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Dive into the research topics where Neil C. Davidson is active.

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Featured researches published by Neil C. Davidson.


Circulation | 2003

Electrical Remodeling of the Atria in Congestive Heart Failure Electrophysiological and Electroanatomic Mapping in Humans

Prashanthan Sanders; Joseph B. Morton; Neil C. Davidson; Steven J. Spence; Jitendra K. Vohra; Paul B. Sparks; Jonathan M. Kalman

Background—Atrial fibrillation (AF) frequently complicates congestive heart failure (CHF). However, the electrophysiological substrate for AF in humans with CHF remains unknown. We evaluated the electrophysiological and electroanatomic characteristics of the atria in patients with CHF. Methods and Results—Twenty-one patients (aged 53.7±13.6 years) with symptomatic CHF (left ventricular ejection fraction 25.5±6.0%) and 21 age-matched controls were studied. The following were evaluated: effective refractory periods (ERPs) from the high and low lateral right atrium (LRA), high septal right atrium, and distal coronary sinus (CS); conduction time along the CS and LRA; corrected sinus node recovery times; P-wave duration; and conduction at the crista terminalis. In a subset, electroanatomic mapping was performed to determine atrial activation, regional conduction velocity, double potentials, fractionated electrograms, regional voltage, and areas of electrical silence. Patients with CHF demonstrated an increase in atrial ERP with no change in the heterogeneity of refractoriness, an increase of atrial conduction time along the LRA and the CS, prolongation of the P-wave duration and corrected sinus node recovery times, and greater number and duration of double potentials along the crista terminalis. Electroanatomic mapping demonstrated regional conduction slowing with a greater number of electrograms with fractionation or double potentials, associated with areas of low voltage and electrical silence (scar). Patients with CHF demonstrated an increased propensity for AF with single extrastimuli, and induced AF was more often sustained. Conclusions—Atrial remodeling due to CHF is characterized by structural changes, abnormalities of conduction, sinus node dysfunction, and increased refractoriness. These abnormalities may be responsible in part for the increased propensity for AF in CHF.


The Lancet | 2010

Cardiovascular effects of marine omega-3 fatty acids.

Palaniappan Saravanan; Neil C. Davidson; Erik Berg Schmidt; Philip C. Calder

Much evidence shows that the marine omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid have beneficial effects in various cardiac disorders, and their use is recommended in guidelines for management of patients after myocardial infarction. However, questions have been raised about their usefulness alongside optimum medical therapies with agents proven to reduce risk of cardiac events in high-risk patients. Additionally, there is some evidence for a possible pro-arrhythmic effect in subsets of cardiac patients. Some uncertainly exists about the optimum dose needed to obtain beneficial effects and the relative merit of dietary intake of omega-3 polyunsaturated fatty acids versus supplements. We review evidence for the effects of omega-3 polyunsaturated fatty acids on various cardiac disorders and the risk factors for cardiac disease. We also assess areas of uncertainty needing further research.


Circulation | 2004

Electrophysiological and Electroanatomic Characterization of the Atria in Sinus Node Disease Evidence of Diffuse Atrial Remodeling

Prashanthan Sanders; Joseph B. Morton; Peter M. Kistler; Steven J. Spence; Neil C. Davidson; Azlan Hussin; Jitendra K. Vohra; Paul B. Sparks; Jonathan M. Kalman

Background—The normal sinus pacemaker complex is an extensive structure within the right atrium. We hypothesized that patients with sinus node disease (SND) would have evidence of diffuse atrial abnormalities. Methods and Results—Sixteen patients with symptomatic SND and 16 age-matched controls were studied. The following were evaluated: effective refractory periods (ERPs) from the high and low lateral right atrium (RA), high septal RA, and distal coronary sinus (CS); conduction time along the CS and lateral RA; P-wave duration; and conduction at the crista terminalis. Electroanatomic mapping was performed to define the sinus node complex and determine regional conduction velocity, double potentials, fractionated electrograms, regional voltage, and areas of electrical silence. Patients with SND demonstrated significant increase in atrial ERP at all right atrial sites, increased atrial conduction time along the lateral RA and CS, prolongation of the P-wave duration, and greater number and duration of double potentials along the crista terminalis. Electroanatomic mapping demonstrated the sinus node complex in SND to be more often unicentric, localized to the low crista terminalis at the site of the largest residual voltage amplitude. There was significant regional conduction slowing with double potentials and fractionation associated with areas of low voltage and electrical silence (or scar). Conclusions—SND is associated with diffuse atrial remodeling characterized by structural change, conduction abnormalities, and increased right atrial refractoriness. There was a change in the nature of sinus pacemaker activity with loss of the normal multicentric pattern of activation, caudal shift of the pacemaker complex, and abnormal and circuitous conduction around lines of conduction block.


Circulation-arrhythmia and Electrophysiology | 2010

Omega-3 Fatty Acid Supplementation Does Not Reduce Risk of Atrial Fibrillation After Coronary Artery Bypass Surgery A Randomized, Double-Blind, Placebo-Controlled Clinical Trial

Palaniappan Saravanan; Ben Bridgewater; Annette L. West; S. C. O'Neill; Philip C. Calder; Neil C. Davidson

Background—Omega-3 polyunsaturated fatty acids (n-3 PUFA) have been reported to reduce the risk of sudden cardiac death presumed to be due to fatal ventricular arrhythmias, but their effect on atrial arrhythmias is unclear. Methods and Results—Patients (n=108) undergoing coronary artery bypass graft surgery were randomly assigned to receive 2 g/d n-3 PUFA or placebo (olive oil) for at least 5 days before surgery (median, 16 days; range, 12 to 21 days). Phospholipid n-3 PUFA were measured in serum at study entry and at surgery and in right atrial appendage tissue at surgery. Echocardiography was used to assess left ventricular function and left atrial dimensions. Postoperative continuous ECG monitoring (Lifecard CF) for 5 days or until discharge, if earlier, was performed with a daily 12-lead ECG and clinical review if patients remained in the hospital beyond 5 days. Lifecard recordings were analyzed for episodes of atrial fibrillation (AF) ≥30 seconds (primary outcome). Clinical AF, AF burden (% time in AF), hospital stay, and intensive care/high dependency care stay were measured as secondary outcomes. One hundred three patients completed the study (51 in the placebo group and 52 in the n-3 PUFA group). There were no clinically relevant differences in baseline characteristics between groups. n-3 PUFA levels were higher in serum and right atrial tissue in the active treatment group. There was no significant difference between groups in the primary outcome of AF (95% confidence interval [CI], −6% to 30%, P=0.28) in any of the secondary outcomes or in AF-free survival. Conclusions—Omega-3 PUFA do not reduce the risk of AF after coronary artery bypass graft surgery. Clinical Trial Registration—www.ukcrn.org.uk. Identifier: 4437.


Journal of Cardiovascular Electrophysiology | 2003

Phased-array intracardiac echocardiography for defining cavotricuspid isthmus anatomy during radiofrequency ablation of typical atrial flutter.

Joseph B. Morton; Prashanthan Sanders; Neil C. Davidson; Paul B. Sparks; Jitendra K. Vohra; Jonathan M. Kalman

Introduction: Cavotricuspid isthmus (CTI) topography includes ridges, pouches, recesses, and trabeculations. These features may limit the success of radiofrequency ablation (RFA) of typical atrial flutter (AFL). The aim of this study was to assess the utility of phased‐array intracardiac echocardiography (ICE) for imaging the CTI and monitoring RFA of AFL.


Circulation-arrhythmia and Electrophysiology | 2010

Risk Assessment for Sudden Cardiac Death in Dialysis Patients

Palaniappan Saravanan; Neil C. Davidson

Patients with end-stage renal disease (ESRD) on long-term dialysis therapy have very high mortality due to predominantly cardiovascular causes1 (Figure 1). Sudden cardiac death (SCD) is the single most common form of death in dialysis patients, accounting for 20% to 30% of all deaths in this cohort.2,3 These patients indeed have a very high burden of coronary artery disease (CAD), and a proportion of SCD events could be due to obstructive CAD.1,2 However, epidemiological and observational studies have reported that the overall incidence of SCD in this population is much greater than the incidence of coronary events,4,5 and the risk of SCD persists even after coronary revascularization.6 These findings suggest a possibility of a primary increase in the risk of fatal ventricular arrhythmias, which is the most common cause of SCD. Dialysis patients with ESRD have several factors that could predispose them to a high risk of ventricular arrhythmias (Table 1). A large number of dialysis patients have diabetes, and thus, autonomic neuropathy as a consequence of both chronic uremia and coexisting diabetes is very common,7 resulting in alterations in autonomic control with a sustained increase in the sympathetic tone reported to be proarrhythmic. Similarly, hypertension is very common, and uremia leads to secondary hyperparathyroidism, both of which lead to considerable left ventricular hypertrophy (LVH).8 In addition, chronic uremia leads to endothelial dysfunction, and the combination of endothelial dysfunction and LVH compromises perfusion reserve and makes the individual susceptible to arrhythmias precipitated by ischemia. Long-standing uremia leads to uremic cardiomyopathy, with typical changes of diffuse myocardial fibrosis,9 which could lead to slowing of conduction and increased dispersion of repolarization, both of which have been shown to be proarrhythmic.10 Significant sudden shifts in electrolytes and fluid volume that surrounds a dialysis session acts as a trigger and can initiate life-threatening arrhythmias in patients with a susceptible substrate.11 Hence, it is conceivable that risk assessment tests that evaluate these variables could be used to identify dialysis patients at risk of SCD. In this review, we discuss the rationale behind the use of specific risk assessments to evaluate the risk of SCD in the dialysis cohort and review the current evidence on the use of some of these tests in dialysis patients with ESRD. Left Ventricular Systolic Dysfunction and Risk of SCD in Dialysis Severe left ventricular systolic dysfunction (LVSD) is reported to be a reliable indicator of high risk of SCD12 and has been used as the single most important variable in selecting patients for implantable cardioverter defibrillators (ICDs). Notably, clinical trials on ICD either actively excluded or had very few patients with ESRD.13 When patients with ESRD received an ICD, the main parameter used to decide on the need for an ICD was severe LVSD.1 A large number of dialysis patients who died suddenly did not have significant LVSD,14 and 1 prospective study of mortality in a dialysis population reported that severe LVSD was not an independent predictor of SCD.3 Thus, it is likely that a significant proportion of patients with ESRD with a high risk of SCD may have preserved left ventricular systolic function and by using LVSD as the main risk identifier, these patients who arguably might have lower risk of nonarrhythmic mortality, particularly that related to pump failure, will be missed. In that context, 1 study reported that the current risk assessment model identifies far fewer patients than would be expected to have a potential risk of SCD, thus indicating a need for specific risk assessment to address the unique features that predispose dialysis patients to SCD15 and enable appropriate intervention, such as an ICD, to be tested in those found to be at highest risk.


Circulation | 2002

Reversal of Atrial Mechanical Stunning After Cardioversion of Atrial Arrhythmias Implications for the Mechanisms of Tachycardia-Mediated Atrial Cardiomyopathy

Prashanthan Sanders; Joseph B. Morton; John G. Morgan; Neil C. Davidson; Steven J. Spence; Jitendra K. Vohra; Jonathan M. Kalman; Paul B. Sparks

Background—Atrial mechanical stunning develops on termination of chronic atrial arrhythmias and is implicated in the genesis of thromboembolic complications after cardioversion. The mechanisms responsible for atrial mechanical stunning are unknown. The effects of atrial rate, isoproterenol, and calcium on atrial mechanical function in patients with atrial stunning have not been evaluated, and it is not known if atrial stunning can be reversed. Methods and Results—Thirty-five patients with chronic atrial flutter (AFL) undergoing radiofrequency ablation were studied. Fifteen patients in sinus rhythm undergoing ablation for paroxysmal AFL were studied as control for effects of the procedure. Left atrial appendage emptying velocities (LAAEVs) and spontaneous echocardiographic contrast (LASEC) were assessed by transesophageal echocardiography during AFL, after reversion to sinus rhythm, during atrial pacing at cycle lengths of 750 to 250 ms, after a postpacing pause, and with isoproterenol or calcium. With termination of AFL, LAAEV decreased from 59.0±3.7 cm/s to 18.8±1.4 cm/s (P <0.0001) and LASEC grade increased from 0.9±0.1 to 2.2±0.2 (P <0.0001). Pacing increased LAAEV to a maximum of 38.4±3.2 cm/s (P <0.0001) and reduced LASEC grade to 1.9±0.2 (P =0.005). Isoproterenol and calcium reversed atrial mechanical stunning with LAAEV increasing to 89.3±12.6 cm/s (P =0.0007) and 50.2±10.5 cm/s (P =0.005), respectively, and LASEC grade decreasing to 0.2±0.1 (P =0.001) and 1.4±0.2 (P =0.01), respectively. The postpacing pause increased LAAEV to 69.3±3.7 cm/s (P <0.0001). No change in LAAEV was observed in the paroxysmal AFL group. Conclusion—Atrial mechanical stunning can be reversed by pacing at increased rates and through the administration of isoproterenol or calcium. These findings suggest a functional contractile apparatus in the mechanically remodeled atrium as a result of chronic atrial flutter.


Internal Medicine Journal | 2002

Immediate and long-term results of radiofrequency ablation of pulmonary vein ectopy for cure of paroxysmal atrial fibrillation using a focal approach.

Prashanthan Sanders; Joseph B. Morton; Vincent R. Deen; Neil C. Davidson; Paul B. Sparks; Jitendra K. Vohra; Jonathan M. Kalman

Background: Atrial fibrillation (AF) is frequently initiated by focal activity originating in the pulmonary veins. We present the early and long‐term results of a focal approach to pulmonary‐vein ablation for cure of paroxysmal AF.


Pacing and Clinical Electrophysiology | 2007

Safety and acceptability of implantation of internal cardioverter-defibrillators under local anesthetic and conscious sedation.

David J. Fox; Neil C. Davidson; David H. Bennett; Bernard Clarke; Clifford J. Garratt; Mark Hall; Amir Zaidi; Kay Patterson; A. Fitzpatrick

Background: Implantation and testing of implantable defibrillators (ICDs) using local anesthetic and conscious sedation is widely practiced; however, some centers still use general anesthesia. We assessed safety and patient acceptability for implantation of defibrillators using local anesthetic and conscious sedation.


Europace | 2016

Low rate of asymptomatic cerebral embolism and improved procedural efficiency with the novel pulmonary vein ablation catheter GOLD: results of the PRECISION GOLD trial

Yves De Greef; Lukas R.C. Dekker; Lucas Boersma; Stephen Murray; Marcus Wieczorek; Stefan G. Spitzer; Neil C. Davidson; Steve Furniss; Mélèze Hocini; J. Christoph Geller; Zoltán Csanádi

Abstract Aims This prospective, multicentre study (PRECISION GOLD) evaluated the incidence of asymptomatic cerebral embolism (ACE) after pulmonary vein isolation (PVI) using a new gold multi-electrode radiofrequency (RF) ablation catheter, pulmonary vein ablation catheter (PVAC) GOLD. Also, procedural efficiency of PVAC GOLD was compared with ERACE. The ERACE study demonstrated that a low incidence of ACE can be achieved with a platinum multi-electrode RF catheter (PVAC) combined with procedural manoeuvres to reduce emboli. Methods and results A total of 51 patients with paroxysmal atrial fibrillation (AF) (age 57 ± 9 years, CHA2DS2-VASc score 1.4 ± 1.4) underwent AF ablation with PVAC GOLD. Continuous oral anticoagulation using vitamin K antagonists, submerged catheter introduction, and heparinization (ACT ≥ 350 s prior to ablation) were applied. Cerebral magnetic resonance imaging (MRI) scans were performed within 48 h before and 16–72 h post-ablation. Cognitive function assessed by the Mini-Mental State Exam at baseline and 30 days post-ablation. New post-procedural ACE occurred in only 1 of 48 patients (2.1%) and was not detectable on MRI after 30 days. The average number of RF applications per patient to achieve PVI was lower in PRECISION GOLD (20.3 ± 10.0) than in ERACE (28.8 ± 16.1; P = 0.001). Further, PVAC GOLD ablations resulted in significantly fewer low-power (<3 W) ablations (15 vs. 23%, 5 vs. 10% and 2 vs. 7% in 4:1, 2:1, and 1:1 bipolar:unipolar energy modes, respectively). Mini-Mental State Exam was unchanged in all patients. Conclusion Atrial fibrillation ablation with PVAC GOLD in combination with established embolic lowering manoeuvres results in a low incidence of ACE. Pulmonary vein ablation catheter GOLD demonstrates improved biophysical efficiency compared with platinum PVAC. Trial registration ClinicalTrials.gov NCT01767558.

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David J. Fox

Manchester Royal Infirmary

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A. Fitzpatrick

Manchester Royal Infirmary

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Paul B. Sparks

University of California

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