(Circulation. 1995;92:1332-1335.)
© 1995 American Heart Association, Inc.
Articles |
Electrophysiological Testing
The Final Court of Appeal for Diagnosis of Syncope?
From the Department of Medicine, University of Western Ontario, London, Ontario, Canada, and the Cardiology Division, Georgetown University Medical Center, Washington, DC, USA.
Correspondence to Dr George J. Klein, University Hospital, 339 Windermere Rd, London, Ontario, Canada N6A 5A5.
Key Words: diagnosis • electrophysiology • tachyarrhythmias • syncope
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Introduction |
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 Top Introduction Diagnostic Evaluation Invasive Electrophysiological...Conclusions Based on...Assessment of Therapeutic...Unresolved Issues References |
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Unexplained 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.1 2 3 4 5 6 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.
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Diagnostic Evaluation |
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TopIntroductionDiagnostic Evaluation Invasive Electrophysiological...Conclusions Based on...Assessment of Therapeutic...Unresolved Issues References |
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The cause of a syncopal episode is frequently problematic if the diagnosis is not evident after the initial clinical and laboratory assessment.1 2 3 4 5 6 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.
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Invasive Electrophysiological Testing |
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TopIntroductionDiagnostic Evaluation Invasive Electrophysiological...Conclusions Based on...Assessment of Therapeutic...Unresolved Issues References |
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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.8 9
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.11 12 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,13 14 15 16 many
investigators have
described their clinical results with this technique for syncope
patients after noninvasive attempts have
failed.17 18 19 20 21 22 23 24 25 26 27 28 29 30
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.
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Conclusions Based on Electrophysiological Testing |
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TopIntroductionDiagnostic Evaluation Invasive Electrophysiological...Conclusions Based on...Assessment of Therapeutic...Unresolved Issues References |
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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
many17 20 23 25 27 28 29
but not all
studies.18 19 22 30 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 |
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TopIntroductionDiagnostic Evaluation Invasive Electrophysiological...Conclusions Based on...Assessment of Therapeutic...Unresolved Issues References |
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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.
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Unresolved Issues |
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TopIntroductionDiagnostic Evaluation Invasive Electrophysiological...Conclusions Based on...Assessment of Therapeutic...Unresolved Issues References |
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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.5 33 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.34 35 (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.30 36 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.
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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 study21 26 38 39 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.41 42 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.43 44 This will be extremely helpful in the
evaluation of patients who test negative and have sporadic episodes of
syncope.
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In conclusion, the limitations of current strategies to diagnose and treat syncope have been appreciated by many contributors to the field.3 4 5 7 16 19 20 28 30 34 35 36 It is time to achieve the next milestone in our understanding and management of this problem, which is vexing for both physician and patient.
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Acknowledgments |
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This study was supported in part by the Heart and Stroke Foundation of Ontario (Canada).
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Footnotes |
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Dr G.J. Klein is a Career Investigator for the Heart and Stroke Foundation of Ontario (Canada).
Received February 9, 1995; revision received March 23, 1995; accepted March 26, 1995.
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References |
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TopIntroductionDiagnostic Evaluation Invasive Electrophysiological...Conclusions Based on...Assessment of Therapeutic...Unresolved Issues References |
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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. [Medline] [Order article via Infotrieve]
2.
Kapoor WN. Evaluation and management of the
patient with syncope. JAMA. 1992;268:2553-2560.
3. Morady F. The evaluation of syncope with electrophysiologic studies. Cardiol Clin. 1986;4:515-526. [Medline] [Order article via Infotrieve]
4. DiMarco JP. Electrophysiologic studies in patients with unexplained syncope. Circulation. 1987;75:140-141.
5. Kapoor WN. Diagnostic evaluation of syncope. Am J Med. 1991;90:91-106. [Medline] [Order article via Infotrieve]
6. 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. [Abstract]
7. Manolis AS, Linzer M, Salem D, Estes NAM. Syncope: current diagnostic evaluation and management. Ann Intern Med. 1990;112:850-863.
8.
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.
9.
Scheinman MM, Peters RW, Modin G, Brennan M, Mies C,
O'Young J. Prognostic value of infranodal conduction time in
patients with chronic bundle branch block.
Circulation. 1977;56:240-244.
10.
Narula OS, Samet P, Javier RP. Significance of
the sinus-node recovery time. Circulation. 1972;45:140-158.
11.
Brugada P, Green M, Abdollah H, Wellens HJJ.
Significance of ventricular arrhythmias
initiated by programmed stimulation.
Circulation. 1984;69:87-92.
12. Prystowsky EN. Electrophysiologic-electropharmacologic testing in patients with ventricular arrhythmias. PACE Pacing Clin Electrophysiol. 1988;11:225-251. [Medline] [Order article via Infotrieve]
13. DiMarco JP, Garan H, Harthorne JW, Ruskin JN. Intracardiac electrophysiologic techniques in recurrent syncope. Ann Intern Med. 1981;95:542-548.
14. Hess DS, Morady F, Scheinman MM. Electrophysiologic testing in the evaluation of patients with syncope of undetermined origin. Am J Cardiol. 1982;50:1309-1015. [Medline] [Order article via Infotrieve]
15. 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. [Medline] [Order article via Infotrieve]
16. 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. [Medline] [Order article via Infotrieve]
17. 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. [Medline] [Order article via Infotrieve]
18.
Muller T, Roy D, Talajic M, Lemery R, Nattel S, Cassidy
D. Electrophysiologic evaluation and outcome of patients with
syncope of unknown origin. Eur Heart J. 1991;12:139-143.
19. Click RL, Gersh BJ, Sugrue DD, Holmes DR, Wood DL, Osborn MJ, Hammill SC. Role of invasive electrophysiologic testing in patients with symptomatic bundle branch block. Am J Cardiol. 1987;59:817-823. [Medline] [Order article via Infotrieve]
20. Denniss AR, Ross DL, Richards DA, Uther JB. Electrophysiologic studies in patients with unexplained syncope. Int J Cardiol. 1992;35:211-217.[Medline] [Order article via Infotrieve]
21. Bachinsky WB, Linzer M, Weld L, Estes NAM. Usefulness of clinical characteristics in predicting the outcome of electrophysiologic studies in unexplained syncope. Am J Cardiol. 1992;69:1044-1049. [Medline] [Order article via Infotrieve]
22. Twidale N, Heddle WF, Ayres BF, Tonkin AM. Clinical implications of electrophysiology study findings in patients with bifascicular block and syncope. Aust N Z J Med. 1988;18:841-847. [Medline] [Order article via Infotrieve]
23. Olshansky B, Mazuz M, Martins JB. Significance of inducible tachycardia in patients with syncope of unknown origin: a long-term follow-up. J Am Coll Cardiol. 1985;5:216-223. [Abstract]
24. Teichman SL, Felder SD, Matos JA, Kim SG, Waspe LE, Fisher JD. The value of electrophysiologic studies in syncope of undetermined origin: report of 150 cases. Am Heart J. 1985;110:469-479. [Medline] [Order article via Infotrieve]
25. Morady F, Higgins J, Peters RW, Schwartz AB, Shen EN, Bhandari A, Scheinman MM, Sauve MJ. Electrophysiologic testing in bundle branch block and unexplained syncope. Am J Cardiol. 1984;54:587-591. [Medline] [Order article via Infotrieve]
26. Krol RB, Morady F, Flaker GC, DiCarlo LA, Baerman JM, Hewett J, DeBuitleir M. Electrophysiologic testing in patients with unexplained syncope: clinical and noninvasive predictors of outcome. J Am Coll Cardiol. 1987;10:358-363. [Abstract]
27. Moazez F, Peter T, Simonson J, Mandel WJ, Vaughn C, Gang E. Syncope of unknown origin: clinical, noninvasive, and electrophysiologic determinants of arrhythmia induction and symptom recurrence during long-term follow-up. Am Heart J. 1991;121:81-88. [Medline] [Order article via Infotrieve]
28. Doherty JU, Pembrook-Rogers D, Grogan EW, Falcone RA, Buxton AE, Marchlinski FE, Cassidy DM, Kienzle MG, Almendral JM, Josephson ME. Electrophysiologic evaluation and follow-up characteristics of patients with recurrent unexplained syncope and presyncope. Am J Cardiol. 1985;55:703-708. [Medline] [Order article via Infotrieve]
29. Morady F, Shen E, Schwartz A, Hess D, Bhandari A, Sung RJ, Scheinman MM. Long-term follow-up of patients with recurrent unexplained syncope evaluated by electrophysiologic testing. J Am Coll Cardiol. 1983;2:1053-1059. [Abstract]
30. Bass EB, Elson JJ, Fogoros RN, Peterson J, Arena VC, Kapoor WN. Long-term prognosis of patients undergoing electrophysiologic studies for syncope of unknown origin. Am J Cardiol. 1988;62:1186-1191. [Medline] [Order article via Infotrieve]
31. Zipes DP, Akhtar M, Denes P, DeSanctis RW, Garson A, Gettes LS, Josephson ME, Mason JW, Myerburg RJ, Ruskin JN, Wellens HJJ. Guidelines for clinical intracardiac electrophysiologic studies. J Am Coll Cardiol. 1989;14:1827-1842. [Medline] [Order article via Infotrieve]
32. Sra JS, Anderson AJ, Sheikh SH, Avitall B, Tchou PJ, Troup PJ, Gilbert CJ, Akhtar M, Jazayeri MR. Unexplained syncope evaluated by electrophysiologic studies and head-up tilt testing. Ann Intern Med. 1991;114:1013-1019.
33. Lipsitz LA. Syncope in the elderly. Ann Intern Med. 1983;99:92-97.
34. Kushner JA, Kou WH, Kadish AH, Morady F. Natural history of patients with unexplained syncope and a nondiagnostic electrophysiologic study. J Am Coll Cardiol. 1989;14:391-396. [Abstract]
35. Fujimura O, Yee R, Klein GJ, Sharma AD, Boahene KA. The diagnostic sensitivity of electrophysiologic testing in patients with syncope caused by transient bradycardia. N Engl J Med. 1989;321:1703-1707. [Abstract]
36. Middlekauff HR, Stevenson WG, Saxon LA. Prognosis after syncope: impact of left ventricular function. Am Heart J. 1993;125:121-127. [Medline] [Order article via Infotrieve]
37.
Cook DJ, Guyatt GH, Laupacis A, Sackett DL.
Rules of evidence and clinical recommendations on the use of
antithrombotic agents. Chest. 1992;102:305S-311S.
38.
Denes P, Uretz E, Ezri MD, Borbola J. Clinical
predictors of electrophysiologic findings in patients with syncope of
unknown origin. Arch Intern Med. 1988;148:1922-1928.
39. Linzer M, Prystowsky EN, Divine GW, Matchar DB, Samsa G, Harrell F, Pressley JC, Pryor DB. 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. [Medline] [Order article via Infotrieve]
40.
Savage DD, Corwin L, McGee DL, Kannel WB, Wolf PA.
Epidemiologic features of isolated syncope: the Framingham
study. Stroke. 1985;16:626-629.
41. 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. [Medline] [Order article via Infotrieve]
42. 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. [Abstract]
43. 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. [Medline] [Order article via Infotrieve]
44. Krahn AD, Klein GJ, Norris C, Yee R. The etiology of syncope in patients with negative tilt table and electrophysiological testing. Circulation. In press.
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