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Dive into the research topics where Matthew T. Bennett is active.

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Featured researches published by Matthew T. Bennett.


Lipids in Health and Disease | 2007

Ezetimibe is effective when added to maximally tolerated lipid lowering therapy in patients with HIV

Matthew T. Bennett; Kevin Johns; Gregory P. Bondy

To determine the efficacy and safety of adding ezetimibe to maximally tolerated lipid lowering therapy in patients with HIV dyslipidemia.Retrospective analysis of lipid parameters was conducted for 33 patients with HIV who had been prescribed ezetimibe 10 mg per day.Mean total cholesterol was reduced 21% (p < 0.001). Mean LDL was reduced 35% (p < 0.001). Mean HDL increased 8% (p = 0.038). Mean triglyceride was reduced 34% (p = 0.006). Mean Apolipoprotein B100 was reduced 33% (p = 0.043). No adverse events occurred.Ezetimibe appears safe and effective in patients with HIV when added to maximally tolerated doses of lipid lowering therapy.


Heart Rhythm | 2010

Utility of the recovery electrocardiogram after exercise: a novel indicator for the diagnosis and genotyping of long QT syndrome?

Ishvinder Chattha; Raymond W. Sy; Raymond Yee; Lorne J. Gula; Allan C. Skanes; George J. Klein; Matthew T. Bennett; Andrew D. Krahn

BACKGROUND Exercise testing has shown modest utility in the ability to diagnose and genotype long QT syndrome (LQTS). Although numerous small studies have shown a genotype-specific repolarization response to exercise, the repolarization responses during recovery from exercise have received less focus. OBJECTIVE The purpose of this study was to characterize genotype-specific QT responses during recovery from exercise and to determine its potential as a diagnostic and genotyping tool. METHODS Seventy-five patients were age and sex matched into three groups (n = 25): LQT1, LQT2, and unaffected controls based on Schwartz score and genetic testing results. Each group underwent upright burst and gradual bicycle exercise testing while being monitored by 12-lead electrocardiogram. RESULTS LQT1 patients had significantly longer corrected QT (QTc) than LQT2 intervals during early recovery (P <.01). Control subjects showed little variation in QTc throughout the recovery period, maintaining a QTc within normal limits. Each group showed a distinct pattern of QTc adaptation during recovery. LQT1 patients began the recovery period at a QTc of 492 +/- 11 ms, after which the QTc decreased by 33 +/- 11 ms during recovery. Conversely, the LQT2 patients began recovery at its lowest mean QTc of 420 +/- 10 ms, which increased by 40 +/- 16 ms. At the end of recovery, a QTc cut-off value of 445 ms distinguished 92% of LQTS patients from unaffected controls, while a start-of-recovery QTc cut-off of 460 ms correctly identified genotype in 80% of LQT1 and 92% of LQT2 patients. CONCLUSIONS Genotype-specific differences exist in QT recovery after exercise. These differences can help to identify LQTS patients and distinguish LQT1 from LQT2 genotypes.


Circulation-arrhythmia and Electrophysiology | 2011

Entrainment for Distinguishing Atypical Atrioventricular Node Reentrant Tachycardia From Atrioventricular Reentrant Tachycardia Over Septal Accessory Pathways With Long-RP Tachycardia

Matthew T. Bennett; Peter Leong-Sit; Lorne J. Gula; Allan C. Skanes; Raymond Yee; Andrew D. Krahn; Ellaina C. Hogg; George J. Klein

Background— The response to right ventricular (RV) entrainment is useful to distinguish atypical AV node reentrant tachycardia from AV reentrant tachycardia using a septal accessory pathway. Whether entrainment can differentiate between AV node reentrant tachycardia and AV reentrant tachycardia in patients with long-RP tachycardia has not been systematically validated. Methods and Results— Twenty-four patients with concealed septal accessory pathways who had an electrophysiology study between January 1, 2000, and January 1, 2010, were included (age, 38±17 years; men, 17). Entrainment was performed from the RV apex pacing at cycle length 20 to 40 ms shorter than tachycardia cycle length (TCL). The mean TCL was 390±80 ms, the mean AH interval during tachycardia was 151±57 ms, and the mean ventriculoatrial (VA) time was 182±103 ms. Twelve patients had typical accessory pathways (VA/TCL <40%), and 12 had slowly conducting accessory pathways (VA/TCL ≥40%). In all patients with typical accessory pathways, the postpacing interval minus the TCL (PPI−TCL) was <115 ms and the difference in the VA interval during pacing and tachycardia (StimA−VA) was <85 ms. On the other hand, in 6 of the 12 patients in the slowly conducting group, the PPI−TCL was >115 ms, and the StimA−VA was >85 ms. Conclusions— Slowly conducting accessory pathways frequently yield RV entrainment criteria traditionally attributable to AV node reentry. Distinguishing AV node reentry from AV reentry in patients with long-RP tachycardia requires other criteria.


Journal of Cardiovascular Electrophysiology | 2010

Repolarization dynamics during exercise discriminate between LQT1 and LQT2 genotypes.

Raymond W. Sy; Ishvinder Chattha; George J. Klein; Lorne J. Gula; Allan C. Skanes; Raymond Yee; Matthew T. Bennett; Andrew D. Krahn

Genotype and Exercise in LQTS. Background: Repolarization dynamics during exercise in patients with long‐QT Syndrome (LQTS) may be influenced by various factors such as a patients genotype. We sought to systematically characterize the repolarization dynamics during exercise in patients with LQTS with a particular focus on the influence of genotype.


Circulation-arrhythmia and Electrophysiology | 2016

Outcome of Apparently Unexplained Cardiac Arrest: Results From Investigation and Follow-Up of the Prospective Cardiac Arrest Survivors With Preserved Ejection Fraction Registry

Adam R.M. Herman; C. Cheung; Brenda Gerull; Christopher S. Simpson; David H. Birnie; George Klein; Jean Champagne; Jeff S. Healey; K. Gibbs; Mario Talajic; Martin Gardner; Matthew T. Bennett; Christian Steinberg; M. Janzen; Michael H. Gollob; Paul Angaran; Raymond Yee; Richard Leather; Santabhanu Chakrabarti; Shubhayan Sanatani; Vijay S. Chauhan; Andrew D. Krahn

Background—The Cardiac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER) enrolls patients with apparently unexplained cardiac arrest and no evident cardiac disease to identify the pathogenesis of cardiac arrest through systematic clinical testing. Exercise testing, drug provocation, advanced cardiac imaging, and genetic testing may be useful when a cause is not apparent. Methods and Results—The first 200 survivors of unexplained cardiac arrest from 14 centers across Canada were evaluated to determine the results of investigation and follow-up (age, 48.6±14.7 years, 41% female). Patients were free of evidence of coronary artery disease, left ventricular dysfunction, or evident repolarization syndromes. Advanced testing determined a diagnosis in 34% of patients at baseline, with a diagnosis emerging during follow-up in 7% of patients. Of those who were diagnosed, 28 (35%) had an underlying structural condition and 53 (65%) had a primary electric disease. During a mean follow-up of 3.15±2.34 years, 23% of patients had either a shock or an appropriate antitachycardia pacing from their implantable cardioverter defibrillator, or both. The implantable cardioverter defibrillator appropriate intervention rate was 8.4% at 1 year and 18.1% at 3 years, with no clear difference between diagnosed and undiagnosed subjects, or between those diagnosed with a primary electric versus structural pathogenesis. Conclusions—Obtaining a diagnosis in previously unexplained cardiac arrest patients requires systematic clinical testing and regular follow-up to unmask the cause. Nearly half of apparently unexplained cardiac arrest patients ultimately received a diagnosis, allowing for improved treatment and family screening. A substantial proportion of patients received appropriate implantable cardioverter defibrillator therapy during medium-term follow-up. Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT00292032.


Canadian Journal of Cardiology | 2017

Canadian Cardiovascular Society/Canadian Heart Rhythm Society 2016 Implantable Cardioverter-Defibrillator Guidelines

Matthew T. Bennett; Ratika Parkash; Pablo B. Nery; Mario Sénéchal; Blandine Mondésert; David H. Birnie; Laurence D. Sterns; Claus Rinne; Derek V. Exner; François Philippon; Jafna L. Cox; Paul Dorian; Vidal Essebag; Andrew D. Krahn; Jaimie Manlucu; F. Molin; Michael P. Slawnych; Mario Talajic

Sudden cardiac death is a major public health issue in Canada. However, despite the overwhelming evidence to support the use of implantable cardioverter defibrillators (ICDs) in the prevention of cardiac death there remains significant variability in implantation rates across Canada. Since the most recent Canadian Cardiovascular Society position statement on ICD use in Canada in 2005, there has been a plethora of new scientific information to assist physicians in their discussions with patients considered for ICD implantation to prevent sudden cardiac death due to ventricular arrhythmias. We have reviewed, critically appraised, and synthesized the pertinent evidence to develop recommendations regarding: (1) ICD implantation in the primary and secondary prevention of sudden cardiac death in patients with and without ischemic heart disease; (2) when it is reasonable to withhold ICD implantation on the basis of comorbidities; (3) ICD implantation in patients listed for heart transplantation; (4) implantation of a single- vs dual-chamber ICD; (5) implantation of single- vs dual-coil ICD leads; (6) the role of subcutaneous ICDs; and (7) ICD implantation infection prevention strategies. We expect that this document, in combination with the companion article that addresses the implementation of these guidelines, will assist all medical professionals with the care of patients who have had or at risk of sudden cardiac death.


Lipids in Health and Disease | 2007

Are HIV positive patients resistant to statin therapy

Kevin Johns; Matthew T. Bennett; Gregory P. Bondy

BackgroundPatients with HIV are subject to development of HIV metabolic syndrome characterized by dyslipidemia, lipodystrophy and insulin resistance secondary to highly active antiretroviral therapy (HAART). Rosuvastatin is a highly potent HMG-CoA reductase inhibitor. Rosuvastatin is effective at lowering LDL and poses a low risk for drug-drug interaction as it does not share the same metabolic pathway as HAART drugs. This study sought to determine the efficacy of rosuvastatin on lipid parameters in HIV positive patients with HIV metabolic syndrome.ResultsMean TC decreased from 6.54 to 4.89 mmol/L (25.0% reduction, p < 0.001). Mean LDL-C decreased from 3.39 to 2.24 mmol/L (30.8% reduction, p < 0.001). Mean HDL rose from 1.04 to 1.06 mmol/L (2.0% increase, p = ns). Mean triglycerides decreased from 5.26 to 3.68 mmol/L (30.1% reduction, p < 0.001). Secondary analysis examining the effectiveness of rosuvastatin monotherapy (n = 70) vs. rosuvastatin plus fenofibrate (n = 43) showed an improvement of 21.3% in TG and a decrease of 4.1% in HDL-C in the monotherapy group. The rosuvastatin plus fenofibrate showed a greater drop in triglycerides (45.3%, p < 0.001) and an increase in HDL of 7.6% (p = 0.08).ConclusionThis study found that rosuvastatin is effective at improving potentially atherogenic lipid parameters in HIV-positive patients. The lipid changes we observed were of a smaller magnitude compared to non-HIV subjects. Our results are further supported by a small, pilot trial examining rosuvastatin effectiveness in HIV who reported similar median changes from baseline of -21.7% (TC), -22.4% (LDL-C), -30.1% (TG) with the exception of a 28.5% median increase in HDL. In light of the results revealed by this pilot study, clinicians may want to consider a possible resistance to statin therapy when treating patients with HIV metabolic syndrome.


Journal of Cardiovascular Electrophysiology | 2015

Early Failure of the Biotronik Linox Implantable Cardioverter Defibrillator Lead

Gareth J. Padfield; Christian Steinberg; Shahzad S. Karim; Stanley Tung; Matthew T. Bennett; John P. Le Maitre; Jamil Bashir

The Linox and Durata implantable cardioverter defibrillator (ICD) leads were introduced to British Columbia (BC) in 2008. We determined their performance and the potential risk factors for lead failure in a large population‐based patient registry.


Circulation-arrhythmia and Electrophysiology | 2016

Retrieval of the Leadless Cardiac Pacemaker: A Multicenter Experience

Vivek Y. Reddy; Marc A. Miller; Reinoud E. Knops; Petr Neuzil; Pascal Defaye; Werner Jung; Rahul N. Doshi; Mark Castellani; Adam Strickberger; R. Hardwin Mead; Harish Doppalapudi; Dhanunjaya Lakkireddy; Matthew T. Bennett; Johannes Sperzel

Background—Leadless cardiac pacemakers have emerged as a safe and effective alternative to conventional transvenous single-chamber ventricular pacemakers. Herein, we report a multicenter experience on the feasibility and safety of acute retrieval (<6 weeks) and chronic retrieval (>6 weeks) of the leadless cardiac pacemaker in humans. Methods and Results—This study included patients enrolled in 3 multicenter trials, who received a leadless cardiac pacemaker implant and who subsequently underwent a device removal attempt. The overall leadless pacemaker retrieval success rate was 94%: for patients whose leadless cardiac pacemaker had been implanted for <6 weeks (acute retrieval cohort), complete retrieval was achieved in 100% (n=5/5); for those implanted for ≥ 6 weeks (chronic retrieval cohort), retrieval was achieved in 91% (n=10/11) of patients. The mean duration of time from implant to retrieval attempt was 346 days (range, 88–1188 days) in the chronic retrieval cohort, and nearly two thirds (n=7; 63%) had been implanted for >6 months before the retrieval attempt. There were no procedure-related adverse events at 30 days post retrieval procedure. Conclusions—This multicenter experience demonstrated the feasibility and safety of retrieving a chronically implanted single-chamber (right ventricle) active fixation leadless pacemaker. Clinical Trial Registration—URL: https://www.clinicaltrials.gov. Unique identifiers: NCT02051972, NCT02030418, and NCT01700244.


Heart Rhythm | 2015

Preventing cardiac implantable electronic device infections

Gareth J. Padfield; Christian Steinberg; Matthew T. Bennett; Santabhanu Chakrabarti; Marc W. Deyell; Jamil Bashir; Andrew D. Krahn

Cardiac implantable electronic devices (CIEDs) have dramatically improved clinical outcomes in patients with heart disease, and the number of CIED-related procedures being performed continues to grow. Unfortunately, the rate of device-related infection (DRI) is increasing disproportionately to the rate of implantation, with DRI rates of >2% in many series. This increase in DRI is a consequence of the increased number of patients with a higher burden of comorbidities, who are more susceptible to infection and are undergoing more complex device procedures. Identification of high-risk patients is an important component of procedural planning, and targeted therapy and surveillance may be beneficial in certain groups. An understanding of the pathophysiology of DRI has facilitated more effective and widespread use of prophylactic antibiotics; however, current guidelines for antibiotic prophylaxis are based on a relatively small evidence base. Clinical equipoise remains regarding the optimal prophylactic regimen, and we are continuing to learn how best to manage these patients. In this review, we discuss the epidemiology and pathophysiology of DRI and its clinical presentation, the risk factors for DRI, and the existing and emerging evidence supporting strategies to prevent DRI.

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Andrew D. Krahn

University of British Columbia

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Santabhanu Chakrabarti

University of British Columbia

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Raymond Yee

University of Western Ontario

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Jason G. Andrade

University of British Columbia

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Marc W. Deyell

University of British Columbia

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Christian Steinberg

University of British Columbia

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Jeff S. Healey

Population Health Research Institute

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Stanley Tung

University of British Columbia

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Allan C. Skanes

University of Western Ontario

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