Publications by authors named "Robert Gow"

48 Publications

The impact of the Auckland cellulitis pathway on length of hospital stay, mortality readmission rate, and antibiotic stewardship.

Clin Infect Dis 2021 Feb 26. Epub 2021 Feb 26.

Department of Infectious Diseases, Auckland District Health Board, Auckland, New Zealand.

Background: The Dundee classification of cellulitis severity, previously shown to predict disease outcomes, provides an opportunity to improve the management of patients with cellulitis.

Methods: We developed and implemented a pathway to guide the management of adults with cellulitis based on their Dundee severity class, and measured its effect on patient outcomes. We compared the outcomes in patients admitted to Auckland City Hospital (ACH) between July 2014 and July 2015 (the baseline cohort) with those in patients admitted between June 2017 and June 2018 (the intervention cohort).

Results: The median length of stay was shorter in the intervention cohort (0.7 days, IQR 0.1 to 3.0 days) than in the baseline cohort (1.8 days, IQR 0.1 to 4.4 days; P<0.001). The 30 day mortality rate declined from 1.8% (19/1092) in the baseline cohort to 0.7% (10/1362; P=0.02) in the intervention cohort. The 30 day cellulitis readmission rate increased from 6% in the baseline cohort to 11% (P<0.001) in the intervention cohort. Adherence to the ACH cellulitis antibiotic guideline improved from 38% to 48% (P<0.01) and was independently associated with reduced length of stay.

Conclusions: The implementation of the Auckland cellulitis pathway, readily generalizable to other settings, improved the outcomes in patients with cellulitis, and resulted in an annual saving of approximately 1,000 bed days.
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http://dx.doi.org/10.1093/cid/ciab181DOI Listing
February 2021

An International Multicenter Evaluation of Type 5 Long QT Syndrome: A Low Penetrant Primary Arrhythmic Condition.

Circulation 2020 02 16;141(6):429-439. Epub 2020 Jan 16.

Department of Cardiovascular Medicine, Division of Heart Rhythm Services, Department of Pediatric and Adolescent Medicine, Division of Pediatric Cardiology, Department of Molecular Pharmacology & Experimental Therapeutics, Windland Smith Rice Sudden Death Genomics Laboratory, Mayo Clinic, Rochester, MN (M.B., J.R.G., M.J.A.).

Background: Insight into type 5 long QT syndrome (LQT5) has been limited to case reports and small family series. Improved understanding of the clinical phenotype and genetic features associated with rare variants implicated in LQT5 was sought through an international multicenter collaboration.

Methods: Patients with either presumed autosomal dominant LQT5 (N = 229) or the recessive Type 2 Jervell and Lange-Nielsen syndrome (N = 19) were enrolled from 22 genetic arrhythmia clinics and 4 registries from 9 countries. variants were evaluated for ECG penetrance (defined as QTc >460 ms on presenting ECG) and genotype-phenotype segregation. Multivariable Cox regression was used to compare the associations between clinical and genetic variables with a composite primary outcome of definite arrhythmic events, including appropriate implantable cardioverter-defibrillator shocks, aborted cardiac arrest, and sudden cardiac death.

Results: A total of 32 distinct rare variants were identified in 89 probands and 140 genotype positive family members with presumed LQT5 and an additional 19 Type 2 Jervell and Lange-Nielsen syndrome patients. Among presumed LQT5 patients, the mean QTc on presenting ECG was significantly longer in probands (476.9±38.6 ms) compared with genotype positive family members (441.8±30.9 ms, <0.001). ECG penetrance for heterozygous genotype positive family members was 20.7% (29/140). A definite arrhythmic event was experienced in 16.9% (15/89) of heterozygous probands in comparison with 1.4% (2/140) of family members (adjusted hazard ratio [HR] 11.6 [95% CI, 2.6-52.2]; =0.001). Event incidence did not differ significantly for Type 2 Jervell and Lange-Nielsen syndrome patients relative to the overall heterozygous cohort (10.5% [2/19]; HR 1.7 [95% CI, 0.3-10.8], =0.590). The cumulative prevalence of the 32 variants in the Genome Aggregation Database, which is a human database of exome and genome sequencing data from now over 140 000 individuals, was 238-fold greater than the anticipated prevalence of all LQT5 combined (0.238% vs 0.001%).

Conclusions: The present study suggests that putative/confirmed loss-of-function variants predispose to QT prolongation, however, the low ECG penetrance observed suggests they do not manifest clinically in the majority of individuals, aligning with the mild phenotype observed for Type 2 Jervell and Lange-Nielsen syndrome patients.
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http://dx.doi.org/10.1161/CIRCULATIONAHA.119.043114DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7035205PMC
February 2020

Stress reactivity in healthy child offspring of parents with anxiety disorders.

Psychiatry Res 2019 02 3;272:756-764. Epub 2019 Jan 3.

University of Ottawa, Ottawa, Ontario, Canada; Institut du savoir Montfort, Ottawa, Ontario, Canada.

Several studies suggest that anxiety disorders (AD) involve dysregulation of the autonomic nervous system (ANS) and hypothalamic-pituitary (HPA) axis. However, it is unknown if alterations in these biological systems are premorbid markers of AD risk or a state-dependent feature of anxiety. This study examined ANS and HPA-axis response to a laboratory stressor in healthy child offspring of parents with (n = 55) and without (n = 98) a history of AD. High frequency heart rate variability (HF-HRV) was assessed during sitting and standing baseline conditions and during a speech task where participants remained standing. Salivary cortisol was measured at baseline and at 15, 30, 45 and 60 min post-speech. Subjective anxiety was assessed with a visual analogue scale. Children of parents with AD displayed reduced HRV and a blunted cortisol response to the speech task compared to children of non-anxious parents. No risk group effect was found for anxiety ratings. These preliminary data suggest that healthy children of anxious parents exhibit altered stress reactivity to an acute laboratory stressor. Further research is needed to confirm findings and identify mechanisms that may account for altered self-regulation processes to a stressor in children at familial risk for AD.
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http://dx.doi.org/10.1016/j.psychres.2018.12.171DOI Listing
February 2019

The mental health of adolescents and pre-adolescents living with inherited arrhythmia syndromes: a systematic review of the literature.

Cardiol Young 2018 May 18;28(5):621-631. Epub 2018 Jan 18.

2Department of Paediatrics, Faculty of Medicine,University of Ottawa,Ottawa,Ontario,Canada.

Potentially fatal arrhythmias add to the mental health challenges of adolescence. This systematic review sought to summarise current knowledge regarding the mental health of adolescents and pre-adolescents diagnosed with inherited arrhythmia syndromes. Searches combining psychological problems with inherited cardiac arrhythmia diagnoses identified 16 studies with paediatric (<18 years) inherited arrhythmia patients. All studies were cross-sectional; 8/16 required an implantable cardioverter defibrillator. Methods were quantitative (n=11), qualitative (n=4), or mixed (n=1), with 14-100% of participants having an inherited arrhythmia syndrome. Mean/median age in 13/16 studies was 12-16 years. Patients and parents reported lower quality of life, particularly in relation to physical function, social relationships, restriction of peer activities, bodily pain, and mental and emotional health. Self-perceptions and behaviour were similar to healthy populations. Rates of anxiety and depression (15-33% of these patients) were not increased in these studies where patients were assessed 2+ years after diagnosis. Higher mental health risk occurred among patients who have a diagnosed sibling, those with cardiomyopathy, and those who report decreased quality of life. Mental health research among youth with inherited arrhythmias is extremely limited and of low quality. Data, primarily from patients 2-4 years after diagnosis or treatment with an implantable cardioverter defibrillator, indicate that quality of life may be decreased and 15-33% experience mental health issues. Future research is required to examine the mental health and quality of life of paediatric patients with inherited arrhythmia syndromes, whether or not they have an implantable cardioverter defibrillator, from time of diagnosis.
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http://dx.doi.org/10.1017/S104795111700289XDOI Listing
May 2018

How to measure a QT interval.

Med J Aust 2017 08;207(3):107-110

Starship Children's Health, Auckland, New Zealand.

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http://dx.doi.org/10.5694/mja16.00442DOI Listing
August 2017

Letter by Gow Regarding Article, "Clinical Management of Catecholaminergic Polymorphic Ventricular Tachycardia: The Role of Left Cardiac Sympathetic Denervation".

Authors:
Robert M Gow

Circulation 2016 Jan;133(4):e365

Inherited Arrhythmia Clinic, Children's Hospital of Eastern Ontario, University of Ottawa Faculty of Medicine, Ottawa, ON, Canada.

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http://dx.doi.org/10.1161/CIRCULATIONAHA.115.018881DOI Listing
January 2016

A novel NaV1.5 voltage sensor mutation associated with severe atrial and ventricular arrhythmias.

J Mol Cell Cardiol 2016 Mar 19;92:52-62. Epub 2016 Jan 19.

Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, NC, United States; Ion Channel Research Unit, Duke University Medical Center, Durham, NC, United States; Department of Neurobiology, Duke University Medical Center, Durham, NC, United States. Electronic address:

Background: Inherited autosomal dominant mutations in cardiac sodium channels (NaV1.5) cause various arrhythmias, such as long QT syndrome and Brugada syndrome. Although dozens of mutations throughout the protein have been reported, there are few reported mutations within a voltage sensor S4 transmembrane segment and few that are homozygous. Here we report analysis of a novel lidocaine-sensitive recessive mutation, p.R1309H, in the NaV1.5 DIII/S4 voltage sensor in a patient with a complex arrhythmia syndrome.

Methods And Results: We expressed the wild type or mutant NaV1.5 heterologously for analysis with the patch-clamp and voltage clamp fluorometry (VCF) techniques. p.R1309H depolarized the voltage-dependence of activation, hyperpolarized the voltage-dependence of inactivation, and slowed recovery from inactivation, thereby reducing the channel availability at physiologic membrane potentials. Additionally, p.R1309H increased the "late" Na(+) current. The location of the mutation in DIIIS4 prompted testing for a gating pore current. We observed an inward current at hyperpolarizing voltages that likely exacerbates the loss-of-function defects at resting membrane potentials. Lidocaine reduced the gating pore current.

Conclusions: The p.R1309H homozygous NaV1.5 mutation conferred both gain-of-function and loss-of-function effects on NaV1.5 channel activity. Reduction of a mutation-induced gating pore current by lidocaine suggested a therapeutic mechanism.
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http://dx.doi.org/10.1016/j.yjmcc.2016.01.014DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4789166PMC
March 2016

Pulse Oximetry Waveform: Important Bedside Tool to Assess Cardiac Tamponade.

J Pediatr 2016 Feb 24;169:320-320.e1. Epub 2015 Nov 24.

University of Ottawa, Ottawa, Ontario, Canada.

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http://dx.doi.org/10.1016/j.jpeds.2015.10.094DOI Listing
February 2016

Impact of a restrictive drug access program on the risk of cardiovascular encounters in children exposed to ADHD medications.

J Popul Ther Clin Pharmacol 2014 8;21(3):e357-69. Epub 2014 Oct 8.

Background: ADHD medications increase clinical encounters for cardiovascular symptoms. Uncertain are the roles of differences in ADHD medications and restrictive practices by drug programs.

Methods: We conducted two nested case-control studies. The first was nested within a cohort of children de novo users of methylphenidate, amphetamines or atomoxetine and the second case-control study was nested within a subcohort of de novo amphetamine or atomoxetine users with no cardiovascular events prior to the first dispensing of either drug. The outcome for both studies was the composite of physician visits, emergency room visits or hospitalizations for cardiovascular reasons. Cases were matched on sex, age and date of entry within the cohorts, with up to 10 controls. Patients with an active dispensation of ADHD medications at the index date (and up to 90 days previously) were considered exposed. Conditional logistic regression was used to calculate odd ratios (OR).

Results: The full cohort comprised 38,495 patients. Among these patients, 3595 (9.3%) had no prior cardiovascular events (the subcohort). In the full cohort, an association was demonstrated with exposure to amphetamine and atomoxetine (but not methylphenidate) and the cardiovascular encounter outcomes. When the sub-cohort was analyzed the associations with amphetamine or atomoxetine were no longer evident.

Conclusion: Reimbursement policies need to be considered when conducting observational studies. Had the analysis been conducted without consideration of these policies the results would have incorrectly identified amphetamine and atomoxetine as important risk factors for cardiovascular encounters.
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June 2015

Do sugar-sweetened beverages cause adverse health outcomes in children? A systematic review protocol.

Syst Rev 2014 Sep 4;3:96. Epub 2014 Sep 4.

Healthy Active Living and Obesity Research Group, Children's Hospital of Eastern Ontario Research Institute, 401 Smyth Road, Ottawa, ON K1H 8L1, Canada.

Background: Cardiovascular disease and type 2 diabetes are examples of chronic diseases that impose significant morbidity and mortality in the general population worldwide. Most chronic diseases are associated with underlying preventable risk factors, such as elevated blood pressure, high blood glucose or glucose intolerance, high lipid levels, physical inactivity, excessive sedentary behaviours, and overweight/obesity. The occurrence of intermediate outcomes during childhood increases the risk of disease in adulthood. Sugar-sweetened beverages are known to be significant sources of additional caloric intake, and given recent attention to their contribution in the development of chronic diseases, a systematic review is warranted. We will assess whether the consumption of sugar-sweetened beverages in children is associated with adverse health outcomes and what the potential moderating factors are.

Methods/design: Of interest are studies addressing sugar-sweetened beverage consumption, taking a broad perspective. Both direct consumption studies as well as those evaluating interventions that influence consumption (e.g. school policy, educational) will be relevant. Non-specific or multi-faceted behavioural, educational, or policy interventions may also be included subject to the level of evidence that exists for the other interventions/exposures. Comparisons of interest and endpoints of interest are pre-specified. We will include randomized controlled trials, controlled clinical trials, interrupted time series studies, controlled before-after studies, prospective and retrospective comparative cohort studies, case-control studies, and nested case-control designs. The MEDLINE®, Embase, The Cochrane Library, CINAHL, ERIC, and PsycINFO® databases and grey literature sources will be searched. The processes for selecting studies, abstracting data, and resolving conflicts are described. We will assess risk of bias using design-specific tools. To determine sets of confounding variables that should be adjusted for, we have developed causal directed acyclic graphs and will use those to inform our risk of bias assessments. Meta-analysis will be conducted where appropriate; parameters for exploring statistical heterogeneity and effect modifiers are pre-specified. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach will be used to determine the quality of evidence for outcomes.

Systematic Review Registration: PROSPERO CRD42014009641.
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http://dx.doi.org/10.1186/2046-4053-3-96DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160918PMC
September 2014

Vital signs after cardiac arrest following withdrawal of life-sustaining therapy: a multicenter prospective observational study.

Crit Care Med 2014 Nov;42(11):2358-69

1Division of Pediatric Critical Care, Children's Hospital of Eastern Ontario, Ottawa, ON, Canada. 2Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON, Canada. 3Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada. 4Montreal Children's Hospital, McGill University Health Centre, Montreal, QC, Canada. 5McGill University Health Centre Research Institute, Montreal, QC, Canada. 6Department of Critical Care, The Keenan Research Centre in the Li Ka Shing Knowledge Institute, St Michael's Hospital, Toronto, ON, Canada. 7Faculty of Medicine, Interdepartmental Division of Critical Care, University of Toronto, ON, Canada. 8Critical Care Medicine and Center for Health Evaluation and Outcome Sciences, St. Paul's Hospital, Vancouver, BC, Canada. 9Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada. 10Ingram School of Nursing McGill University, McGill University Health Centre, Montreal, QC, Canada. 11Faculty of Medicine Biomedical Ethics Unit, McGill University, Montreal, QC, Canada. 12Department of Critical Care Medicine and Department of Medicine, Sunnybrook Health Sciences Centre, Toronto, ON, Canada. 13Pediatric Cardiology, Children's Hospital of Eastern Ontario, Ottawa, ON, Canada. 14Neurosciences Intensive Care Unit, University of Alberta Hospital, Edmonton, AB, Canada. 15Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada. 16Critical Care, The Ottawa Hospital, Ottawa, ON, Canada. 17Department of Medicine, University of Ottawa, Ottawa, ON, Canada. 18The Ottawa Health Research Institute, Ottawa, ON, Canada. 19The Clinical Epidemiology Program Methods Centre, University of Ottawa, Ottawa, ON, Canada. 20Department of Epidemiology and Community Medicine, University of Ottawa, Ottawa, ON, Canada. 21National GE3LS Program, Genome Canada, Ottawa, ON, Canada. 22Information Systems, Children's Hospital of Eastern Ontario, Ottawa, ON, Canada. 23Department of Clinical Neurological Sciences, London Health Scien

Objective: Controversies regarding the process and timing of the determination of death for controlled organ donation after circulatory death persist. This study assessed the feasibility of conducting a prospective, observational study of continuous monitoring of vital signs for 30 minutes after the clinical determination of death in five Canadian ICUs. Waveform data were analyzed.

Design: Prospective observational cohort study.

Setting: One pediatric and four adult Canadian ICUs.

Patients: One month of age or older, admitted to the ICU, and for whom a consensual decision to withdraw life-sustaining therapies had been made, with an anticipation of imminent death.

Interventions: None.

Measurements And Main Results: Invasive arterial blood pressure, electrocardiogram, and oxygen saturation plethysmography activity were recorded and reviewed for 30 minutes after declaration of death. Feasibility was assessed (recruitment, consent rate, protocol compliance, and staff satisfaction). Of 188 subjects screened over 16 months, 41 subjects were enrolled (87% consent rate). Data collection was complete for 30 subjects (73% protocol compliance). In four subjects, arterial blood pressure resumed following cessation of activity. The longest period of cessation of arterial blood pressure before resumption was 89 seconds. The duration of resumed activity ranged from 1 to 172 seconds. No cases of sustained resumption of arterial blood pressure activity were recorded, and no instances of clinical autoresuscitation were reported. In nearly all patients (27 of 30), electrocardiogram activity continued after the disappearance of arterial blood pressure.

Conclusions: This is the first observational study to prospectively collect waveform data for 30 minutes after the declaration of death. A future larger study may support initial data suggesting that circulatory function does not resume after more than 89 seconds of absence. Furthermore, persistence of cardiac electrical activity with the documented absence of circulation may not be relevant to declaration of death.
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http://dx.doi.org/10.1097/CCM.0000000000000417DOI Listing
November 2014

Procainamide infusion in the evaluation of unexplained cardiac arrest: from the Cardiac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER).

Heart Rhythm 2014 Jun 18;11(6):1047-54. Epub 2014 Mar 18.

Queen׳s University, Kingston, Ontario, Canada.

Background: Provocative testing with sodium channel blockers is advocated for the evaluation of unexplained cardiac arrest (UCA) with the primary purpose of unmasking the typical ECG features of Brugada syndrome. The Cardiac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER) systematically assesses subjects with UCA or a family history of sudden death (FHSD).

Objective: The purpose of this study was to determine the clinical yield of procainamide infusion in a national registry of subjects with either UCA or a FHSD.

Methods: Subjects with either UCA or a FHSD without evidence of a Brugada pattern at baseline underwent procainamide testing (15 mg/kg to a maximum of 1 g at 50 mg/min). A test was considered positive for Brugada pattern if there was an increase in ST elevation >1 mm or if there was >1 mm of new ST elevation in leads V1 and/or V2. Genetic testing was performed on the basis of phenotype detection.

Results: Procainamide testing was performed in 174 subjects (age 46.8 ± 15.4 years, 47% female). Testing provoked a Brugada pattern in 12 subjects (6.9%), 5 of whom had no ST abnormalities at baseline. No subjects with a negative procainamide challenge were subsequently diagnosed with Brugada syndrome. Genetic testing was conducted in 10 of the 12 subjects with a provoked Brugada pattern and was positive for a mutation in the SCN5A gene in 1.

Conclusion: Irrespective of the baseline ECG, procainamide testing provoked a Brugada pattern in a significant proportion of subjects with UCA or a FHSD, thereby facilitating a diagnosis of Brugada syndrome, and is recommended in the workup of UCA.
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http://dx.doi.org/10.1016/j.hrthm.2014.03.022DOI Listing
June 2014

Sudden cardiac death in children and adolescents between 1 and 19 years of age.

Heart Rhythm 2014 Feb 13;11(2):239-45. Epub 2013 Nov 13.

Department of Pediatrics, Children's Hospital of Eastern Ontario, University of Ottawa, Ottawa, Ontario, Canada. Electronic address:

Background: Understanding pediatric sudden cardiac death (SCD) may inform age-specific prevention strategies.

Objective: To characterize potential underlying causes of SCD in children and adolescents

Methods: We performed a retrospective population-based study in Ontario, Canada, of all SCD cases in a 5-year period (2005-2009) involving persons aged 1-19 years identified from the comprehensive database of the Office of the Chief Coroner. Of 1204 coroner's cases, 351 potential SCD cases were reviewed.

Results: Of 116 cases of adjudicated SCD, there was no identifiable cause of death in 60 (52%). The majority were males (66%), and median age was 12.7 years. The incidence of SCD was greatest between 1 and 2 years (3.14 per 100,000 person-years), decreased, and then increased to 1.01 per 100,000 person-years (15-19 years). Autopsy findings were normal in 29 of 35 (83%) of children younger than 5 years and were more likely to be abnormal in those 10 years and older (odds ratio 9.0; 95% confidence interval 3.3-24.9). In 9%, the pathology findings may be of uncertain significance. Most events occurred in the home (68%). Activity level at the time of the event was associated with both age group (χ(2) = 34.9; P < .001) and autopsy findings (χ(2) = 28.9; P < .001). Events during moderate or vigorous activity were more common in those older than 10 years 16 of 66 (24%), and the majority had abnormal autopsy findings 13 of 18 (72%).

Discussion: Death in the very young is often caused by presumed primary arrhythmia syndromes, and death during exertion is typically seen in those with structural heart disease.

Conclusion: These differences should inform age-specific diagnostic and prevention strategies.
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http://dx.doi.org/10.1016/j.hrthm.2013.11.006DOI Listing
February 2014

Charting a course for cardiac electrophysiology training in Canada: the vital role of fellows in advanced cardiovascular care.

Can J Cardiol 2013 Nov;29(11):1527-30

Royal Jubilee Hospital, Victoria, British Columbia, Canada. Electronic address:

Canadian electrophysiology (EP) fellowship programs have evolved in an ad hoc fashion over 30 years. This evolution has occurred in many fields in medicine and is natural when innovators and pioneers attract research fellows who help change the status quo from predominantly research to a predominantly clinical application and focus. Fellows not only push their supervisors and their centres into new areas of inquiry but also function at the most advanced level to encourage and teach junior trainees and to provide examples of excellence to residents, medical students, and other health professionals. Funding for fellows has never been provided in the traditional way through the Ministry of Health or the Ministry of Advanced Education. Each Canadian centre has over the years found novel ways to fund fellowship programs, and many centres have used value-adds from procurement programs. These sources of funding are eroding as provincial government agencies are beginning to assume procurement responsibilities and local flexibility to fund fellowships is lost. In particular, provincial government agencies feel that valuable financial resources should be restricted to Canadian trainees only, despite the international consensus that fellowship is an essential time for advanced trainees to travel abroad to acquire a broad a range of experience, learn new techniques and approaches, make lifelong research connections, and hopefully return home with these skills and expertise. This article summarizes the long history of EP fellowship training in Canada, as well as EP fellowship experiences at home and abroad by Canadian electrophysiologists, in an attempt to contextualize these new realities.
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http://dx.doi.org/10.1016/j.cjca.2013.08.019DOI Listing
November 2013

Lone atrial fibrillation in the pediatric population.

Can J Cardiol 2013 Oct;29(10):1227-33

Division of Pediatric Cardiology, University of Ottawa, Ottawa, Ontario, Canada.

Background: There are few reports of pediatric studies of atrial fibrillation (AF). We sought to describe the clinical characteristics, management strategies, and recurrence rates and to identify predictors of AF recurrence in a contemporary pediatric population.

Methods: A retrospective review was performed of patients ≤ 18 years with lone AF who were seen at 4 pediatric institutions from 1996-2011. Patients with AF in the setting of thyroid disease, ventricular pre-excitation, coexisting congenital heart disease, or a history of cardiac surgery were excluded. Demographics, clinical presentation, investigations, treatment, and follow-up were analyzed.

Results: Forty-two patients were diagnosed with a first episode of lone AF, and 4 of these cases were later classified as persistent AF. Thirty-one (74%) were male patients, median age was 15.3 years, and median (interquartile range [IQR]) duration of AF episode was 12 (IQR, 7-24) hours. AF recurred in 39% (15 of 38) of patients. The Kaplan-Meier median time to estimated recurrence was 19 months. By univariate analysis, initial AF episode duration was associated with a higher risk of recurrence (hazard ratio [HR], 1.01; 95% confidence interval [CI], 1-1.02; P = 0.034). Sex, age, family history, size of the left atrium, and history of cardioversion were not associated with recurrence. Recurrence with another supraventricular tachyarrhythmia (SVT) was observed in 6 of 38 (16%) patients, and 12 patients underwent electrophysiology (EP) study, with 6 patients receiving ablation.

Conclusions: Our reported rate of recurrence of 39% is important when counseling pediatric patients and their parents on the expected course and treatment goals.
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http://dx.doi.org/10.1016/j.cjca.2013.06.014DOI Listing
October 2013

Activity intensity during free-living activities in children and adolescents with inherited arrhythmia syndromes: assessment by combined accelerometer and heart rate monitor.

Circ Arrhythm Electrophysiol 2013 Oct 30;6(5):939-45. Epub 2013 Aug 30.

Department of Pediatrics.

Background: International guidelines recommend restriction of activities for many children and adolescents with inherited arrhythmia syndromes to moderate activity (<7 metabolic equivalents [METs]). We hypothesized that moderate levels of intensity would be exceeded during free-living daily activity in these individuals when assessed objectively by combined heart rate and accelerometry monitor (Actiheart).

Methods And Results: Participants wore the Actiheart for ≤7 days on 2 occasions after a maximal exercise test that was used to calibrate the monitor individually against intensity levels. Of 16 participants, 13 (81%) had long QT syndrome, 9 (56%) were female, and median age was 12 years. Monitors were worn for a median (range) of 13 (6-14) days, and a mean (SD) of 11.3 (1.7) hours per day. Vigorous (7 MET) and very vigorous (10 MET) thresholds were exceeded by 15 and 13 participants, respectively. The median (interquartile range), individual, total weekly time spent >7 MET threshold was 113 (65-330) minutes, whereas such time spent >10 MET threshold was 53 (9-115) minutes. Total time>7 MET threshold was 2.3% of monitor wear time. There were no differences in time above threshold between male and female participants (P=0.357) or among those with different levels of activity restriction (P=0.769).

Conclusions: Current recommended activity guidelines are frequently exceeded during routine free-living activities in young participants with inherited arrhythmia syndromes. Whether this indicates increased risk for these individuals or excessively restrictive guidelines remains to be determined.
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http://dx.doi.org/10.1161/CIRCEP.113.000514DOI Listing
October 2013

Scope and nature of sudden cardiac death before age 40 in Ontario: a report from the cardiac death advisory committee of the office of the chief coroner.

Heart Rhythm 2013 Apr 8;10(4):517-23. Epub 2012 Dec 8.

Department of Medicine, University of Western Ontario, London, Ontario, Canada.

Background: Understanding sudden cardiac death in the young may inform prevention strategies.

Objective: To determine the scope and nature of sudden death in a geographically defined population.

Methods: We performed a retrospective population-based cohort study in Ontario, Canada, of all sudden cardiac death cases involving persons aged 2-40 years identified from the 2008 comprehensive Coroner database. Of 1741 Coroner's cases, 376 were considered potential sudden cardiac death cases and underwent review.

Results: There were 174 cases of adjudicated sudden cardiac death from a population of 6,602,680 persons aged 2-40 years. Structural heart disease was present in 126 cases (72%), 78% of which was unrecognized. There was no identifiable cause of death in 48 cases (28%), representing primary arrhythmia syndromes. The majority of decedents were men (76%) over the age of 18 (90%). The overall incidence of sudden cardiac death increased with age from 0.7/100,000 (2-18 years) to 2.4/100,000 (19-29 years) to 5.3/100,000 (30-40 years) person-years. Persons experiencing sudden cardiac death before age 30 were more likely to have a primary arrhythmia syndrome (odds ratio 2.97; P<.001). The majority of events occurred in the home (72%); 33% of the events in children/adolescents and 9% of the events in adults occurred during reported moderate or vigorous exercise (P = .002). There were no pediatric deaths during organized competitive sports.

Conclusions: The incidence of sudden cardiac death increases with age, typically occurring in a man at rest in the home with unrecognized underlying heart disease or a primary arrhythmia syndrome. Prevention strategies should consider targeting identification of unrecognized structural heart disease and primary arrhythmia syndromes.
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http://dx.doi.org/10.1016/j.hrthm.2012.12.003DOI Listing
April 2013

The QT and corrected QT interval in recovery after exercise in children.

Circ Arrhythm Electrophysiol 2011 Aug 23;4(4):448-55. Epub 2011 May 23.

Royal Children's Hospital, Melbourne, Victoria, Australia.

Background: Prolongation of the QT interval after exercise can be used to help diagnose long-QT syndrome, especially when the resting QT interval is borderline. The aim of this study was to determine the normal ranges for QT and corrected QT in the recovery phase after exercise in children.

Methods And Results: Ninety-four volunteer boys and girls aged 8 to < 17 years without any history of heart disease underwent exercise testing and had a 12-lead ECG performed in the supine position for 10 minutes of recovery. The QT was measured using a standardized tangent method, with the baseline defined as the Q-Q line. The recovery QT was maximally short at 1 minute of recovery in 93 of 94 children then lengthened and stabilized at 4 to 5 minutes recovery. The recovery QT lengthens as heart rate decreases in an approximately linear fashion with a mean increase of 15 ms per 10-beat decrease in heart rate. The 98 th percentiles for the corrected QT using the Bazett formula during minutes 4 to 6 in recovery were from 482 to 491 ms. There was excellent intraobserver and interobserver reliability, with intraclass correlation coefficients of 0.95 and 0.88, respectively.

Conclusions: There is substantial individual variability of the normal repolarization process in the postexercise recovery period in children. The study provides a reference for normal responses for similar populations using a specific measurement protocol that can be easily applied.
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http://dx.doi.org/10.1161/CIRCEP.110.961094DOI Listing
August 2011

Atrial fibrillation in a LQTS patient with an ICD programmed for managed ventricular pacing: what is the cause?

Pacing Clin Electrophysiol 2012 Mar 23;35(3):357-9. Epub 2011 May 23.

Department of Pediatrics, The Children's Hospital of Eastern Ontario, Ottawa, Canada.

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http://dx.doi.org/10.1111/j.1540-8159.2011.03120.xDOI Listing
March 2012

Recommendations for the use of genetic testing in the clinical evaluation of inherited cardiac arrhythmias associated with sudden cardiac death: Canadian Cardiovascular Society/Canadian Heart Rhythm Society joint position paper.

Can J Cardiol 2011 Mar-Apr;27(2):232-45

Division of Cardiology, University of Ottawa Heart Institute, Ottawa, Ontario, Canada.

The era of gene discovery and molecular medicine has had a significant impact on clinical practice. Knowledge of specific genetic findings causative for or associated with human disease may enhance diagnostic accuracy and influence treatment decisions. In cardiovascular disease, gene discovery for inherited arrhythmia syndromes has advanced most rapidly. The arrhythmia specialist is often confronted with the challenge of diagnosing and managing genetic arrhythmia syndromes. There is now a clear need for guidelines on the appropriate use of genetic testing for the most common genetic conditions associated with a risk of sudden cardiac death. This document represents the first ever published recommendations outlining the role of genetic testing in various clinical scenarios, the specific genes to be considered for testing, and the utility of test results in the management of patients and their families.
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http://dx.doi.org/10.1016/j.cjca.2010.12.078DOI Listing
June 2011

Arrhythmia characterization and long-term outcomes in catecholaminergic polymorphic ventricular tachycardia.

Heart Rhythm 2011 Jun 9;8(6):864-71. Epub 2011 Feb 9.

University of Western Ontario, Ontario, Canada.

Background: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is characterized by adrenergically induced ventricular tachycardia (VT) associated with syncope and sudden death.

Objective: This study sought to characterize arrhythmias associated with CPVT with respect to provocation by exercise and drugs, electrocardiographic characteristics, and association with long-term outcomes; and to explore the relation between age and clinical presentation.

Methods: Seventy patients from 16 families were evaluated with exercise and selective adrenaline challenge, and screened for RyR2 mutations. CPVT was diagnosed in probands with symptoms and stress- or adrenaline-provoked VT, or in asymptomatic relatives with provoked VT or RyR2 mutations. Patients were followed up for recurrent syncope, VT, and sudden death.

Results: Twenty-seven patients including 16 probands were identified (median age 35 years, 67% female). Presentation was cardiac arrest in 33% and syncope in 56%, and 11% were asymptomatic. Polymorphic or bidirectional VT was provoked with exercise in 63% and adrenaline in 82%. The initiating beat of VT was late-coupled and wide (coupling interval 418 ± 42 ms; QRSd 131 ± 17 ms), and QRS morphology suggested an outflow tract origin in 59%. During follow-up of 6.2 ± 5.7 years, 2 patients died despite an implantable cardioverter-defibrillator (ICD), 4 patients received ICD therapy for VT, and 5 patients had inappropriate therapy for supraventricular tachycardia. Patients presenting with late-onset CPVT (age > 21; n = 10) were often female (80%) and less likely to have RyR2 (Ryanodine receptor type 2) mutations (33%), and fatal events were not observed during follow-up (4.1 ± 3.6 years).

Conclusion: Ventricular arrhythmia in CPVT is often initiated from the outflow tract region. Despite β-blocker therapy and selective ICD implantation, breakthrough arrhythmias occur and may be associated with adverse outcomes.
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http://dx.doi.org/10.1016/j.hrthm.2011.01.048DOI Listing
June 2011

Characterization of a novel mutation in the cardiac ryanodine receptor that results in catecholaminergic polymorphic ventricular tachycardia.

Channels (Austin) 2010 Jul-Aug;4(4):302-10. Epub 2010 Jul 14.

Department of Physiology and Pharmacology, University of Calgary, Calgary, AB, Canada.

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an arrhythmogenic disease that manifests as syncope or sudden death during high adrenergic tone in the absence of structural heart defects. It is primarily caused by mutations in the cardiac ryanodine receptor (RyR2). The mechanism by which these mutations cause arrhythmia remains controversial, with discrepant findings related to the role of the RyR2 binding protein FKBP12.6. The purpose of this study was to characterize a novel RyR2 mutation identified in a kindred with clinically diagnosed CPVT. Single-strand conformational polymorphism analysis and direct DNA sequencing were used to screen the RyR2 gene for mutations. Site-directed mutagenesis was employed to introduce the mutation into the mouse RyR2 cDNA. The impact of the mutation on the interaction between RyR2 and a 12.6 kDa FK506 binding protein (FKBP12.6) was determined by immunoprecipitation and immunoblotting and its effect on RyR2 function was characterized by single cell Ca(2+) imaging and [(3)H]ryanodine binding. A novel CPVT mutation, E189D, was identified. The E189D mutation does not alter the affinity of the channel for FKBP12.6, but it increases the propensity for store-overload-induced Ca(2+) release (SOICR). Furthermore, the E189D mutation enhances the basal channel activity of RyR2 and its sensitivity to activation by caffeine. The E189D RyR2 mutation is causative for CPVT and functionally increases the propensity for SOICR without altering the affinity for FKBP12.6. These observations strengthen the notion that enhanced SOICR, but not altered FKBP12.6 binding, is a common mechanism by which RyR2 mutations cause arrhythmias.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3322479PMC
http://dx.doi.org/10.4161/chan.4.4.12666DOI Listing
March 2011

Complications associated with revision of Sprint Fidelis leads: report from the Canadian Heart Rhythm Society Device Advisory Committee.

Circulation 2010 Jun 24;121(22):2384-7. Epub 2010 May 24.

Queen Elizabeth II Health Sciences Centre, Halifax, Nova Scotia.

Background: It has been observed that replacement of an implantable cardioverter-defibrillator generator in response to a device advisory may be associated with a substantial rate of complications, including death. The risk of lead revision in response to a lead advisory has not been determined previously.

Methods And Results: Twenty-five implantable cardioverter-defibrillator implantation and follow-up centers from the Canadian Heart Rhythm Society Device Advisory Committee were surveyed to assess complication rates as a result of lead revisions due to the Sprint Fidelis advisory issued in October 2007. As of June 1, 2009, there had been 310 lead failures found in 6237 Sprint Fidelis leads in Canada (4.97%) over a follow-up of 40 months. There were 469 leads to be revised, 66% for confirmed fracture. Of the patients who underwent revision, 95% had a new lead inserted, whereas 4% had a pace/sense lead added. The lead was removed in 248 cases (53%), by simple traction in 61% and by laser lead extraction in 33%. Complications were encountered in 14.5% of the lead revisions; 7.25% of these were major, whereas 7.25% were minor. There were 2 deaths (0.43%). The overall risk of complications (19.8%) was greater in those who underwent lead removal at the time of revision than in those whose leads were abandoned (8.6%; P=0.0008).

Conclusions: The overall rate of major complications that arose from lead revision due to the Sprint Fidelis advisory was significant. This must be taken into account when lead revision is planned in those patients who have not yet demonstrated an abnormality in lead performance.
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http://dx.doi.org/10.1161/CIRCULATIONAHA.109.924357DOI Listing
June 2010

Preventing sudden cardiac death in the young: Is electrocardiogram screening the most effective means?

Authors:
Robert Gow

Paediatr Child Health 2009 Mar;14(3):185-8

Department of Paediatrics, The Children's Hospital of Eastern Ontario, Ottawa, Ontario.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2690551PMC
http://dx.doi.org/10.1093/pch/14.3.185DOI Listing
March 2009

Understanding ethical issues, ICD, and DNR orders: an obstacle to imminent death?

Heart Rhythm 2010 Jun 11;7(6):858-60. Epub 2010 Feb 11.

University of Ottawa, Children's Hospital of Eastern Ontario, Ottawa, Ontario, Canada.

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http://dx.doi.org/10.1016/j.hrthm.2010.02.009DOI Listing
June 2010

Formation of a national network for rapid response to device and lead advisories: The Canadian Heart Rhythm Society Device Advisory Committee.

Can J Cardiol 2009 Jul;25(7):403-5

The Canadian Heart Rhythm Society (CHRS) Device Advisory Committee was commissioned to respond to advisories regarding cardiac rhythm device and lead performance on behalf of the CHRS. In the event of an advisory, the Chair uses an e-mail network to disseminate advisory information to Committee members broadly representative of the Canadian device community. A consensus recommendation is prepared by the Committee and made available to all Canadian centres on the CHRS Web site after approval by the CHRS executive. This collaborative approach using an e-mail network has proven very efficient in providing a rapid national response to device advisories. The network is an ideal tool to collect specific data on implanted device system performance and allows for prompt reporting of clinically relevant data to front-line clinicians and patients.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2723023PMC
http://dx.doi.org/10.1016/s0828-282x(09)70502-1DOI Listing
July 2009

Pacemaker therapy of postoperative arrhythmias after pediatric cardiac surgery.

Pediatr Crit Care Med 2010 Jan;11(1):133-8

From the Pediatric Intensive Care Unit, Children's Heart Centre, British Columbia Children's Hospital, BC, Canada.

Objective: To summarize the practical operation of temporary pacemakers in common use pertinent to the intensivist caring for the postcardiac patient. Pacemaker therapy is commonly required in the postoperative period after congenital cardiac surgery.

Data Synthesis: Monitoring the hemodynamic status and availability of equipment for resuscitation is always important in any patient requiring a temporary pacemaker. Two important scenarios to consider in the pediatric intensive care unit are: 1) the patient in whom pacing has been initiated to optimize cardiac function; and 2) the patient without demonstrable spontaneous electrical activity or with extreme bradycardia. A number of different models of temporary pacemaker are available. Management of the child requiring cardiac pacing requires an understanding of the indications for pacing, a thorough knowledge of the available pacemaker, and an ability to troubleshoot problems.

Conclusions: As the most common arrhythmias post congenital cardiac surgery involve either rate or conduction abnormalities, temporary pacemaker systems are a common form of electrical therapy in the postoperative period.
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http://dx.doi.org/10.1097/PCC.0b013e3181ae5b8aDOI Listing
January 2010

The measurement of the QT and QTc on the neonatal and infant electrocardiogram: a comprehensive reliability assessment.

Ann Noninvasive Electrocardiol 2009 Apr;14(2):165-75

The Children's Hospital of Eastern Ontario, University of Ottawa Faculty of Medicine, 401 Smyth Road, Ottawa, Ontario, Canada.

Background: An electrocardiogram has been proposed to screen for prolonged QT interval that may predispose infants to sudden death in the first year of life. Understanding the reliability of QT interval measurement will inform the design of a screening program.

Methods: Three pediatric cardiologists measured the QT/RR intervals on 60 infant electrocardiograms (median age 46 days), from leads II, V5 and V6 on three separate occasions, 7 days apart, according to a standard protocol. The QTc was corrected by Bazett's (QTcB), Fridericia's (QT(CFrid)), and Hodges' (QTcH) formulae. Intraobserver and interobserver reliability were assessed by intraclass correlation coefficients (ICC), limits of agreement and repeatability coefficients for single, average of two and average of three measures. Agreement for QTc prolongation (> 440 msec) was assessed by kappa coefficients.

Results: QT interval intraobserver ICC was 0.86 and repeatability coefficient was 25.9 msec; interobserver ICC increased from 0.88 for single observations to 0.94 for the average of 3 measurements and repeatability coefficients decreased from 22.5 to 16.7 msec. For QTcB, intraobserver ICC was 0.67, and repeatability was 39.6 msec. Best interobserver reliability for QTcB was for the average of three measurements (ICC 0.83, reproducibility coefficient 25.8 msec), with further improvement for QTcH (ICC 0.92, reproducibility coefficient 16.69 msec). Maximum interobserver kappa for prolonged QTc was 0.77. Misclassification around specific cut points occurs because of the repeatability coefficients.

Conclusions: Uncorrected QT measures are more reliable than QTcB and QT(CFrid). An average of three independent measures provides the most reliable QT and QTc measurements, with QTcH better than QTcB.
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http://dx.doi.org/10.1111/j.1542-474X.2009.00292.xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6932280PMC
April 2009