Ben Freedman
University of Sydney
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Featured researches published by Ben Freedman.
The Lancet | 2016
Ben Freedman; Tatjana S. Potpara; Gregory Y.H. Lip
Atrial fibrillation is found in a third of all ischaemic strokes, even more after post-stroke atrial fibrillation monitoring. Data from stroke registries show that both unknown and untreated or under treated atrial fibrillation is responsible for most of these strokes, which are often fatal or debilitating. Most could be prevented if efforts were directed towards detection of atrial fibrillation before stroke occurs, through screening or case finding, and treatment of all patients with atrial fibrillation at increased risk of stroke with well-controlled vitamin K antagonists or non-vitamin K antagonist anticoagulants. The default strategy should be to offer anticoagulant thromboprophylaxis to all patients with atrial fibrillation unless defined as truly low risk by simple validated risk scores, such as CHA2DS2-VASc. Assessment of bleeding risk using the HAS-BLED score should focus attention on reversible bleeding risk factors. Finally, patients need support from physicians and various other sources to start anticoagulant treatment and to ensure adherence to and persistence with treatment in the long term.
Circulation | 2017
Ben Freedman; John Camm; Hugh Calkins; Jeff S. Healey; Mårten Rosenqvist; Jiguang Wang; Christine M. Albert; Craig S. Anderson; Sotiris Antoniou; Emelia J. Benjamin; Giuseppe Boriani; Johannes Brachmann; Axel Brandes; Tze-Fan Chao; David Conen; Johan Engdahl; Laurent Fauchier; David A Fitzmaurice; Leif Friberg; Bernard J. Gersh; David J Gladstone; Taya V. Glotzer; Kylie Gwynne; Graeme J. Hankey; Joseph Harbison; Graham S Hillis; Mellanie True Hills; Hooman Kamel; Paulus Kirchhof; Peter R. Kowey
Approximately 10% of ischemic strokes are associated with atrial fibrillation (AF) first diagnosed at the time of stroke. Detecting asymptomatic AF would provide an opportunity to prevent these strokes by instituting appropriate anticoagulation. The AF-SCREEN international collaboration was formed in September 2015 to promote discussion and research about AF screening as a strategy to reduce stroke and death and to provide advocacy for implementation of country-specific AF screening programs. During 2016, 60 expert members of AF-SCREEN, including physicians, nurses, allied health professionals, health economists, and patient advocates, were invited to prepare sections of a draft document. In August 2016, 51 members met in Rome to discuss the draft document and consider the key points arising from it using a Delphi process. These key points emphasize that screen-detected AF found at a single timepoint or by intermittent ECG recordings over 2 weeks is not a benign condition and, with additional stroke factors, carries sufficient risk of stroke to justify consideration of anticoagulation. With regard to the methods of mass screening, handheld ECG devices have the advantage of providing a verifiable ECG trace that guidelines require for AF diagnosis and would therefore be preferred as screening tools. Certain patient groups, such as those with recent embolic stroke of uncertain source (ESUS), require more intensive monitoring for AF. Settings for screening include various venues in both the community and the clinic, but they must be linked to a pathway for appropriate diagnosis and management for screening to be effective. It is recognized that health resources vary widely between countries and health systems, so the setting for AF screening should be both country- and health system-specific. Based on current knowledge, this white paper provides a strong case for AF screening now while recognizing that large randomized outcomes studies would be helpful to strengthen the evidence base.
Circulation | 2006
George T. Lau; Lloyd J Ridley; Paul G. Bannon; Louise A. Wong; Joseph Trieu; David Brieger; Harry C. Lowe; Ben Freedman; Leonard Kritharides
Background— The use of saphenous vein grafts (SVG) in coronary artery bypass surgery is established but little is known of SVG remodeling during the first year in vivo. Methods and Results— The feasibility of measuring total vessel diameter (lumen plus wall), lumen diameter, and wall thickness by a novel computed tomography (CT) method was established in phantom model tubes (r=0.98 for lumen diameter and r=0.98 for wall thickness) and in an initial clinical study of 14 patients correlating CT and intravascular ultrasound measurements of SVG (r=0.88 for total vessel diameter, r=0.85 for lumen diameter and r=0.89 for wall thickness). In a separate group of 42 patients (aged 66±10 years; 36 male, 6 female) undergoing coronary artery bypass grafting, SVG total vessel diameter, lumen diameter, and wall thickness were determined prospectively with multi-slice CT angiography at 1 and 12 months postoperatively. Mean total vessel diameter decreased from 5.95±0.83 mm to 5.39±0.87 mm, P<0.001 (range, −39% to +8% change). Twenty-six patients (62%) had a decrease of SVG vessel diameter (negative remodeling) >5%. Mean lumen diameter decreased from 3.69±0.66 mm to 3.36±0.68 mm, P<0.001, (range, −40 to +11% change). Surprisingly, mean wall thickness decreased from 1.14±0.27 mm to 1.01±0.21 mm (P<0.001; range, −48 to +33% change). Conclusions— Lumen loss in SVG between postoperative months 1 and 12 is predominantly caused by negative remodeling of the whole vessel rather than to changes in wall thickness. Therapies targeting negative remodeling may be required for optimal maintenance of SVG lumen in the first postoperative year.
Thrombosis and Haemostasis | 2016
Ben Freedman; Gregory Y.H. Lip
“Unreal world” or “real world” data in oral anticoagulant treatment of atrial fibrillation -
BMJ | 2016
Carlos Martinez; Samy Suissa; Stephan Rietbrock; Anja Katholing; Ben Freedman; At Cohen; David J. Handelsman
Objective To determine the risk of venous thromboembolism associated with use of testosterone treatment in men, focusing particularly on the timing of the risk. Design Population based case-control study Setting 370 general practices in UK primary care with linked hospital discharge diagnoses and in-hospital procedures and information on all cause mortality. Participants 19 215 patients with confirmed venous thromboembolism (comprising deep venous thrombosis and pulmonary embolism) and 909 530 age matched controls from source population including more than 2.22 million men between January 2001 and May 2013. Exposure of interest Three mutually exclusive testosterone exposure groups were identified: current treatment, recent (but not current) treatment, and no treatment in the previous two years. Current treatment was subdivided into duration of more or less than six months. Main outcome measure Rate ratios of venous thromboembolism in association with current testosterone treatment compared with no treatment were estimated using conditional logistic regression and adjusted for comorbidities and all matching factors. Results The adjusted rate ratio of venous thromboembolism was 1.25 (95% confidence interval 0.94 to 1.66) for current versus no testosterone treatment. In the first six months of testosterone treatment, the rate ratio of venous thromboembolism was 1.63 (1.12 to 2.37), corresponding to 10.0 (1.9 to 21.6) additional venous thromboembolisms above the base rate of 15.8 per 10 000 person years. The rate ratio after more than six months’ treatment was 1.00 (0.68 to 1.47), and after treatment cessation it was 0.68 (0.43 to 1.07). Increased rate ratios within the first six months of treatment were observed in all strata: the rate ratio was 1.52 (0.94 to 2.46) for patients with pathological hypogonadism and 1.88 (1.02 to 3.45) for those without it, and 1.41 (0.82 to 2.41) for those with a known risk factor for venous thromboembolism and 1.91 (1.13 to 3.23) for those without one. Conclusions Starting testosterone treatment was associated with an increased risk of venous thromboembolism, which peaked within six months and declined thereafter.
JAMA Cardiology | 2016
Ben Freedman; Carlos Martinez; Anja Katholing; Stephan Rietbrock
Residual Risk of Stroke and Death in AnticoagulantTreated Patients With Atrial Fibrillation Despite the impressive reduction of risk of stroke and death in patients with atrial fibrillation (AF) conferred by anticoagulation with warfarin or non–vitamin K antagonist oral anticoagulants,1,2 there is still an appreciable stroke risk during anticoagulant treatment, approximating 1.7% per year for warfarin and 1.4% per year for non–vitamin K antagonist oral anticoagulants at 2.2 years’ follow-up.2 This residual stroke rate is often regarded as treatment failure, but, to our knowledge, it has not been compared with a matched control population and could instead reflect the stroke rate in people of a comparable baseline risk without AF.
Nature Reviews Cardiology | 2017
Ben Freedman; Giuseppe Boriani; Taya V. Glotzer; Jeff S. Healey; Paulus Kirchhof; Tatjana S. Potpara
Cardiac implanted electronic devices (CIEDs), including pacemakers and implantable defibrillators that perform atrial sensing typically using an atrial electrode, frequently detect subclinical atrial high-rate episodes (AHREs). When the intracardiac electrograms are carefully examined, the majority of AHREs are atrial fibrillation (AF) or other atrial tachyarrhythmias, which have been shown to be associated with both an increased risk of stroke, and subsequent development of clinical AF. However, the absolute risk of stroke among patients with AHREs is less than might be expected for clinically diagnosed paroxysmal AF. In addition, a close temporal relationship between AHREs and stroke is seen in only 15% of strokes in patients with a CIED: the majority have either no AHREs before the stroke, or AHREs very distant from incident stroke, suggesting that AHREs might be more of a risk marker than a risk factor for stroke. Management of AHREs should not be the same as for clinical AF, and a degree of uncertainty underpins the rationale for much-needed, ongoing, randomized trials of oral anticoagulation in patients with CIED-detected AHREs. We propose a management algorithm that takes into account both the stroke risk and the AHRE burden, but highlights the current uncertainty and evidence gaps for this condition.
Journal of the American Heart Association | 2016
Ben Freedman
Atrial fibrillation (AF) is a growing problem in cardiovascular disease and is associated with an increased risk of severe stroke, heart failure, and death. Indeed, recent stroke registries indicate that AF is associated with a third of all ischemic strokes.[1][1] Anticoagulation with warfarin or
Europace | 2018
Dipak Kotecha; Günter Breithardt; A. John Camm; Gregory Y.H. Lip; Ulrich Schotten; Anders Ahlsson; David O. Arnar; Dan Atar; Angelo Auricchio; Jeroen J. Bax; Stefano Benussi; Carina Blomström-Lundqvist; M. Borggrefe; Giuseppe Boriani; Axel Brandes; Hugh Calkins; Barbara Casadei; Manuel Castellá; Winnie W. L. Chua; Harry J.G.M. Crijns; Dobromir Dobrev; Larissa Fabritz; Martin Feuring; Ben Freedman; Andrea Gerth; Andreas Goette; Eduard Guasch; Doreen Haase; Stéphane N. Hatem; Karl Georg Haeusler
There are major challenges ahead for clinicians treating patients with atrial fibrillation (AF). The population with AF is expected to expand considerably and yet, apart from anticoagulation, therapies used in AF have not been shown to consistently impact on mortality or reduce adverse cardiovascular events. New approaches to AF management, including the use of novel technologies and structured, integrated care, have the potential to enhance clinical phenotyping or result in better treatment selection and stratified therapy. Here, we report the outcomes of the 6th Consensus Conference of the Atrial Fibrillation Network (AFNET) and the European Heart Rhythm Association (EHRA), held at the European Society of Cardiology Heart House in Sophia Antipolis, France, 17-19 January 2017. Sixty-two global specialists in AF and 13 industry partners met to develop innovative solutions based on new approaches to screening and diagnosis, enhancing integration of AF care, developing clinical pathways for treating complex patients, improving stroke prevention strategies, and better patient selection for heart rate and rhythm control. Ultimately, these approaches can lead to better outcomes for patients with AF.
Heart Lung and Circulation | 2015
David Colquhoun; Ben Freedman; David Cross; Ben Fitzgerald; Brett Forge; David L. Hare; James Tatoulis; John Wicks; A. Wilson; Robert Zecchin
This position paper provide guidelines on the minimum requirements of both personnel and equipment for the safe performance of clinical exercise electrocardiography, and for the adequate interpretation and assessment of results. This document was originally developed by Professor Ben Freedman and members of the Rehabilitation, Exercise and Prevention Working Group in 1996. It has been recently reviewed by a Working Group chaired by Associate Professor David Colquhoun. The resulting, revised Statement was considered by the Continuing Education and Recertification Committee and ratified at the CSANZ Board meeting held on 1st August 2014.