Electrophysiological Testing
1995; Lippincott Williams & Wilkins; Volume: 92; Issue: 5 Linguagem: Inglês
10.1161/01.cir.92.5.1332
ISSN1524-4539
AutoresGeorge J. Klein, Bernard J. Gersh, Raymond Yee,
Tópico(s)Cardiac electrophysiology and arrhythmias
ResumoHomeCirculationVol. 92, No. 5Electrophysiological Testing Free AccessResearch ArticleDownload EPUBAboutView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticleDownload EPUBElectrophysiological Testing The Final Court of Appeal for Diagnosis of Syncope? George J. Klein, Bernard J. Gersh and Raymond Yee George J. KleinGeorge J. Klein From the Department of Medicine, University of Western Ontario, London, Ontario, Canada, and the Cardiology Division, Georgetown University Medical Center, Washington, DC, USA. , Bernard J. GershBernard J. Gersh From the Department of Medicine, University of Western Ontario, London, Ontario, Canada, and the Cardiology Division, Georgetown University Medical Center, Washington, DC, USA. and Raymond YeeRaymond Yee From the Department of Medicine, University of Western Ontario, London, Ontario, Canada, and the Cardiology Division, Georgetown University Medical Center, Washington, DC, USA. Originally published1 Sep 1995https://doi.org/10.1161/01.CIR.92.5.1332Circulation. 1995;92:1332–1335Unexplained syncope is a relatively frequent cause of admission to emergency departments, and it continues to pose a clinical dilemma, despite the development of new diagnostic techniques.123456 For the patient, the syndrome is a source of morbidity and, to a lesser extent, mortality. Recurrences may have a substantial and deleterious effect on lifestyle, the sense of physical well-being, and employment opportunities. Understandably, the search for treatable or preventable causes and identification of cost-effective approaches to syncope continue to remain a focus of clinical interest. Diagnostic Evaluation The cause of a syncopal episode is frequently problematic if the diagnosis is not evident after the initial clinical and laboratory assessment.123456 The major obstacle to diagnosis is the periodic and unpredictable frequency of events, with months and years separating spells and a high spontaneous remission rate.7 This creates a prohibitive barrier for recording of the ECG during a spontaneous episode in most patients, and even aggressive and prolonged ECG monitoring may yield only a 16% diagnosis rate over a 6-month period.5 Perhaps the most valuable clinical tools for the diagnosis of syncope are the clinical history and, in some patients, the use of additional tests to identify structural heart disease. An abnormal ECG frequently is present in patients with syncope but rarely identifies the specific cause. Prolonged ambulatory monitoring has been used widely as a diagnostic tool, but most frequently it identifies nonspecific arrhythmias in the absence of symptoms. Despite the widespread acceptance of ambulatory monitoring as a key aspect of our diagnostic armamentarium for syncope, documentation of significant arrhythmias or syncope during ambulatory monitoring is extremely rare. The use of patient-activated recorders is most productive in motivated patients who experience relatively frequent episodes. Invasive Electrophysiological Testing In the absence of an ECG tracing or other record during spontaneous syncope, the only diagnostic gold standard, clinicians may rely on abnormal laboratory results to provide a presumptive diagnosis for initiating therapy. The goals of tilt testing and electrophysiological testing are to provoke symptoms under controlled conditions to arrive at a diagnosis. Reproducing symptoms can be more convincing than recording asymptomatic abnormalities, especially if a unique prodrome is reproduced. Reproducing symptoms is still a surrogate for the spontaneous event, however, and it is readily appreciated that sudden loss of consciousness in an individual may be subjectively similar regardless of the mode of induction. On the basis of the premise that most cardiogenic syncope is related to an arrhythmia, tachyarrhythmia, or bradyarrhythmia, electrophysiological testing has great intuitive appeal. Intracardiac recording can measure conduction time over the AV node and His-Purkinje system.89 Pacing and extrastimuli can assess the response of the sinus node to overdrive stimulation and stress the AV conduction system.10 Many "clinical" arrhythmias, including those due to AV reentry, AV node reentry, and monomorphic ventricular tachycardia, can be reproducibly induced in the electrophysiology laboratory.1112 In patients with unexplained syncope, however, there is no diagnostic gold standard to assess the validity of the result.5 The abnormalities observed are generally accepted as "specific" or "diagnostic" if markedly abnormal or if the abnormality is infrequently seen in healthy persons, as with sustained monomorphic ventricular tachycardia (VT). Since the earliest studies using electrophysiological studies for syncope,13141516 many investigators have described their clinical results with this technique for syncope patients after noninvasive attempts have failed.1718192021222324252627282930 Table 1 summarizes some larger studies in the range of ≥100 patients. All these studies have described abnormalities, most frequently sustained VT, that have been defined as "diagnostic," have based treatment on these abnormalities, and have reported the results of therapy. Patients who had negative study results had therapy withheld or were treated empirically. Table 1 demonstrates many of the complexities involved in analyzing the use of electrophysiological testing in the diagnosis of syncope. The overall impressions are that test results are positive in ≈50% of patients and that half the study population has organic heart disease. The likelihood of recurrence is low in patients who had positive test results (and who presumably were receiving electrophysiological testing-guided therapy). On the other hand, the results at first glance for patients who tested negative appear to be similar, with the exception of a lower cardiovascular disease mortality in this group as a manifestation of a lower incidence of underlying structural heart disease. Conclusions Based on Electrophysiological Testing A great deal has been learned from these studies. (1) The yield of abnormalities is higher in patients with heart disease, and the test is most productive in this group. (2) Patients who have positive electrophysiological study results (generally VT) have a poorer prognosis than those who tested negative (Table 1). Since patients with inducible VT have more severe heart disease and left ventricular dysfunction, the independent contribution of this variable has not been rigidly established. (3) Patients in whom therapy is predicted to be effective fare better than their counterparts who do not have predictive therapy in many17202325272829 but not all studies.18192230 If patients who do not have predicted effective therapy have a poor prognosis, it is uncertain whether this is related to absence of therapy or to identification of a higher-risk group whose VT cannot be suppressed adequately. (4) Every clinician performing these studies has been impressed by dramatic individual cases in which frequent episodes of syncope are eliminated after identification and treatment of the offending problem. Assessment of Therapeutic Efficacy: Statistical Limitations In most patients, assessment of the efficacy of therapy is hampered by the sporadic nature of syncopal events, the temporal proximity of the study, and the initiation of therapy to the most recent episode. The last reason is frequently the precipitant of the evaluation that consequently led to the introduction of therapy The effect of treatment on subsequent outcome is difficult to analyze statistically unless follow-up is lengthy or unless the patient has a history of frequent episodes occurring consistently over a prolonged period, which is an uncommon clinical syndrome. This circumstance is likely to bias the data in favor of a "favorable" response to therapy without a recurrence, but it may be a reflection of selection bias, in that the majority of patients would have had a recent episode before the electrophysiology study and would be reasonably expected to be free of recurrence for some time after the study. This could be entirely unrelated to the treatment instituted. Unresolved Issues The American Heart Association and the American College of Cardiology31 recommend electrophysiological testing if a diagnosis is not obtained by noninvasive techniques, especially in the patient with organic heart disease. But electrophysiological testing has significant shortcomings as a "court of last appeal" in this patient population (Table 2): (1) Inspection of Table 1 reveals that 14% to 70% of patients will have a nondiagnostic study performed. The tilt test has been used widely to screen patients for vasodepressor syncope, and routine use of this test (which was not used for any study in Table 1) undoubtedly would have improved diagnostic yield. In a study specifically addressing the yields of both electrophysiology studies and tilt tests, 26% of patients remained undiagnosed after both studies.32 Although these patients are said to have a good prognosis, it is small consolation to the individual faced with the specter of recurrent spells, which may limit their choice of occupation, recreational activities, and ability to drive. (2) Patients with severe organic heart disease and the elderly frequently have multiple abnormalities pointing to potential bradycardia or tachycardia.533 These abnormalities are not definitive, and since therapy is often invasive and complex (eg, permanent pacemaker implantation, antitachycardia devices, or antiarrhythmic drugs), the abnormal results place the physician and the patient in a quandary. Unfortunately, the specificity of these findings is unknown. (3) Diagnostic yield for patients with intermittent AV block and sinus node dysfunction may be low.3435 (4) Criteria for a "specific" abnormality have been established on reasonable principles but without rigid validation and with many gray areas. For example, are "borderline" abnormalities meaningful? Is sustained monomorphic VT at cycle length 180 as meaningful as that at cycle length 300, or is it "ventricular flutter" and not specific? Is a His-ventricular (HV) time diagnostic at 80 milliseconds but nonspecific at 70 milliseconds? What is the specificity? (5) How is organic heart disease defined? It is well established that clinical sustained monomorphic VT is induced most reliably and reproducibly in patients who have coronary artery disease and previous infarction and is induced considerably less reliably in other patients.4 Should electrophysiological testing be restricted to this group? Does noninducibility in a patient with valvular heart disease and left ventricular dilatation rule out ventricular tachycardia as a cause of syncope? (6) Does electrophysiological testing provide data that result in cure of syncope? Although such testing clearly does in individuals and may do so in general, this is difficult to prove with available data. Table 1 shows a "cure" rate of ≈84% in patients who tested positive and a cure rate of ≈78% in those who tested negative. It is reasonable to argue that a positive study selects a "sicker" group of patients who might otherwise have had an even lower cure rate. However, this clearly cannot be proved by treating all patients who tested positive and is not evident from data currently available. (7) Does electrophysiologically guided therapy improve the mortality rate in patients who experience syncope? The mortality rate in patients who have syncope and accompanying significant heart disease is high (Table 1), and electrophysiological testing is recommended in this group with the implicit hope that mortality can be prevented.31 Again, Table 1 shows that patients who tested positive continue to have a high mortality rate. Smaller studies have suggested that positive electrophysiology studies may identify higher-risk patients, but the mortality rate appears to be related to severity of heart disease and is not clearly altered by electrophysiological testing.3036 It is certainly arguable that the mortality rate in the electrophysiological study groups who tested positive in Table 1 would have been higher if patients were not treated, but this is not established clearly. Rules of evidence have been described for grading the quality of a "recommendation" on the basis of available data from level 1 (best) through level 5 (most tenuous).37 Electrophysiological testing for syncope is supported at best by level 4 evidence, since neither randomized nor concurrent cohort comparison data are available to validate the utility of this test for preventing syncope and reducing the mortality rate. Invasive electrophysiological testing for the diagnosis of syncope has been embraced enthusiastically by the electrophysiological community. The optimistic descriptor "diagnostic yield" is preferred in many publications over the alternative designation of "yield of abnormal results," and "sensitivity" is used with the assumption that the abnormal test result is the cause of syncope. Research has been focused to provide noninvasive predictors of a positive study21263839 rather than to validate the meaning of a positive test. This is not surprising, given the relative futility of other diagnostic techniques and the attractions of electrophysiological testing, which include a comprehensive assessment of the conduction system and the inducibility of supraventricular or ventricular arrhythmia. Nonetheless, although the logic of this diagnostic strategy, which has been in place for almost 15 years, is indisputable, the sensitivity and specificity of electrophysiological testing and the results of test-guided therapy on the recurrence of syncope have not been subjected to rigorous scrutiny. A major impediment to the evaluation of treatments that are based on this approach is the understandable reluctance of physicians to use placebo therapy, particularly in patients with syncope and underlying structural heart disease. Emerging technological advances would suggest that this is a trial whose time has now come (Figure). High-risk patients could be treated with implantable defibrillators or pacemakers that have the diagnostic capability to record subsequent events. This, in turn, would validate the result of the electrophysiological test that initially dictated the therapy. Patients can be randomized to therapy or no therapy if they are considered to be at low risk of sudden death.40 Alternatively, such patients could be randomized prospectively to strategies that did or did not incorporate electrophysiological testing. In patients with presumed vasodepressor syncope, there are conflicting data concerning the utility of pharmacological therapy that are based on the results of repeat tilt-table testing.4142 A positive tilt test result may expose a tendency toward vasodepressor syncope in an individual but does not prove that this caused syncope. The long-term reproducibility of a positive tilt test result is not clear.42 A large, multicenter trial is needed to assess our ability to treat this troublesome condition with pharmacological therapy and ways of assessing therapeutic efficacy ahead of time. The quest for diagnostic gold standards can be reestablished by a new technique that is capable of long-term ambulatory ECG monitoring for periods of months and years, as opposed to days and weeks.4344 This will be extremely helpful in the evaluation of patients who test negative and have sporadic episodes of syncope. In conclusion, the limitations of current strategies to diagnose and treat syncope have been appreciated by many contributors to the field.34571619202830343536 It is time to achieve the next milestone in our understanding and management of this problem, which is vexing for both physician and patient. Dr G.J. Klein is a Career Investigator for the Heart and Stroke Foundation of Ontario (Canada).Download figureDownload PowerPoint Figure 1. Potential framework for a randomized trial. ICD indicates implantable cardioverter defibrillator. Table 1. Electrophysiological Testing in Syncope Studyn (Follow-up1 )Mean Age, yMean Follow-up, moRatio of Male to Female PatientsSHD, %Positive Test, %Negative Test, %Posi-tiveNRCardiovascular Mortality RateNega-tiveNRCardiovascular Mortality RateTeichman et al24150 (137)62311.7507585> 92553>12Doherty2 et al28119 (85)51271.45266681334764Olshansky2 et al23105 (97)6025.81.6543973861800Click23 et al19112 (110)64306.2…86801914820Twidale23 et al2293 (90)73392.23548964755279335Denes2 et al3889 (82)56471.972719118299310Muller et al1813459221.9533081870811Lacroix2 et al17100 (98)61231.46548871552732Bachinsky et al21141 (140)592442.1693182569821Denniss et al2011159201.36633951767767TOTAL1154 (1084)Mean60292.25753841647787HD indicates structural heart disease; NR, no recurrent syncope. 1Available for follow-up. 2Carotid sinus massage considered part of electrophysiological study. 3Study restricted to bundle-branch block or bifascicular block. 4Median. 5Total mortality rate. Table 2. Unresolved Issues in Electrophysiological Testing for Syncope1.How does one manage the patient with negative test results?2.Which abnormality should be addressed when multiple potential causes are suggested?3.How does one assess "borderline" abnormalities?4.How does one define "structural heart disease"?5.What is the true efficacy of electrophysiologically guided therapy?6.Does electrophysiologically guided therapy improve mortality rates?This study was supported in part by the Heart and Stroke Foundation of Ontario (Canada). FootnotesCorrespondence to Dr George J. Klein, University Hospital, 339 Windermere Rd, London, Ontario, Canada N6A 5A5. References 1 Kapoor WN, Hammill SC, Gersh BJ. Diagnosis and natural history of syncope and the role of invasive electrophysiologic testing. Am J Cardiol.1989; 63:730-734. CrossrefMedlineGoogle Scholar2 Kapoor WN. Evaluation and management of the patient with syncope. JAMA.1992; 268:2553-2560. CrossrefMedlineGoogle Scholar3 Morady F. The evaluation of syncope with electrophysiologic studies. Cardiol Clin.1986; 4:515-526. CrossrefMedlineGoogle Scholar4 DiMarco JP. Electrophysiologic studies in patients with unexplained syncope. Circulation.1987; 75:140-141. Google Scholar5 Kapoor WN. Diagnostic evaluation of syncope. Am J Med.1991; 90:91-106. CrossrefMedlineGoogle Scholar6 Kapoor WN, Karpf M, Weiand S, Peterson JR, Levey GS. A prospective evaluation and follow-up of patients with syncope. N Engl J Med.1983; 309:197-204. CrossrefMedlineGoogle Scholar7 Manolis AS, Linzer M, Salem D, Estes NAM. Syncope: current diagnostic evaluation and management. Ann Intern Med.1990; 112:850-863. CrossrefMedlineGoogle Scholar8 Dhingra RC, Wyndham C, Bauernfeind R, Swiryn S, Deedwania PC, Smith T, Denes P, Rosen KM. Significance of block distal to the His bundle induced by atrial pacing in patients with chronic bifascicular block. Circulation.1979; 60:1455-1464. 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Electrophysiologic testing in the evaluation of patients with syncope of undetermined origin. Am J Cardiol.1982; 50:1309-1015. CrossrefMedlineGoogle Scholar15 Gulamhusein S, Naccarelli GV, Ko PT, Prystowsky EN, Zipes DP, Barnett HJM, Heger JJ, Klein GJ. Value and limitations of clinical electrophysiologic study in assessment of patients with unexplained syncope. Am J Med.1982; 73:700-705. CrossrefMedlineGoogle Scholar16 Akhtar M, Shenasa M, Denker S, Gilbert CJ, Rizwi N. Role of cardiac electrophysiologic studies in patients with unexplained syncope. PACE Pacing Clin Electrophysiol.1983; 6:192-201. CrossrefMedlineGoogle Scholar17 Lacroix D, Dubuc M, Kus T, Savard P, Shenasa M, Nadeau R. Evaluation of arrhythmic causes of syncope: correlation between Holter monitoring, electrophysiologic testing, and body surface potential mapping. Am Heart J.1991; 122:1346-1354. CrossrefMedlineGoogle Scholar18 Muller T, Roy D, Talajic M, Lemery R, Nattel S, Cassidy D. 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Predicting the outcomes of electrophysiologic studies of patients with unexplained syncope: preliminary validation of a derived model. J Gen Intern Med.1991; 6:113-120. CrossrefMedlineGoogle Scholar40 Savage DD, Corwin L, McGee DL, Kannel WB, Wolf PA. Epidemiologic features of isolated syncope: the Framingham study. Stroke.1985; 16:626-629. CrossrefMedlineGoogle Scholar41 Milstein S, Bvetikofer J, Dunnigan A, Benditt DG, Gornick C, Reyes WJ. Usefulness of disopyramide for prevention of upright tilt-induced hypotension-bradycardia. Am J Cardiol.1990; 65:1339-1344. CrossrefMedlineGoogle Scholar42 Morillo CA, Leitch JW, Yee R, Klein GJ. A placebo-controlled trial of intravenous and oral disopyramide for prevention of neurally mediated syncope induced by head-up tilt. J Am Coll Cardiol.1993; 22:1843-1848. CrossrefMedlineGoogle Scholar43 Murdock CJ, Klein GJ, Yee R, Leitch JW, Teo WS, Norris C. Feasibility of long-term electrocardiographic monitoring with an implanted device for syncope diagnosis. PACE Pacing Clin Electrophysiol.1990; 13:1374-1378. CrossrefMedlineGoogle Scholar44 Krahn AD, Klein GJ, Norris C, Yee R. The etiology of syncope in patients with negative tilt table and electrophysiological testing. Circulation. In press. Google Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Olshansky B and Sullivan R (2015) Syncope in Patients with Organic Heart Disease, Cardiology Clinics, 10.1016/j.ccl.2015.04.013, 33:3, (449-463), Online publication date: 1-Aug-2015. Olshansky B and Sullivan R (2013) Syncope in Patients with Organic Heart Disease, Cardiac Electrophysiology Clinics, 10.1016/j.ccep.2013.08.006, 5:4, (495-509), Online publication date: 1-Dec-2013. Olshansky B and Sullivan R (2013) Sudden Death Risk in Syncope: The Role of The Implantable Cardioverter Defibrillator, Progress in Cardiovascular Diseases, 10.1016/j.pcad.2012.10.015, 55:4, (443-453), Online publication date: 1-Jan-2013. Rosanio S, Schwarz E, Ware D and Vitarelli A (2013) Syncope in adults: Systematic review and proposal of a diagnostic and therapeutic algorithm, International Journal of Cardiology, 10.1016/j.ijcard.2011.11.021, 162:3, (149-157), Online publication date: 1-Jan-2013. Angaran P, Klein G, Yee R, Skanes A, Gula L, Leong-Sit P and Krahn A (2011) Syncope, Neurologic Clinics, 10.1016/j.ncl.2011.07.005, 29:4, (903-925), Online publication date: 1-Nov-2011. Morillo C and Expósito-García V (2010) Unexplained Syncope Clinical Approach to Sudden Cardiac Death Syndromes, 10.1007/978-1-84882-927-5_3, (25-35), . 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September 1, 1995Vol 92, Issue 5 Advertisement Article InformationMetrics Copyright © 1995 by American Heart Associationhttps://doi.org/10.1161/01.CIR.92.5.1332 Manuscript receivedFebruary 9, 1995Manuscript acceptedMarch 26, 1995Originally publishedSeptember 1, 1995Manuscript revisedMarch 23, 1995 Keywordsdiagnosissyncopeelectrophysiologytachyarrhythmias Advertisement
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