurally normal heart was admitted for percutaneous ablation. Electrocardiography showed a bigeminal unifocal ventricular ectopic pattern, with a right bundle branch block configuration and superior axis, indicating likely origin at the inferior left ventricle.During mapping at the inferior left ventricle, multiple sites with good morphological match to the ectopic beats during pace mapping, and with early local electrograms relative to the QRS complex, were identified. Despite this, the proximal electrograms at these sites consistently preceded the distal bipolar electrograms (Figure 1A) with the mapping catheter oriented perpendicularly to the inferior left ventricular wall (Figures 1B and 1C). Figure 1D shows the good pace matches obtained from these sites. The locations of these sites were roughly in a circle (Figure 1B), presumed to represent sites encircling the posteromedial papillary muscle, with the origin of the ectopic activity at the mid–papillary muscle, which would account for the consistent finding of proximal electrograms preceding distal electrograms at the surrounding sites.

Journal article

Luther V, Linton NW, Jamil-Copley S, Koa-Wing M, Lim PB, Qureshi N, Ng FS, Hayat S, Whinnett Z, Davies DW, Peters NS, Kanagaratnam Pet al., 2016, A prospective study of ripple mapping the post-infarct ventricular scar to guide substrate ablation for ventricular tachycardia, Circulation: Arrhythmia and Electrophysiology, Vol: 9, Pages: 1-12, ISSN: 1941-3084

BACKGROUND: Post-infarct ventricular tachycardia is associated with channels of surviving myocardium within scar characterized by fractionated and low-amplitude signals usually occurring late during sinus rhythm. Conventional automated algorithms for 3-dimensional electro-anatomic mapping cannot differentiate the delayed local signal of conduction within the scar from the initial far-field signal generated by surrounding healthy tissue. Ripple mapping displays every deflection of an electrogram, thereby providing fully informative activation sequences. We prospectively used CARTO-based ripple maps to identify conducting channels as a target for ablation. METHODS AND RESULTS: High-density bipolar left ventricular endocardial electrograms were collected using CARTO3v4 in sinus rhythm or ventricular pacing and reviewed for ripple mapping conducting channel identification. Fifteen consecutive patients (median age 68 years, left ventricular ejection fraction 30%) were studied (6 month preprocedural implantable cardioverter defibrillator therapies: median 19 ATP events [Q1-Q3=4-93] and 1 shock [Q1-Q3=0-3]). Scar (<1.5 mV) occupied a median 29% of the total surface area (median 540 points collected within scar). A median of 2 ripple mapping conducting channels were seen within each scar (length 60 mm; initial component 0.44 mV; delayed component 0.20 mV; conduction 55 cm/s). Ablation was performed along all identified ripple mapping conducting channels (median 18 lesions) and any presumed interconnected late-activating sites (median 6 lesions; Q1-Q3=2-12). The diastolic isthmus in ventricular tachycardia was mapped in 3 patients and colocated within the ripple mapping conducting channels identified. Ventricular tachycardia was noninducible in 85% of patients post ablation, and 71% remain free of ventricular tachycardia recurrence at 6-month median follow-up. CONCLUSIONS: Ripple mapping can be used to identify conduction channels within scar to guide functional substrate

Journal article

Leong KMW, Ng FS, Yao C, Yates S, Taraborrelli P, Linton NW, Whinnett Z, LeFroy D, Davies DW, Lim PB, Peters NS, Harding SE, Kanagaratnam P, Varnava Aet al., 2016, Contribution of Conduction and Repolarisation Abnormalities to the Type I Brugada Pattern: A Study Using Non-Invasive Electrocardiographic Imaging, Annual Conference of the British Cardiovascular Society (BCS) on Prediction and Prevention, Publisher: BMJ Publishing Group, Pages: A105-A106, ISSN: 1468-201X

Conference paper

Leong KMW, Chow J-J, Ng FS, Yates S, Wright I, Luther V, David L, Qureshi N, Koa-Wing M, Whinnett Z, Linton NW, Davies DW, Lim PB, Peters NS, Kanagaratnam P, Varnava Aet al., 2016, Risk Stratification in Hypertrophic Cardiomyopathy: Evaluation of the European Society of Cardiology Sudden Cardiac Death Risk Scoring System, Annual Conference of the British Cardiovascular Society (BCS) on Prediction and Prevention, Publisher: BMJ Publishing Group, Pages: A104-A105, ISSN: 1355-6037

Conference paper

Ng FS, Ariff B, Punjabi PP, Hanna GB, Cousins J, Peters NS, Kanagaratnam P, Lim PBet al., 2016, Pyopneumopericardium Secondary to Pericardioesophageal Fistula After Radiofrequency Ablation of Atrial Fibrillation, JACC: Clinical Electrophysiology, Vol: 2, Pages: 397-399, ISSN: 2405-500X

Journal article

Ng FS, Kalindjian JM, Cooper SA, Chowdhury RA, Patel PM, Dupont E, Lyon AR, Peters NSet al., 2016, Enhancement of Gap Junction Function During Acute Myocardial Infarction Modifies Healing and Reduces Late Ventricular Arrhythmia Susceptibility, JACC. Clinical electrophysiology, Vol: 2, Pages: 574-582, ISSN: 2405-5018

Objectives: To investigate the effects of enhancing gap junction (GJ) coupling during acute myocardial infarction (MI) on the healed infarct scar morphology and late post-MI arrhythmia susceptibility. Background: Increased heterogeneity of myocardial scarring after MI is associated with greater arrhythmia susceptibility. We hypothesized that short-term enhancement of GJ coupling during acute MI can produce more homogeneous infarct scars, reducing late susceptibility to post-MI arrhythmias. Methods: Following arrhythmic characterisation of the rat 4-week post-MI model (n=24), a further 27 Sprague-Dawley rats were randomised to receive rotigaptide to enhance GJ coupling (n=13) or saline control (n=14) by osmotic minipump immediately prior to, and for the first 7 days following surgical MI. At 4 weeks post-MI, hearts were explanted for ex vivo programmed electrical stimulation (PES) and optical mapping. Heterogeneity of infarct border zone (IBZ) scarring was quantified by histomorphometry. Results: Despite no detectable difference in infarct size at 4 weeks post-MI, rotigaptide-treated hearts had reduced arrhythmia susceptibility during PES (Inducibility score: rotigaptide 2.40.8, control 5.00.6, p=0.02) and less heterogeneous IBZ scarring (standard deviation of IBZ Complexity Score: rotigaptide 1.10.1, control 1.40.1, p=0.04), associated with an improvement in IBZ conduction velocity (rotigaptide 43.13.4 cm/s, control 34.82.0 cm/s, p=0.04). Conclusions: Enhancement of GJ coupling for only 7 days at the time of acute MI produced more homogeneous IBZ scarring and reduced arrhythmia susceptibility at 4 weeks post-MI. Short-term GJ modulation at the time of MI may represent a novel treatment strategy to modify the healed infarct scar morphology and reduce late post-MI arrhythmic risk.

Journal article

Zuliani C, Ng FS, Alenda A, Eftekhar A, Peters NS, Toumazou Cet al., 2016, An array of individually addressable micro-needles for mapping pH distributions, Analyst, Vol: 141, Pages: 4659-4666, ISSN: 1364-5528

This work describes the preparation of an array of individually addressable pH sensitive microneedles which are sensitized by electrodepositing iridium oxide. The impact of the deposition potential, storage conditions and interferents on the sensor characteristics such as slope, offset, intra- and inter-batch reproducibility is investigated. The device may be a useful tool for carrying out direct pH measurements of soft and heterogeneous samples such as tissues and organs. For example, we demonstrated that the microneedle array can be employed for real-time mapping of the cardiac pH distribution during cycles of global ischemia and reperfusion.

Journal article

Luther V, Linton NW, Koa-Wing M, Lim PB, Jamil-Copley S, Qureshi N, Ng FS, Hayat S, Whinnett Z, Davies DW, Peters NS, Kanagaratnam Pet al., 2016, A prospective study of ripple mapping in atrial tachycardias: a novel approach to interpreting activation in low-voltage areas, Circulation: Arrhythmia and Electrophysiology, Vol: 9, Pages: 1-13, ISSN: 1941-3084

BACKGROUND: Post ablation atrial tachycardias are characterized by low-voltage signals that challenge current mapping methods. Ripple mapping (RM) displays every electrogram deflection as a bar moving from the cardiac surface, resulting in the impression of propagating wavefronts when a series of bars move consecutively. RM displays fractionated signals in their entirety thereby helping to identify propagating activation in low-voltage areas from nonconducting tissue. We prospectively used RM to study tachycardia activation in the previously ablated left atrium.METHODS AND RESULTS: Patients referred for atrial tachycardia ablation underwent dense electroanatomic point collection using CARTO3v4. RM was played over a bipolar voltage map and used to determine the voltage "activation threshold" that differentiated functional low voltage from nonconducting areas for each map. Ablation was guided by RM, but operators could perform entrainment or review the isochronal activation map for diagnostic uncertainty. Twenty patients were studied. Median RM determined activation threshold was 0.3 mV (0.19-0.33), with nonconducting tissue covering 33±9% of the mapped surface. All tachycardias crossed an isthmus (median, 0.52 mV, 13 mm) bordered by nonconducting tissue (70%) or had a breakout source (median, 0.35 mV) moving away from nonconducting tissue (30%). In reentrant circuits (14/20) the path length was measured (87-202 mm), with 9 of 14 also supporting a bystander circuit (path lengths, 147-234 mm). In breakout tachycardias, splitting of wavefronts resulted in 2 to 4 incomplete circuits. RM-guided ablation interrupted the tachycardia in 19 of 20 cases with the first ablation set. CONCLUSIONS: RM helps to define activation through low-voltage regions and aids ablation of atrial tachycardias.

Journal article

Kim M-Y, Ng FS, Ariff B, Hanna GB, Whinnett Z, Kanagaratnam P, Tanner M, Lim PBet al., 2015, Extensive Intramural Esophageal Hematoma After Transesophageal Echocardiography During Atrial Fibrillation Ablation, CIRCULATION, Vol: 132, Pages: 1847-1849, ISSN: 0009-7322

Journal article

Boukens BJ, Sulkin MS, Gloschat CR, Fu SN, Vigmond EJ, Efimov IRet al., 2015, Transmural APD gradient synchronizes repolarization in the human left ventricular wall, CARDIOVASCULAR RESEARCH, Vol: 108, Pages: 188-196, ISSN: 0008-6363

Journal article

Cantwell CD, Roney CH, Ng FS, Siggers JH, Sherwin SJ, Peters NSet al., 2015, Techniques for automated local activation time annotation and conduction velocity estimation in cardiac mapping, Computers in Biology and Medicine, Vol: 65, Pages: 229-242, ISSN: 0010-4825

Measurements of cardiac conduction velocity provide valuable functional and structural insight into the initiation and perpetuation of cardiac arrhythmias, in both a clinical and laboratory context. The interpretation of activation wavefronts and their propagation can identify mechanistic properties of a broad range of electrophysiological pathologies. However, the sparsity, distribution and uncertainty of recorded data make accurate conduction velocity calculation difficult. A wide range of mathematical approaches have been proposed for addressing this challenge, often targeted towards specific data modalities, species or recording environments. Many of these algorithms require identification of activation times from electrogram recordings which themselves may have complex morphology or low signal-to-noise ratio. This paper surveys algorithms designed for identifying local activation times and computing conduction direction and speed. Their suitability for use in different recording contexts and applications is assessed.

Journal article

Ng FS, Lyon AR, Shadi IT, Chang ETY, Chowdhury RA, Dupont E, Peters NSet al., 2015, Modulation of Gap Junctional Coupling as an Anti-Arrhythmic Strategy to Prevent Reperfusion Ventricular Fibrillation, SET for Britain 2010 (House of Commons, UK Parliament)

Conference paper

Ng FS, Lyon AR, Shadi IT, Chang ETY, Chowdhury RA, Dupont E, Peters NSet al., 2015, Gap Junctional Uncoupling with Carbenoxolone Slows Conduction and Increases Vulnerability to Ventricular Arrhythmias in Structurally Normal Hearts: An Optical Mapping Study, British Cardiovascular Society Annual Conference 2010, Pages: A5-A6

Conference paper

Tzortzis KN, Roney CH, Qureshi NA, Ng FU, Lim PHANGBOON, Sherwin S, Peters NS, Cantwell Cet al., 2015, Influence of left atrial geometry on rotor core trajectories in a model of atrial fibrillation, Computing in Cardiology, Publisher: IEEE, Pages: 481-484, ISSN: 2325-8861

Left atrial anatomy and myocardial architecture areknown to influence rotor initiation and maintenance.However, identifying their relative contribution clinicallyis challenging. The present study aims to investigate insilico the effect of left atrial geometry in isolation onrotor generation and evolution through thespatiotemporal tracking of phase singularities. Aftermeandering for a short period of time, rotors areattracted to specific areas of the chamber where there ishigh curvature, primarily near the base of the left atrialappendage and the junctions of the pulmonary veins. Thissuggests that the left atrial anatomy could play a key rolein the perpetuation of fibrillatory activity.

Conference paper

Ng FS, Roney CH, Debney MT, Eichhorn C, Nachiappan A, Qureshi N, Chowdhury RA, Kanagaratnam P, Lyon AR, Peters NSet al., 2015, Anatomical and functional determinants of preferential rotor locations and stability in atrial fibrillation, Congress of the European-Society-of-Cardiology (ESC), Publisher: OXFORD UNIV PRESS, Pages: 568-568, ISSN: 0195-668X

Conference paper

Ng FS, Behradfar E, Debney MT, Nygren A, Hartley A, Lyon AR, Efimov IR, Vigmond E, Peters NSet al., 2015, Activation of normally quiescent Purkinje-myocardial junctions during acute myocardial ischaemia - an unexplored arrhythmogenic mechanism, Congress of the European-Society-of-Cardiology (ESC), Publisher: OXFORD UNIV PRESS, Pages: 214-214, ISSN: 0195-668X

Conference paper

Leong KMW, Ng FS, Roney C, Lim PB, Peters NS, Varnava A, Kanagaratnam Pet al., 2015, DYNAMIC CHARACTERISATION OF THE ELECTROPHYSIOLOGICAL SUBSTRATE IN BRUGADA SYNDROME DURING PHYSIOLOGICAL AUTONOMIC STIMULATION, British-Cardiac-Society (BCS) Annual Conference on Hearts and Genes, Publisher: BMJ PUBLISHING GROUP, Pages: A36-A37, ISSN: 1355-6037

Conference paper

Tondato F, Zeng H, Goodchild T, Ng FS, Chronos N, Peters NSet al., 2015, Autologous Dermal Fibroblast Injections Slow Atrioventricular Conduction and Ventricular Rate in Atrial Fibrillation in Swine, Circulation-Arrhythmia and Electrophysiology, Vol: 8, Pages: 439-446, ISSN: 1941-3149

Journal article

Roney CH, Tzortzis KN, Cantwell CD, Qureshi NA, Ali RL, Lim PB, Siggers JH, Ng FS, Peters NSet al., 2015, A Technique for Visualising Three-Dimensional Left Atrial Cardiac Activation Data in Two Dimensions with Minimal Distance Distortion, 37th Annual International Conference of the IEEE-Engineering-in-Medicine-and-Biology-Society (EMBC), Publisher: IEEE, Pages: 7296-7299, ISSN: 1557-170X

Conference paper

Sulkin MS, Boukens BJ, Tetlow M, Gutbrod SR, Ng FS, Efimov IRet al., 2014, Mitochondrial depolarization and electrophysiological changes during ischemia in the rabbit and human heart, AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, Vol: 307, Pages: H1178-H1186, ISSN: 0363-6135

Journal article

Ng FS, Debney MT, Protti A, Lyon AR, Shah AM, Peters NSet al., 2014, 15Early pharmacological enhancement of gap junction coupling with rotigaptide reduces arrhythmia vulnerability and modulates structural remodelling in reperfused myocardial infarction., Europace, Vol: 16 Suppl 3

Survivors of myocardial infarction (MI) are at increased risk of late ventricular arrhythmias and sudden cardiac death with infarct size and scar heterogeneity as key determinants of arrhythmic risk. Current preventative strategies are limited to few, select antiarrhythmic drugs or an implantable cardioverter-defibrillator. Cardiac gap junctions (GJ) have a key role in allowing the passage of small molecules between cells and may mediate the spread of acute myocardial infarction. We hypothesised that enhancing GJ coupling in the acute phase of MI may beneficially modify the extent and pattern of necrosis and infarction acutely, thus affording a protective effect against late arrhythmogenesis.

Journal article

Ng FS, Holzem KM, Koppel AC, Janks D, Gordon F, Wit AL, Peters NS, Efimov IRet al., 2014, Adverse Remodeling of the Electrophysiological Response to Ischemia-Reperfusion in Human Heart Failure Is Associated With Remodeling of Metabolic Gene Expression, CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY, Vol: 7, Pages: 875-U234, ISSN: 1941-3149

Journal article

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