Chapter 29 Electrophysiological Evaluation of Syncope
Electrophysiology Testing
Indications
EP testing can provide important diagnostic information in patients presenting with syncope. The results of EP testing can be useful in establishing a diagnosis of sick sinus syndrome, carotid sinus hypersensitivity, heart block, supraventricular tachycardia (SVT), and ventricular tachycardia (VT). The indications for EP testing in the evaluation of patients with syncope are outlined in detail in the European Society of Cardiology (ESC) Guidelines on Management of Syncope (Table 29-1).1 It is generally accepted that EP testing should be performed in patients when the initial evaluation suggests an arrhythmic cause of syncope (class 1). This group of patients includes those with an abnormal electrocardiogram (ECG), structural heart disease, or both. Patients whose clinical history suggests an arrhythmic cause of syncope and those with a family history of sudden death are also included in this group. It is also generally accepted that EP testing should not be performed in patients with a normal ECG and no heart disease and in whom the clinical history does not suggest an arrhythmic cause of syncope (class 3). Class 2 indications for performing an EP study are shown in Table 31-1. These indications suggest that EP testing is appropriate when the results may affect treatment and in patients with “high-risk” occupations, in which case every effort should be expended to determine the probable cause of syncope.
Table 29-1 Indications for Electrophysiology Testing in the Evaluation of Patients with Syncope
| CLASS 1 |
| When the initial evaluation of syncope suggests an arrhythmic cause of syncope |
| In patients with abnormal electrocardiography, structural heart disease, or both |
| In patients with syncope associated with palpitations or a family history of sudden death |
| CLASS 2 |
| To evaluate the exact nature or mechanism of an arrhythmia that has been identified as the cause of syncope |
| In patients with cardiac disorders in which arrhythmia induction has a bearing on the selection of therapy |
| In patients with syncope who are in a high-risk occupation and in whom every effort to exclude a cardiac cause of syncope is warranted |
| CLASS 3 |
| In patients with normal electrocardiograms and no heart disease and no palpitations |
Electrophysiology Testing Protocol
When EP testing is undertaken in a patient with syncope, a comprehensive EP evaluation should be performed. This should include an evaluation of sinus node function by measuring the sinus node recovery time (SNRT) and an evaluation of atrioventricular (AV) conduction by measurement of the H-V interval (His bundle to ventricle conduction time) at baseline, with atrial pacing, and following pharmacologic challenge with intravenous procainamide. In addition, programmed electrical stimulation using standard techniques should be performed to evaluate the inducibility of ventricular and supraventricular arrhythmias. The minimal suggested EP protocol recommended by the ESC is provided in Table 29-2. Although the minimal suggested EP protocol recommended by the ESC includes only double extrastimuli and two basic drive train cycle lengths, it is common practice in the United States to include triple extrastimuli and three basic drive train cycle lengths. It is also common practice to limit the shortest coupling interval to 200 ms. In select patients, when a ventricular arrhythmia is highly suspected, EP testing with atrial and ventricular programmed stimulation may be repeated after an infusion of isoproterenol. In my experience, this is of particular importance in the presence of suspicion of a supraventricular arrhythmia such as AV nodal re-entrant tachycardia or orthodromic AV reciprocating tachycardia as the cause of syncope.
Table 29-2 Minimal Suggested Protocol for Electrophysiology Testing for the Diagnosis of Syncope
| Measurement of sinus node recovery time and corrected sinus node recovery time by repeated 30- to 60-second sequences of atrial pacing at 10 to 20 beats/min higher than the sinus rate and at two faster pacing rates. |
| Measurement of the H-V interval (His bundle to ventricle) during sinus rhythm and with incremental atrial pacing. If the baseline study is inconclusive, pharmacologic provocation with an infusion of procainamide (10 mg/kg IV) is recommended. |
| To evaluate the exact nature or mechanism of an arrhythmia that has been identified as the cause of syncope. |
| Programmed electrical stimulation in the ventricle to assess ventricular inducibility. |
| Programmed stimulation should be performed at the apex and outflow tract and at two basic drive cycle lengths with up to two extrastimuli. |
| Programmed electrical stimulation to evaluate the substrate for inducibility of supraventricular arrhythmias. |
Assessment of Sinus Node Function
Sinus node function is evaluated during EP testing primarily by determining the SNRT, which is determined by pacing the right atrium at cycle lengths between 600 and 350 ms for 30 to 60 seconds. The SNRT is defined as the interval between the last paced atrial depolarization and the first spontaneous atrial depolarization resulting from activation of the sinus node. The SNRT is corrected for the underlying sinus cycle length (SCL) and expressed as the corrected SNRT (CSNRT = SNRT – SCL). An SNRT longer than 1.6 seconds or a corrected SNRT greater than 525 ms is generally considered abnormal. A secondary pause is defined as an inappropriately long pause between the beats that follow the first sinus recovery beat after atrial overdrive pacing. Evaluation of secondary pauses increases the sensitivity of the SNRT in the detection of sinus node dysfunction. Identification of sinus node dysfunction as the cause of syncope is uncommon during EP tests (<5%). The sensitivity of an abnormal SNRT or CSNRT is approximately 50% to 80%. The specificity of an abnormal SNRT or CSNRT is greater than 95%.2 The prognostic value of an abnormal CSNRT or SNRT has not been well defined. Gann and colleagues demonstrated a relationship between an abnormal SNRT and the effect of pacemaker placement on symptoms.3 Another study reported that patients with a markedly prolonged CSNRT (>800 ms) had a risk of syncope eight times higher than that with CSNRTs less than 800 ms.4 It is important to note that the absence of evidence of sinus node dysfunction during EP testing does not exclude a bradyarrhythmia as the cause of syncope.5
Assessment of Atrioventricular Conduction
During EP testing, AV conduction is assessed by measuring the A-H interval (AV node to His bundle conduction time) and the H-V interval by determining the response of AV conduction to incremental atrial pacing and atrial premature stimuli. If the results of an initial assessment of AV conduction in the baseline state are inconclusive, procainamide (10 mg/kg) may be administered intravenously and atrial pacing and programmed stimulation repeated. According to the 2004 ESC Guidelines on Management of Syncope, the findings at EP study that establish heart block as the probable cause of syncope are bi-fasicular block and a baseline HV interval longer than 100 ms or demonstration of second- or third-degree His-Purkinje block during incremental atrial pacing or when provoked by an infusion of procainamide (Table 29-3).1 According to these guidelines, the finding of an H-V interval between 70 and 100 ms is of less certain diagnostic value. Among studies that have reported the results of EP testing in evaluating patients with syncope, AV block was identified as the probable cause of syncope in approximately 10% to 15% of patients. Donateo and colleagues reported the results of a systematic evaluation of patients with syncope in the setting of a bundle branch block on their baseline ECG.6 Of 347 patients referred for evaluation of syncope, 55 had a baseline bundle branch block pattern. Systematic evaluation of these patients, including EP testing, resulted in a diagnosis of cardiac syncope in 25 patients (45%): AV block in 20 (36%), sick sinus syndrome in 2 (3.6%), VT in 1 (1.8%), and aortic stenosis in 2 (3.6%). Neurally mediated syncope was diagnosed in 22 patients (40%) and syncope remained unexplained in 8 (15%).
Table 29-3 Diagnostic Findings of Electrophysiology Testing for Syncope
| Class 1 | A normal EP study cannot completely exclude a tachyarrhythmia or a bradyarrhythmia as the cause of syncope. |
| When an arrhythmia is believed to be the likely cause of syncope, further evaluation, perhaps with a loop recorder, is recommended. | |
| An abnormal finding on EP testing may not be diagnostic of the cause of syncope. | |
| An EP study is considered to be diagnostic of the cause of syncope in the following situations: | |
| Sinus bradycardia and a markedly prolonged CSNRT | |
| Bi-fasicular block and a baseline H-V interval (His bundle to ventricle) of >100 ms or second- or third-degree His-Purkinje block with incremental atrial pacing | |
| High-degree His-Purkinje block provoked with IV procainamide | |
| Induction of sustained monomorphic VT | |
| Induction of rapid SVT that reproduces the patient’s symptoms or results in hypotension | |
| Class 2 | The diagnostic value of an EP study is less well established: |
| When the H-V interval is >70 ms but <100 ms | |
| With induction of PMVT or VF in patients with Brugada syndrome, ARVD, and those resuscitated from cardiac arrest | |
| Class 3 | The induction of PMVT or VF has a low predictive value in patients with an ischemic or dilated cardiomyopathy. |
EP, Electrophysiology; CSNRT, corrected sinus node recovery time; IV, intravenous; VT, ventricular tachycardia; SVT, supravenricular tachycardia; VF, ventricular fibrillation; ARVD, arrhythmogenic right ventricular dysplasia; PMVT, pacemaker-modulated VT.
The role of EP testing in the assessment of AV conduction and as a predictor of AV block in patients with syncope has been derived from a large number of studies. Scheinman et al evaluated the prognostic value of the HV interval.7 The rate of progression to AV block at 4 years was 4%, 2%, and 12%, respectively, for patients with H-V intervals less than 55 ms, 55 to 69 ms, and greater than 70 ms, respectively. The risk of progression to AV block was 24% among those with an H-V interval greater than 100 ms. Other studies have investigated the prognostic value of development of intra-His block or infra-His block with incremental atrial pacing. These studies demonstrated that the presence of these blocks in response to incremental atrial pacing is a specific but insensitive parameter. Dini et al, for example, demonstrated that pacing-induced AV block was observed in 7% of 85 patients who were evaluated.8 Complete AV block developed within 2 years in 30% of these patients. The diagnostic value of acute intravenous pharmacologic stress testing has been performed with ajmaline, procainamide, and disopyramide. High-degree AV block is seen in approximately 15% of these studies.8–10 During 24 to 63 months of follow-up, 43% to 100% of these patients develop spontaneous AV block. It has therefore been concluded that induction of AV block during pharmacologic stress testing of AV conduction is highly predictive of development of AV block. It is important to note, however, that a negative EP assessment of AV conduction does not eliminate AV block as the cause of syncope, nor does it exclude that AV block may develop over time. Link et al reported that at 30 months of follow-up, permanent AV block occurred in 18% of patients with syncope who had a negative EP test.11 Similarly, Gaggioli reported that 19% of patients with syncope and a negative EP evaluation developed permanent AV block within 62 months of follow-up.12
Programmed Electrical Stimulation to Evaluate Supraventricular Arrhythmias as the Cause of Syncope
Although it is uncommon for an SVT to result in syncope, this is an important diagnosis to establish as most types of supraventricular arrhythmias can be cured with catheter ablation. Therefore the identification of an SVT as the probable cause of syncope is important because it represents one of the most easily treatable causes of syncope. The usual setting in which an SVT may result in syncope is when a patient with underlying heart disease, limited cardiovascular reserve, or both experiences an SVT that is of abrupt onset and with an extremely rapid rate or when a patient has the propensity for the development of neurally mediated syncope. The typical pattern that is observed is the development of syncope or near-syncope at the onset of the SVT because of an initial drop in blood pressure. The patient often regains consciousness despite the continuation of the arrhythmia because of the activation of a compensatory mechanism. Completion of a standard EP test allows accurate identification of most types of supraventricular arrhythmias that may have caused the syncope. The study should be repeated during an isoproterenol infusion to increase the sensitivity of the study, particularly for detecting AV nodal re-entrant tachycardia in a patient with dual AV node physiology or catecholamine-sensitive atrial fibrillation (AF). According to the 2004 ESC Guidelines on Management of Syncope, an EP study is considered diagnostic of SVT as the cause of syncope in the presence of induction of a rapid supraventricular arrhythmia that reproduces hypotensive or spontaneous symptoms (see Table 29-3).1 A supraventricular arrhythmia is diagnosed as the probable cause of syncope in less than 5% of patients who undergo EP testing for the evaluation of syncope of unknown origin. The probability of SVT as the cause of syncope is higher in patients who report a history of palpitations or heart racing before syncope.
Programmed Electrical Stimulation to Evaluate Ventricular Arrhythmias as the Cause of Syncope
According to the 2004 ESC Guidelines on Management of Syncope, an EP study is considered diagnostic of VT as the cause of syncope in the presence of induction of sustained monomorphic VT (see Table 29-3).1 According to these guidelines, findings on EP testing that have less certain diagnostic value include the induction of polymorphic VT or VF in patients with Brugada syndrome or arrhythmogenic right ventricular dysplasia (ARVD) and in patients resuscitated from a cardiac arrest. These guidelines also state that the induction of polymorphic VT or VF in patients with ischemic or dilated cardiomyopathy has low predictive value.
Carotid Sinus Hypersensitivity
Syncope caused by carotid sinus hypersensitivity results from the stimulation of carotid sinus baroreceptors, which are located in the internal carotid artery above the bifurcation of the common carotid artery. Carotid sinus hypersensitivity is diagnosed by applying gentle pressure over the carotid pulsation just below the angle of the jaw, where the carotid bifurcation is located. According to the ESC 2004 Guidelines on Syncope, carotid sinus massage (CSM) is recommended in patients over the age of 40 years with syncope of unknown etiology after an initial evaluation.1 CSM should not be performed in patients with known carotid artery disease because of an increased risk of stroke. Pressure should be applied for 5 to 10 seconds while continuously monitoring the ECG and blood pressure. If the response to CSM in the supine position is normal, the importance of repeating CSM in the upright position has now been well established.13,14 The TT test makes it easier to perform CSM in both the supine and upright positions. The main complications associated with CSM are neurological. Because of this, CSM should be avoided in patients who have experienced transient ischemic attacks (TIAs), stroke within the past 3 months, or carotid bruits.
A normal response to CSM is a transient decrease in the sinus rate, slowing of AV conduction, or both. Carotid sinus hypersensitivity is defined as a sinus pause of more than 3 seconds’ duration and a fall in systolic blood pressure of 50 mm Hg or more. The response to CSM can be classified as cardio-inhibitory (asystole), vasodepressive (fall in systolic blood pressure), or both. Carotid sinus hypersensitivity is detected in approximately one third of older patients who present with syncope or for falls.1,15 The sensitivity of CSM for the diagnosis of carotid sinus hypersensitivity is increased by performing CSM with the patient in both the supine and upright positions.13,14 Although it is common practice to perform CSM as part of a diagnostic EP study for syncope, a negative response to CSM in the supine position during an EP procedure does not exclude the diagnosis. Therefore repeat CSM in the standing position should be performed either before the EP study or at some point after the EP study. It is important to recognize, however, that carotid sinus hypersensitivity is also commonly observed in asymptomatic older patients.16 Thus the diagnosis of carotid sinus hypersensitivity should be approached cautiously after excluding all other causes of syncope. Once diagnosed, dual-chamber pacemaker implantation is recommended for patients with recurrent syncope or falls resulting from carotid sinus hypersensitivity.17,18
Tilt-Table Testing
The TT test is valuable for evaluating patients with syncope.1,19 The recommendations for TT testing protocols are shown in Table 29-4.1 Upright TT testing is generally performed for 20 to 45 minutes at an angle between 60 and 70 degrees. The sensitivity of the test can be increased, with an associated fall in specificity, by the use of longer tilt durations, steeper tilt angles, and provocative agents such as isoproterenol or nitroglycerin. When isoproterenol is used as a provocative agent, it is recommended that the infusion rate be increased incrementally from 1 to 3 µg/min to increase the heart rate to 20% to 25% greater than baseline. When nitroglycerin is used, a fixed dose of 400-µg nitroglycerine spray should be administered sublingually with the patient in the upright position. These two provocative approaches are equivalent in diagnostic accuracy. In the absence of pharmacologic provocation, the specificity of the test has been estimated to be 90%. It is important to recognize, however, that the specificity of TT testing decreases significantly when provocative agents are used.
| Supine pretilt phase of 5 minutes when no venous cannulation |
| Supine pretilt phase of at least 20 minutes when venous cannulation is used |
| Table tilted to 60 to 70 degrees |
| Passive tilt for 20 to 45 minutes |
| Use of either isoproterenol or sublingual nitroglycerine if the passive phase is negative (20 minutes) |
| For isoproterenol, infusion of 1 to 3 µg/min to achieve 20% to 25% increase in heart rate |
| For nitroglycerine, administration of 400 µg as a sublingual spray with the patient in the upright position |
| Positive result if syncope occurs |
The indications for TT testing are shown in Table 29-5.1 It is generally agreed that upright TT testing is indicated in patients following a single episode of syncope in high-risk settings or in patients with recurrent syncope who do not have structural heart disease or in those with structural heart disease once cardiac causes of syncope have been excluded.1 Upright TT testing is not necessary in patients who have experienced only a single syncopal episode that was highly typical for neurally mediated syncope and during which no injury occurred. It is also important to recognize that TT testing should not be used to assess treatment because (1) the reproducibility of a positive response to TT testing varies from 31% to 92%, (2) half of patients with an initial positive tilt response demonstrate a normal tilt response to either treatment or placebo, and (3) the mechanism of a positive response during TT testing does not correlate to that observed during spontaneous syncope as demonstrated with a loop monitor.20–28
Table 29-5 Indications for Tilt-Table Testing
| Class 1 | Single unexplained episode of syncope in a high-risk setting |
| Recurrent episodes of syncope in the absence of structural heart disease or in the presence of structural heart disease after other cardiac causes of syncope have been excluded | |
| When it will be of clinical value to demonstrate susceptibility to neurally mediated syncope | |
| Class 2 | When an understanding of the hemodynamic pattern may alter the therapeutic approach |
| For differentiating syncope from the jerky movements of epilepsy | |
| For evaluating patients with recurrent unexplained falls | |
| For assessing recurrent presyncope or dizziness | |
| Class 3 | Assessment of treatment |
| A single episode of syncope without injury and not in a high-risk setting | |
| Syncope with features typical of syncope because of neurally mediated hypotension when the result of the test will not affect treatment |
Key References
Benditt DG, Sutton R. Tilt-table testing in the evaluation of syncope. J Cardiovasc Electrophysiol. 2005;16:356-358.
Bergfeldt L, Edvardsson N, Rosenqvist M, et al. Atrioventricular block progression in patients with bifascicular block assessed by repeated electrocardiography and a bradycardia-detecting pacemaker. Am J Cardiol. 1994;74:1129-1132.
Blanc JJ, Mansourati J, Maheu B, et al. Reproducibility of a positive passive upright tilt test at a seven-day interval in patients with syncope. Am J Cardiol. 1993;72:469-471.
Brignole M, Alboni P, Benditt DG, et al. Guidelines on management (diagnosis and treatment) of syncope. Update 2004. Eur Heart J. 2004;25:2054-2072.
Brooks R, Ruskin IN, Powell AC, et al. Prospective evaluation of day-to-day reproducibility of upright tilt table testing in unexplained syncope. Am J Cardiol. 1993;71:1289-1292.
De Buitler M, Grogan EWJr, Picone MF, et al. Immediate reproducibility of the tilt table test in adults with unexplained syncope. Am J Cardiol. 1993;71:304-307.
Fujimura O, Yee R, Klein G, et al. The diagnostic sensitivity of electrophysiologic testing in patients with syncope caused by transient bradycardia. N Engl J Med. 1989;321:1703-1707.
Grubb BP, Wolfe D, Temesy Armas P, et al. Reproducibility of head upright tilt-table test in patients with syncope. Pacing Clin Electrophysiol. 1992;15:1477-1481.
Kenny RA, Richardson DA, Bexton RS, et al. Carotid sinus syndrome: A modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol. 2001;38:1491-1496.
Kerr SR, Pearce MS, Brayne C, et al. Carotid sinus hypersensitivity in asymptomatic older persons. Arch Intern Med. 2006;166:515-520.
Maya A, Permanyer-Miralda G, Sagrista-Sauleda J, et al. Limitations of head-up tilt test for evaluating the efficacy of therapeutic interventions in patients with vasovagal syncope: Results of a controlled study of etilefrine versus placebo. J Am Coll Cardiol. 1995;25:65-69.
Parry SW, Richardson D, O’Shea D, et al. Diagnosis of carotid sinus hypersensitivity in older adults: Carotid sinus massage in the upright position is essential. Heart. 2000;83:22-23.
Parry SW, Steen IN, Baptist M, Kenny RA. Amnesia for loss of consciousness in carotid sinus syndrome. J Am Coll Cardiol. 2005;45:1840-1843.
Scheinman MM, Peters RW, Sauve MJ, et al. Value of the H-Q interval in patients with bundle branch block and the role of prophylactic permanent pacing. Am J Cardiol. 1982;50:1316-1322.
Sheldon R, Splawinski J, Killam S. Reproducibility of isoproterenol tilt-table tests in patients with syncope. Am J Cardiol. 1992;69:1300-1305.
1 Brignole M, Alboni P, Benditt DG, et al. Guidelines on management (diagnosis and treatment) of syncope. Update 2004. Eur Heart J. 2004;25:2054-2072.
2 Benditt DG, Gornick C, Dunbar D, et al. Indications for electrophysiological testing in diagnosis and assessment of sinus node dysfunction. Circulation. 1987;75(Suppl III):93-99.
3 Gann D, Tolentino A, Samet P. Electrophysiologic evaluation of elderly patients with sinus bradycardia. A long-term follow-up study. Ann Intern Med. 1979;90:24-29.
4 Menozzi D, Brignole M, Alboni P, et al. The natural course of untreated sick sinus syndrome and identification of the variables predictive of unfavorable outcome. Am J Cardiol. 1998;82:1205-1209.
5 Fujimura O, Yee R, Klein G, et al. The diagnostic sensitivity of electrophysiologic testing in patients with syncope caused by transient bradycardia. N Engl J Med. 1989;321:1703-1707.
6 Donateo P, Brignole M, Alboni P, et al. A standardized conventional evaluation of the mechanism of syncope in patients with bundle branch block. Europace. 2002;4:357.
7 Scheinman MM, Peters RW, Sauve MJ, et al. Value of the H-Q interval in patients with bundle branch block and the role of prophylactic permanent pacing. Am J Cardiol. 1982;50:1316-1322.
8 Dini P, Iaolongo D, Adinolfi E, et al. Prognostic value of His-ventricular conduction after ajmaline administration. In: Masoni A, Alboni P, editors. Cardiac electrophysiology today. London: Academic Press, 1982.
9 Bergfeldt L, Edvardsson N, Rosenqvist M, et al. Atrioventricular block progression in patients with bifascicular block assessed by repeated electrocardiography and a bradycardia-detecting pacemaker. Am J Cardiol. 1994;74:1129-1132.
10 Gronda M, Magnani A, Occhetta E, et al. Electrophysiologic study of atrioventricular block and ventricular conduction defects. G Ital Cardiol. 1984;14:768-773.
11 Link M, Kim KM, Homoud M, et al. Long-term outcome of patients with syncope associated with coronary artery disease and a nondiagnostic electrophysiological evaluation. Am J Cardiol. 1999;83:1334-1337.
12 Gaggioli G, Bottoni N, Brignote M, et al. Progression to second or third-degree atrioventricular block in patients electrostimulated for bundle branch block: A long-term study. G Ital Cardiol. 1994;24:409-416.
13 Brignole M, Sartore B, Prato R. Role of body position during carotid sinus stimulation test in the diagnosis of cardioinhibitory carotid sinus syndrome. G Ital Cardiol. 1983;14:69-72.
14 Parry SW, Richardson D, O’Shea D, et al. Diagnosis of carotid sinus hypersensitivity in older adults: Carotid sinus massage in the upright position is essential. Heart. 2000;83:22-23.
15 Parry SW, Steen IN, Baptist M, Kenny RA. Amnesia for loss of consciousness in carotid sinus syndrome. J Am Coll Cardiol. 2005;45:1840-1843.
16 Kerr SR, Pearce MS, Brayne C, et al. Carotid sinus hypersensitivity in asymptomatic older persons. Arch Intern Med. 2006;166:515-520.
17 Gregoratos G, Abrams J, Epstein AE, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: Summary article: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). Circulation. 2002;106:2145-2161.
18 Kenny RA, Richardson DA, Bexton RS, et al. Carotid sinus syndrome: A modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol. 2001;38:1491-1496.
19 Benditt DG, Sutton R. Tilt-table testing in the evaluation of syncope. J Cardiovasc Electrophysiol. 2005;16:356-358.
20 Sheldon R, Splawinski J, Killam S. Reproducibility of isoproterenol tilt-table tests in patients with syncope. Am J Cardiol. 1992;69:1300-1305.
21 Grubb BP, Wolfe D, Temesy Armas P, et al. Reproducibility of head upright tilt-table test in patients with syncope. Pacing Clin Electrophysiol. 1992;15:1477-1481.
22 De Buitler M, Grogan EWJr, Picone MF, et al. Immediate reproducibility of the tilt table test in adults with unexplained syncope. Am J Cardiol. 1993;71:304-307.
23 Brooks R, Ruskin IN, Powell AC, et al. Prospective evaluation of day-to-day reproducibility of upright tilt table testing in unexplained syncope. Am J Cardiol. 1993;71:1289-1292.
24 Blanc JJ, Mansourati J, Maheu B, et al. Reproducibility of a positive passive upright tilt test at a seven-day interval in patients with syncope. Am J Cardiol. 1993;72:469-471.
25 Maya A, Permanyer-Miralda G, Sagrista-Sauleda J, et al. Limitations of head-up tilt test for evaluating the efficacy of therapeutic interventions in patients with vasovagal syncope: Results of a controlled study of etilefrine versus placebo. J Am Coll Cardiol. 1995;25:65-69.
26 Morillo CA, Leitch JW, Vee R, et al. 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.
27 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;99:1452-1457.
28 Maya A, Brignote M, Menozzi C, et al. Mechanism of syncope in patients with isolated syncope and in patients with tilt-positive syncope. Circulation. 2001;104:1261-1267.
