The ACCF/AHA Scientific Statement on Syncope:
a document in need of thoughtful revision
David G. Benditt on behalf of the A...
Proper definitions
Clinicians need clear, practical, and accurate definitions of
syncope and related terminology before they...
circumstances and limitations of ICD or pacemaker utiliz-
ation in syncope patients. For instance, although ICDs may
preve...
Rose-Anne Kenny
Institute of Neuroscience, Trinity College, Dublin 2, Ireland
Institute for the Health of the Elderly, Uni...
19. Connolly SJ, Sheldon R, Roberts RS, Gent M Vasovagal Pacemaker Study
Investigators. The North American vasovagal pacem...
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Revisão guideline americano síncope

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Revisão guideline americano síncope

  1. 1. The ACCF/AHA Scientific Statement on Syncope: a document in need of thoughtful revision David G. Benditt on behalf of the Ad Hoc Syncope Consortium{ Cardiovascular Division, Cardiac Arrhythmia Center, University of Minnesota Medical School, Mail Code 508, 420 Delaware St SE, Minneapolis, MN 55455, USA Received 26 July 2006; accepted after revision 22 August 2006 The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have recently published, in both the Journal of the American College of Cardiology (JACC) and Circulation, a Scientific Statement on the Evaluation of Syncope (‘Statement’). This Scientific Statement was commis- sioned to provide guidance for clinicians regarding the evaluation of patients who present with ‘syncope’. The Statement was not intended to be a formal set of practice guidelines. However, in the absence of generally accepted practice guidelines in North America, the Statement’s potential impact on clinical care may be more far-reaching than expected; it may erroneously be considered to be the authoritative ‘de-facto’ guideline document. This commentary, submitted by a multidisciplin- ary consortium of more than 60 physicians with expertise in the management of transient loss of consciousness (TLOC), points out that in many respects the ACCF/AHA Syncope Statement fails to address long-standing clinical errors associated with the evaluation of episodes of apparent TLOC, including syncope. If not appropriately revised, the current Statement may lead to both inadequate patient care as well as a potentially damaging legal environment for physicians undertaking evaluation of patients who present with transient loss of consciousness. KEYWORDS Syncope; Practice guidelines; Diagnosis; Evaluation; Management Introduction Recently, the American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) published, in both Journal of the American College of Cardiology (JACC) and Circulation, a scientific statement on the evalu- ation of syncope (‘statement’).1 This scientific statement was commissioned to provide guidance for clinicians regard- ing the evaluation of patients who present with ‘syncope’. The ACCF/AHA statement was not intended to be a formal set of practice guidelines. Nonetheless, in the absence of formal practice guidelines endorsed by professional societies in North America, the statement’s impact on clini- cal care may be far-reaching. In fact, given its carrying the imprimatur of the ACCF, the AHA, and the Heart Rhythm Society, the statement may be erroneously considered to be the authoritative de facto guideline document. The Ad Hoc Syncope Consortium is a multidisciplinary group of more than 60 physicians with expertise in the management of patients presenting with transient loss of consciousness (TLOC), including syncope. The consortium formed primarily as a result of its individual members having identified important concerns with the ACCF/AHA syncope statement. Apart from alerting readers to the syncope statement’s shortcomings, the consortium’s goals are to support thoughtful revision of the syncope statement and to promote development of guidelines for management of patients with TLOC that takes into account the multifa- ceted nature of the problem. To this end, the Ad Hoc Consortium has published a commentary regarding the syncope statement on Heart.org and a brief letter addres- sing some of our concerns with the statement in JACC. Circulation has declined publishing any critique of the statement. In the consortium’s opinion, the ACCF/AHA syncope state- ment does not adequately address many long-standing clini- cal errors associated with the evaluation of episodes of apparent self-limited TLOC, including syncope. In addition, the statement’s messages and conclusions are often impre- cise and seem to lack balance. Although, in some instances, our disagreements with the statement’s positions may simply reflect honest differences of opinion, there are clear-cut oversights in the statement that deserve attention. Several important shortcomings are highlighted subsequently. & The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org Corresponding author. Tel: þ1 612 625 4401; fax: þ1 612 624 4937. E-mail address: bendi001@umn.edu { The list of co-authors belonging to the AD Hoc Syncope Consortium is given in the appendix. Europace (2006) 8, 1017–1021 doi:10.1093/europace/eul134
  2. 2. Proper definitions Clinicians need clear, practical, and accurate definitions of syncope and related terminology before they can begin their diagnostic evaluation. The ACCF/AHA statement does not provide accurate definitions. For instance, it is critical in our opinion that a document focusing on the syncope evalu- ation addresses the fundamental issue, ‘what is syncope?’. The statement’s approach is inadequate; it does not establish the distinction between syncope and the broader problem of TLOC.2–4 For the statement to be useful, it must address what syncope is and how it differs from other forms of TLOC (e.g. concussion due to trauma, epileptic seizures due to a primary electrical problem, and apparent TLOC such as in con- version disorders). To be fair, failure to distinguish syncope from other forms of TLOC is an error,5 which is also found in other prominent medical writings.6,7 The absence of clarity regarding the central topic of the statement’s interest only serves to aggravate other long-standing misunderstandings. By way of example, the statement itself continues to foster the misconception that ‘vasovagal’ and ‘neurocardiogenic’syncopes are synonymous. The former is, in fact, a subset of the neurocardiogenic faints (the preferred term being neurally mediated reflex faints 8 ). This may appear to be a minor point, and certainly elimination of all errors is not a reasonable expectation, but it is indicative of the need for careful and critical review of statements from professional societies prior to publication. The consequence of imprecise definitions is propagation of unclear thinking among clinicians. The outcome is uncer- tainty leading to excessive and generally futile overuse of inappropriate medical tests.9–12 The statement missed an opportunity to rectify this major problem; one that leads to unnecessary costs and possible patient harm. Absence of citations to many published contemporary statements and documents The ACCF/AHA statement offers as a goal ‘to summarize the data that direct the evaluation of the patient with syncope’. However, the statement fails to cite important recent contributions to the syncope evaluation. Most importantly, the European Society of Cardiology (ESC) Syncope Guideline statements8,13 published in 2001 and revised in 2004 are missing. In this regard, a number of Consortium’s members (Ã ) admit a potential conflict of interest, having participated in the ESC guideline development. Contrary to the preferred current practice in which the best available medical evidence is used to support clinical recommendations, the statement ignores the majority of recently published controlled trials in the field. For instance, although the statement’s authors cite three ICD trials14–16 and one drug trial,17 none of which focused primarily on a syncope population per se, they only reference a single non-ICD trial that did enroll true syncope patients.18 Further, the authors failed to cite either of the two major North American pacing trials targeting syncope patients (VPS-1 and VPS-219,20 ), or the single large beta-blocker trial (POST21,22 ), or the only trial examining the utility of an organized syncope management unit in a North American hospital (SEEDS23 ). Moreover, the current statement omits citing any of the several European randomized and/or controlled clinical trials that assessed various aspects of the syncope evaluation, and several of which were published in the North American journals. With the exception of the citation of SAFE-PACE,24 published clinical trials such as EGSYS,25 OESIL,26 OESIL2,27 ISSUE-1,28–30 ISSUE-2,31 VASIS,32,33 SYDIT,34 and SYNPACE35 were not referenced. It is true that the statement was commissioned to focus on ‘evaluation’ (not on treatment) and apparently had space limitations that may have precluded citing all pertinent literatures. Further, many, but not all, of the missing cita- tions examined aspects of syncope treatment rather than diagnostic evaluation. In contrast, it is impractical to try to divorce evaluation and treatment completely. All of the pub- lished studies provide important insights into the optimal evaluation process. Indeed, many of the studies that were cited in the statement were no less treatment-oriented than were the multitude of studies that were omitted. The rationale for the evaluation of syncope is not solely to provide a mortality risk assessment According to the statement, the primary ‘purpose of the (syncope) evaluation’ is ‘to determine whether the patient is at increased risk for death’. We agree that mortality risk assessment is a valid concern. However, the vast majority of these patients has disturbing or disabling condition, which is not life threatening, but may diminish quality of life and lead to physical injury.2,6,36–40 Consequently, the rationale for the syncope evaluation should be a more fun- damental one, namely, to establish the cause of the patient’s symptoms with sufficient confidence to assess prognosis and recommend an effective treatment strategy.8,13,36,37 Appropriate clinical perspective The statement focuses on the relatively small, albeit important, subset of high-risk patients (at most 20% of those with syncope) who may require treatment with cardio- vascular interventions such as implantable cardioverter- defibrillators (ICDs) or pacemakers. However, thoughtful consideration of far more prevalent causes of syncope, namely, those of neurally mediated reflex or orthostatic origin, are hardly addressed.36,37,39–42 These latter con- ditions account overall for more than half of all syncope cases, although rarely life-threatening can result in substan- tial morbidity. Furthermore, certain types of faints (e.g. vasovagal syncope and situational faints) are particularly important in children and young adults. The relevance of patient age to the syncope evaluation process (i.e. the like- lihood of one or other form of syncope being more or less probable) is inadequately addressed in the statement. The fact that neurally mediated and orthostatic fainting con- ditions have been the subject of many recent published studies and reviews36,37,40–52 does not exempt the state- ment from providing practitioners with an appropriate perspective on the problem. Even regarding ICD and pacemaker therapies, the state- ment lacks a comprehensive and carefully defined approach. Specifically, the statement does not provide practitioners with sufficient depth of insight into the appropriate 1018 Editorial Comment
  3. 3. circumstances and limitations of ICD or pacemaker utiliz- ation in syncope patients. For instance, although ICDs may prevent arrhythmic death, they may not alleviate syncope. This vital aspect of the treatment of the high-risk fainter is a common dilemma in patients with structural heart disease, as well as in individuals with less common con- ditions such as long QT syndrome and Brugada syndrome. It remains unexplored in the statement. In the case of syncope patients with normal hearts, the statement underemphasizes the importance of a thorough evaluation. The statement implies that aggressive diagnostic effort is only needed in the most severe (‘malignant’) forms of syncope, where ‘malignant’ is ‘defined as an episode of syncope that occurs with little or no warning and results in significant injury or property damage’. This teaching unfor- tunately tends to diminish the importance of symptoms in the vast majority of fainters, individuals who we know have substantially reduced quality of life,53 and who may be at future risk of injury, accident, or economic loss because of occupational issues. The statement should encourage effective diagnostic assessment in all types of syncope patients. Beyond ICDs and pacemakers, clinicians should be made aware of evol- ving treatment options for vasovagal fainters, or patients with orthostatic hypotension, including those suffering from various dysautonomias.43–51 A revised statement should incorporate a more thoughtful assessment of the important role that medical specialists outside the cardiovascular disease arena play in the evalu- ation of TLOC/syncope. Neuroscience, internal medicine, paediatrics, and geriatric specialties, among others, con- tribute daily to the care of patients who present with appar- ent loss of consciousness spells. Without input from leaders in these fields, recommendations for the syncope evalu- ation, such as those provided in the ACCF/AHA statement, cannot be considered complete and credible. In conclusion, we would like to emphasize our concern that the current ACCF/AHA statement may be mistakenly construed as an authoritative text. In the absence of a well- considered set of practice guidelines, the statement could unfortunately become an inappropriate ‘standard’ for all syncope evaluations in the USA and Canada. As such, its current contents may lead to both less than optimal patient care and a potentially damaging legal environment for physicians undertaking the evaluation of patients who present with TLOC. It is clear that development of interna- tionally applicable multidisciplinary formal practice guide- lines must receive high priority. Appendix Wouter Wieling Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands Haruhiko Abe The Second Department of Internal Medicine,University of Occupational and Environmental Health, Yahatanishi, Kitakyushu 807-8555, Japan Paolo Alboni Divisione di Cardiologia, Ospedale Civile, Cento, Italy Dietrich Andresen Direktor der Klinik fu¨r Innere Medizin-Kardiologie/Angiologie/ konserv, Intensivmedizin, Vivantes-Klinikum Am Urban/Im Friedrichshain 10 967, Berlin Felicia B. Axelrod New York University School of Medicine, Carl Seaman Family Professor of Dysautonomia Treatment and Research, Pediatrics, NYU Medical Center, New York, NY, USA Eduardo Bennaroch Department of Neurology, Mayo Medical School, Mayo Clinic, Rochester, MN, USA Lennart Bergfeldt Department of Cardiology, Sahlgrenska Academy, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden Jean Jacques Blanc Departement de Cardiologie, Universite de Brest, Hopital de la Cavale Blanche, CHU de Brest, France Michele Brignole Department of Cardiology and Arrhythmologic Centre, Ospedali del Tigullio, 16033 Lavagna, Italy A. John Camm St George’s Medical School of London, Cranmer Terrace, London, UK Thomas Chelimsky Case Western Reserve University, American Academy of Neurology, University Hospitals of Cleveland, Cleveland, OH, USA Pietro Cortelli Alma Mater Studiorum-Universita’di Bologna, Dipartimento di Scienze Neurologiche, 40123 Bologna, Italy J. Gert van Dijk Department of Neurology and Clinical Neurophysiology, Leiden University Medical Centre, Leiden, The Netherlands Nynke van Dijk Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands Murray Esler Monash University, Melbourne, Australia Baker Heart Research Institute, Melbourne, Victoria 8008, Australia Adam Fitzpatrick Manchester Heart Centre, Royal Infirmary, Manchester, UK Fetnat Fouad-Tarazi Department of Cardiology, Cleveland Clinic Foundation, Cleveland, OH, USA Roy Freeman Harvard Medical School, Center for Autonomic and Peripheral Nerve Disorders, Beth Israel Deaconess Medical Center, Boston, MA, USA MaryAnn Goldstein Pediatric Emergency Medicine, Minneapolis, MN, USA Blair Grubb Medical College of Ohio, Toledo, OH, USA Bengt Herweg University of South Florida, Tampa, FL, 33606, USA Max J. Hilz Department of Neurology, University Erlangen-Nuremberg, Erlangen, Germany American Academy of Neurology, New York University School of Medicine, New York, NY, USA Giris Jacob Rambam Medical Center and Technion IIT, Hiafa, Israel David Jardine Christchurch School of Medicine, University of Otago, Christchurch, New Zealand Jens Jordan Franz-Volhard Centrum fu¨r Klinische Forschung, 13125 Berlin, Germany Michael J. Joyner Mayo Clinic, Rochester, MN, USA Wishwa Kapoor Department of Internal Medicine, University of Pittsburgh, Pittsburgh, PA, USA Horacio Kaufmann Mount Sinai School of Medicine, New York, NY, USA Editorial Comment 1019
  4. 4. Rose-Anne Kenny Institute of Neuroscience, Trinity College, Dublin 2, Ireland Institute for the Health of the Elderly, University of Newcastle Upon Tyne, Royal,Victoria Infirmary, Newcastle upon Tyne, UK Andrew Krahn Arrhythmia Monitoring Unit, London Health Sciences Centre, University of Western Ontario, London, Ontario, Canada Chu-Pak Lau Department of Medicine, Hong Kong University and Queen Mary Hospital, Hong Kong, China Benjamin D. Levine Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, TX 75231, USA Johannes J. van Lieshout Department of Internal Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands Lewis Lipsitz Hebrew Senior Life Institute for Aging Research, Boston, MA, USA Philip Low Mayo Clinic College of Medicine, Mayo Clinic, Rochester, MN, USA Keith G. Lurie University of Minnesota Medical School and Central Minnesota Heart Center, Hennepin County Hospital, Minneapolis, MN, USA St Cloud Hospital, St Cloud Minnesota, USA Christopher J. Mathias Neurovascular Medicine Unit, Faculty of Medicine, Imperial College London at St Mary’s Hospital, The Queen Elizabeth, The Queen Mother Wing, London W2 1NY, UK Autonomic Unit, National Hospital for Neurology and Neurosurgery, Queen Square and Institute of Neurology, University College London, London WC1 N 3BG, UK Angel Moya Department of Cardiology, Hospital General Vall d’Hebron, 08035 Barcelona, Spain Brian Olshansky University of Iowa Medical School, Iowa City, IA, USA Satish R. Raj Vanderbilt University, Nashville, TN, USA Antonio Raviele Divisione di Cardiologia, Ospedale Umberto I, Mestre-Venice, Italy Sanjeev Saksena Robert Wood Johnson Medical School, Millburn, NJ, USA Francois P. Sarasin Hopital Cantonal, University of Geneva Medical School, 1211 Geneva 14, Switzerland Philip J. Saul Medical University of South Carolina, Charleston, SC, USA Ronald Schondorf Department of Neurology McGill University, SMBD Jewish General Hospital, Montreal, Quebec, Canada Jean-Michel Senard School of Medicine, University of Toulouse III, Faculte´ de Me´decine, 31000 Toulouse, France Robert Sheldon Libin Cardiovascular Institute of Alberta, University of Calgary, Calgary, Alberta, Canada Win-Kuang Shen Mayo Medical School, Mayo Clinic, Rochester, MN, USA Jasbir Sra University of Wisconsin- Milwaukee, Milwaukee, WI, USA John Stephenson Fraser of Allander Neurosciences Unit, Royal Hospital for Sick Children, Glasgow G3 8SJ, Scotland Division of Developmental Medicine, University of Glasgow, Scotland Julian M. Stewart Center for Hypotension, New York Medical College, Hawthorne, NY 10532, USA Richard Sutton Royal Brompton Hospital, London, UK Hidetaka Tanaka Department of Developmental Pediatrics, Osaka Medical College Hospital, Osaka 569-8686, Japan George Theodorakis 28 Department of Cardiology, Onassis Cardiac Surgery Center, Athens, Greece Andrea Ungar Department of Critical Care Medicine and Surgery—Unit of Geriatrics and Gerontology, University of Florence, 50141 Florence, Italy A.A.M. Wilde Department of Cardiology, Academic Medical Center Amsterdam, 1105 AZ Amsterdam, The Netherlands References 1. Strickberger SA, Benson DW Jr, Biagggioni I et al. AHA/ACCF scientific statement on the evaluation of syncope. J Am Coll Cardiol 2006;47: 473–84; Circulation 2006;113:316–27. 2. Blanc JJ, Benditt DG. Syncope: definition, classification, and multiple potential causes. In: Benditt DG, Blanc JJ, Brignole M, Sutton R, eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura/Black- well Publishing; 2003. p3–10. 3. Thijs RD, Wieling W, Kaufmann H, van Dijk G. Defining and classifying syncope. Clin Autonom Res 2004;14 (Suppl. 1):4–8. 4. Mathias CJ. Role of autonomic evaluation in the diagnosis and manage- ment of syncope. Clin Autonom Res 2004;14 (Suppl. 1):45–54. 5. Thijs RD, Benditt DG, Mathias CJ et al. Unconscious confusion. A litera- ture search for definitions of syncope and related disorders. Clin Auton Res 2005;15:35–9. 6. Soteriades ES, Evans JC, Larson MG et al. Incidence and prognosis of syncope. N Engl J Med 2002;347:878–85. 7. Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. Br Med J 2004;329:336–41. 8. Brignole M, Alboni P, Benditt DG et al. Guidelines on management (diag- nosis and treatment) of syncope. Eur Heart J 2001;22:1256–306. 9. Kapoor W, Karpf M, Maher Y et al. Syncope of unknown origin: the need for a more cost-effective approach to its diagnostic evaluation. JAMA 1982;247:2687–91. 10. Nyman J, Krahn A, Bland P, Criffiths S, Manda V. The costs of recurrent syncope of unknown origin in elderly patients. PACE 1999;22:1386–94. 11. Kenny RA, O’Shea D, Walker HF. Impact of a dedicated syncope and falls facility for older adults on emergency beds. Age Ageing 2002;31:272–5. 12. Sun BC, Emond JA, Camargo CA Jr. Direct medical costs of syncope-related hospitalizations in the United States. Am J Cardiol 2005;95:668–71. 13. Brignole M, Alboni P, Benditt DG et al. Guidelines on management (diag- nosis and treatment) of syncope—update 2004. Europace 2004;6:467–537. 14. Moss AJ, Zareba W, Hall WJ et al. for the Multicenter Automatic Defibrillator Implantation Trial II Investigators. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejec- tion fraction. N Engl J Med 2002;346:877–83. 15. Bardy GH, Lee KL, Mark DB, et al. for the Sudden Cardiac death in Heart failure trial (SCD-HeFT) Investigators. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med 2005;352:225–37. 16. Kadish A, Dyer A, Daubert DP, for the Defibrillators in Nonischemic Cardiomyopathy Evaluation (DEFINITE) Investigators. Prophylactic defi- brillator implantation in patients with nonischemic dilated cardiomyopa- thy. N Engl J Med 2004;350:2151–8. 17. Packer M, Bristow MR, Cohn JN et al. The effect of carvedilol on morbid- ity and mortality in patients with chronic heart failure: US Carvedilol Heart Failure Study group. N Engl J Med 1996;334:1349–55. 18. Krahn A, Klein GJ, Yee R, Skanes AC. Randomized assessment of syncope trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation 2001;104:46–51. 1020 Editorial Comment
  5. 5. 19. Connolly SJ, Sheldon R, Roberts RS, Gent M Vasovagal Pacemaker Study Investigators. The North American vasovagal pacemaker study (VPS): a randomized trial of permanent cardiac pacing for the prevention of vasovagal syncope. J Am Coll Cardiol 1999;33:16–20. 20. Connolly S, Sheldon R, Thorpe KE et al. Pacemaker therapy for preven- tion of syncope in patients with recurrent vasovagal syncope. JAMA 2003;289:2224–9. 21. Sheldon R, Rose S, Connolly S. Prevention of Syncope Trial (POST): a ran- domized clinical trial of beta blockers in the prevention of vasovagal syncope; rationale and study design. Europace 2003;5:71–5. 22. Sheldon RS, Connelly S, Rose S et al. The prevention of syncope trial (POST). A randomized, placebo-controlled study of metoprolol in the pre- vention of vasovagal syncope. Circulation 2006;113:1164–70. 23. Shen WK, Decker WW, Smars PA et al. Syncope Evaluation in the Emergency Department Study (SEEDS): a multidisciplinary approach to syncope management. Circulation 2004;110:3636–45. 24. Kenny RA, Richardson DA, Steen N et al. Carotid sinus syndrome: a modifiable risk factor for non-accidental falls in older adults (SAFE PACE). J Am Coll Cardiol 2001;38:1491–6. 25. Brignole M, Disertori M, Menozzi C et al. Evaluation of guidelines in syncope study group. Management of syncope referred urgently to general hospitals with and without syncope units. Europace 2003;5:293–8. 26. Ammirati F, Colivicchi F, Minardi G et al. Hospital management of syncope: the OESIL study. G Ital Cardiol 1999;29:533–9. 27. Ammirati F, Colivicchi F, Santini M et al. Diagnosing syncope in clinical practice. Implementation of a simplified diagnostic algorithm in a multi- centre prospective trial—the OESIL 2 study (Observatorio Epidemiologico della Sincope nel Lazio). Eur Heart J 2000;21:935–40. 28. Moya A, Brignole M, Menozzi C, Garcia-Civera R, Tognarini S, Mont L et al., ISSUE Investigators. Mechanism of syncope in patients with iso- lated syncope and in patients with tilt-positive syncope. Circulation 2001;104:1261–7. 29. Brignole M, Menozzi C, Moya A et al. Mechanism of syncope in patients with bundle branch block and negative electrophysiologic test. Circulation 2001;104:2045–50. 30. Menozzi C, Brignole M, Garcia-Civera R et al. Mechanism of syncope in patients with heart disease and negative electrophysiologic test. Circulation 2002;105:2741–5. 31. Brignole M. Randomized clinical trials of neurally mediated syncope. J - Cardiovasc Electrophysiol 2003;14 (Suppl.):S64–9. 32. Raviele A, Brignole M, Sutton R et al. Effect of etilefrine in preventing syncopal recurrence in patients with vasovagal syncope: a double-blind, randomized, placebo-controlled trial. The Vasovagal Syncope International Study. Circulation 1999;99:1452–57. 33. Sutton R, Brignole M, Menozzi C, Raviele A, Alboni P, Giani P et al., for the VASIS Investigators. Dual-chamber pacing is efficacious in treatment of neurally-mediated tilt-positive cardioinhibitory syncope. Pacemaker versus no therapy: a multicentre randomized study. Circulation 2000;102:294–9. 34. Ammirati F, Colivicchi F, Santini M et al. Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope. A multicenter, randomized, controlled trial. Circulation 2001;104:52–6. 35. Raviele A, Giada F, Menozzi C, Speca G, Orazi S, Gasparini G et al., Vasovagal Syncope and Pacing Trial Investigators. A randomized, double-blind, placebo-controlled study of permanent cardiac pacing for the treatment of recurrent tilt-induced vasovagal syncope. The Vasovagal Syncope and Pacing trial (SYNPACE). Eur Heart J 2004;25:1741–8. 36. Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:160–75. 37. Colman N, Nahm K, van Dijk JG, Reitsma JB, Wieling W, Kaufmann H. Diagnostic value of history taking in reflex syncope. Clin Auton Res 2004;14 (Suppl. 1):37–44. 38. Blanc J-J, L’Her C, Touiza A et al. Prospective evaluation and outcome of patients admitted for syncope over a 1-year period. Eur Heart J 2002; 23:815–20. 39. Chen LY, Gersh BJ, Hodge DO et al. Prevalence and clinical outcomes of patients with multiple potential causes of syncope. Mayo Clin Proc 2003;78:414–20. 40. Colman N, Nahm K, Ganzeboom KS et al. Epidemiology of reflex syncope. Clin Auton Res 2004;14 (Suppl. 1):9–17. 41. Mathias CJ, Deguchi K, Schatz I. Observations on recurrent syncope and presyncope in 641 patients. Lancet 2001;357:348–53. 42. Ganzeboom KS, Colman N, Reitsma JB, Shen WK, Wieling W. Prevalence and triggers for syncope in medical students. Am J Cardiol 2003; 91:1006–8. 43. Ector H, Reybrouck T, Heidbuchel H, Gewillig M, Van de Werf F. Tilt train- ing: a new treatment for recurrent neurocardiogenic syncope or severe orthostatic intolerance. PACE 1998;21:193–6. 44. Di Girolamo E, Di Iorio C, Leonzio L, Sabatini P, Barsotti A. Usefulness of a tilt training program for prevention of refractory neurocardiogenic syncope in adolescents. A controlled study. Circulation 1999;100: 1798–801. 45. Abe H, Kondo S, Kohshi K et al. Usefulness of orthostatic self-training for the prevention of neurocardiogenic syncope. PACE 2002;25:1454–8. 46. Abe H, Kohshi K, Nakashima Y. Home orthostatic self-training in neurocar- diogenic syncope. PACE 2005;28 (Suppl. 1):S246–8. 47. Wieling W, Van Lieshout JJ, Van Leeuwen AM. Physical maneuvers that reduce postural hypotension in autonomic failure. Clin Auton Res 1993;3:57–65. 48. Van Lieshout JJ, Ten Harkel ADJ, Wieling W. Combating orthostatic dizzi- ness in autonomic failure by physical maneuvers. Lancet 1992;339: 897–8. 49. Van Dijk N, Sprangers MA, Colman N et al. Clinical factors associated with quality of life in patients with transient loss of consciousness. J Cardiovasc Electrophysiol 2006;17:1–5. 50. Melby DP, Cytron JA, Benditt DG. New approaches to the treatment and prevention of neurally-medicated reflex (neurocardiogenic) syncope. Curr Cardiol Rep 2004;6:385–90. 51. van Dijk N, de Bruin IG, Gisolf J, de Bruin-Bon HA, Linzer M, van Lieshout JJ et al. Hemodynamic effects of leg crossing and skeletal muscle tensing during free standing in patients with vasovagal syncope. J Appl Physiol 2005;98:584–90. 52. Benditt DG, Ferguson DW, Grubb BP et al. Tilt table testing for assessing syncope. ACC expert consensus document. J Am Coll Cardiol 1996;28: 263–75. 53. Linzer M, Pontinen M, Gold DT, Divine GW, Felder A, Brooks WB. Impairment of physical and psychosocial function in recurrent syncope. J Clin Epidemiol 1991;44:1037–43. Editorial Comment 1021

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