Aetna considers tilt table testing, alone or in combination with administration of provocative agents (e.g., isoproterenol), medically necessary for the evaluation of members with recurrent unexplained syncope who have an inconclusive history and physical examination, as well as negative non-invasive tests of cardiac structure and function.
Aetna considers the use of tilt table testing experimental and investigational for all other indications, including any of the following (not an all inclusive list) because there is little support in the peer-reviewed medical literature for tilt table testing for these indications:
Determining the effectiveness of medications in treating recurrent unexplained syncope; or
Differential diagnosis of parkinsonian syndromes (e.g., Parkinson's disease, multiple system atrophy and progressive supranuclear palsy); or
Guiding surgical decision-making as well as predicting the clinical response to surgical decompression of Chiari type I-malformation (Chiari drop attacks); or
Identifying members with chronic fatigue syndrome and/or evaluating treatment effectiveness of this condition.
There is sufficient evidence that tilt table testing, with or without isoproterenol, is safe and effective as a diagnostic tool for the evaluation of patients with recurrent unexplained syncope. The reported sensitivity, specificity, and reproducibility of tilt table testing ranged from 65 to 87 %, 55 to 96 %, and 71 to 88 %, respectively. This procedure helps to identify a largely benign disorder and, indirectly, exclude other possibly life-threatening conditions. Tilt table testing performed early in the evaluation may obviate extensive and expensive tests such as intra-cardiac electrophysiological studies, CAT scan, and MRI of the brain. In contrast, there is insufficient evidence that tilt table testing following intravenous infusion of metoprolol can accurately predict the effectiveness of oral metoprolol therapy in treating patients with recurrent unexplained syncope. This procedure has not been shown to provide any additional information than would have been obtained from a trial of oral therapy.
There is inadequate evidence of the effectiveness of tilt-table testing for identifying chronic fatigue syndrome (CFS) patients who would respond to medications to increase their blood pressure. Several case series have shown that patients with known CFS frequently have abnormal responses to tilt-table testing, and CFS patients in these series also frequently appear to respond to anti-hypotensive medications commonly used in patients with neurally mediated hypotension. These case studies fail to demonstrate, however, any value of tilt-table testing in distinguishing CFS patients that would respond to these medications from those who would not.
Straus and colleagues (2009) stated that Chiari I malformation (CM1) is characterized by impaired cerebrospinal fluid flow through the foramen magnum. Dysfunctional autonomic cardiovascular regulation may result in syncope, which may be the primary presenting symptom of CM1 (a syndrome termed Chiari drop attack). It has been postulated that Chiari drop attack is secondary to dysautonomia caused by hind-brain compression. These researchers studied patients with Chiari drop attacks who had negative work-ups for cardiac syncope, followed by tilt table testing and subsequent surgical decompression. They reported test results and clinical outcomes following CM1 decompression. A total of 10 patients met the inclusion criteria: 5 patients had positive and 5 negative tilt table tests. Following decompression, 7 had symptomatic improvement or resolution and 3 failed to improve. The sensitivity and specificity of the tilt table test for detecting clinical improvement with surgical decompression was 43 % and 33 %, respectively. Tilt table testing had 40 % accuracy in predicting clinical response to decompression. The authors concluded that in this short series, surgical decompression of CM1 has a high success rate (70 %) for patients with Chiari drop attacks. Moreover, tilt table testing has poor predictive value in judging the clinical response to surgical decompression and is not a useful test to guide surgical decision-making.
Uno and colleagues (2009) noted that although it is well known that autonomic dysfunction in obstructive sleep apnea syndrome (OSAS) is associated with hypertension, its relationship to hypotension and orthostatic dysregulation is still unclear. These investigators examined the response of blood pressure (BP) and cardiovascular autonomic function to head-up tilt (HUT) test in patients with OSAS. In this study, a total of 14 patients (mean age of 65 +/- 2 years old, male/female: 11/3) with diagnosed OSAS by over-night polysomnography and 84 healthy subjects (mean age of 62 +/- 1 years old, male/female: 46/38) underwent HUT test (from 5 to 10 mins at 45 degrees). Autonomic functions were evaluated by spectrum analysis of BP and heart rate variability. In healthy subjects, systolic BP was unchanged by HUT test due to the enhancement of sympathetic nerve activity and the inhibition of parasympathetic nerve activity. In contrast, autonomic responses were unchanged and systolic BP tended to be decreased by HUT test in OSAS patients. The authors concluded that the findings of this study suggested that baroreflex function is impaired in patients with OSAS. Furthermore, HUT test with spectrum analysis may be useful to evaluate autonomic functions in OSAS patients.
Oliveira et al (2009) stated that the autonomic nervous system (ANS) is known to be an important modulator in the pathogenesis of paroxysmal atrial fibrillation (PAF). Changes in ANS control of heart rate variability (HRV) occur during orthostatism to maintain cardiovascular homeostasis. Wavelet transform has emerged as a useful tool that provides time-frequency decomposition of the signal under investigation, enabling intermittent components of transient phenomena to be analyzed. These investigators studied HRV during HUT with wavelet transform analysis in PAF patients and healthy individuals (normals). A total of 21 patients with PAF (8 men; age of 58 +/- 14 yrs) were examined and compared with 21 normals (7 men, age of 48 +/- 12 yrs). After a supine resting period, all subjects underwent passive HUT (60 degrees) while in sinus rhythm. Continuous monitoring of electroencephalography and BP was carried out. Acute changes in RR-intervals were assessed by wavelet analysis and low-frequency power (LF: 0.04 to 0.15 Hz), high-frequency power (HF: 0.15 to 0.60 Hz) and LF/HF (sympatho-vagal) were calculated for (i) the last 2 mins of the supine period; (ii) the 15 secs of tilting movement (TM); and (iii) the 1st (TT1) and 2nd (TT2) min of HUT. Data were expressed as means +/- SEM. Baseline and HUT RR-intervals were similar for the 2 groups. Supine basal BP was also similar for the 2 groups, with a sustained increase in PAF patients, and a decrease followed by an increase and then recovery in normals. Basal LF, HF and LF/ HF values in PAF patients were 632 +/- 162 ms2, 534 +/- 231 ms2 and 1.95 +/- 0.39, respectively, and 1,058 +/- 223 ms2, 789 +/- 244 ms2 and 2.4 +/- 0.36, respectively, in normals (p = NS). During TM, LF, HF and LF/HF values for PAF patients were 747 +/- 277 ms2, 387 +/- 94 ms2 and 2.9 +/- 0.6, respectively, and 1316 +/- 315 ms2, 698 +/- 148 ms2 and 2.8 +/- 0.6, respectively, in normals (p < 0.05 for LF and HF). During TF1, LF, HF and LF/ HF values for PAF patients were 1,243 +/- 432 ms2, 302 +/- 88 ms2 and 7.7 +/- 2.4, respectively, and 1,992 +/- 398 ms2, 333 +/- 76 ms2 and 7.8 +/- 0.98, respectively, for normals (p < 0.05 for LF). During TF2, LF, HF and LF/HF values for PAF patients were 871 +/- 256 ms2, 242 +/- 51 ms2 and 4.7 +/- 0.9, respectively, and 1263 +/- 335 ms2, 317 +/- 108 ms2 and 8.6 +/- 0.68, respectively, for normals (p < 0.05 for LF/HF). The dynamic profile of HRV showed that LF and HF values in PAF patients did not change significantly during TM or TT2, and LF/HF did not change during TM but increased in TT1 and TT2. The authors concluded that patients with PAF present alterations in HRV during orthostatism, with decreased LF and HF power during TM, without significant variations during the first minutes of HUT. These findings suggested that wavelet transform analysis may provide new insights when assessing autonomic heart regulation and highlight the presence of ANS disturbances in PAF. The findings of these small preliminary studies need to be validated by well-designed studies.
Riley and Chelimsky (2003) stated that formal laboratory testing of autonomic function is reported to distinguish between patients with Parkinson's disease (PD) and those with multiple system atrophy (MSA), but such studies segregated patients according to clinical criteria that select those with autonomic dysfunction for the MSA category. These researchers attempted to characterize the profiles of autonomic disturbances in patients in whom the diagnosis of PD or MSA used criteria other than autonomic dysfunction. A total of 47 patients with parkinsonism and autonomic symptoms who had undergone autonomic laboratory testing were identified and their case records reviewed for non-autonomic features. They were classified clinically into 3 diagnostic groups: (i) PD (n = 19), MSA (n = 14), and uncertain (n = 14). The performance of the patients with PD was compared with that of the MSA patients on 5 autonomic tests: (i) R-R interval variations during deep breathing, (ii) heart rate changes with the Valsalva maneuvre, (iii) tilt table testing, (iv) the sudomotor axon reflex test, and (v) thermoregulatory sweat testing. None of the tests distinguished one group from the other with any statistical significance, alone or in combination. Parkinson's disease and MSA patients showed similar patterns of autonomic dysfunction on formal testing of cardiac sympathetic and parasympathetic, vasomotor, and central and peripheral sudomotor functions. The authors concluded that these findings supported the clinical observation that PD is often indistinguishable from MSA when it involves the autonomic nervous system. The clinical combination of parkinsonism and dysautonomia is as likely to be caused by PD as by MSA. Current clinical criteria for PD and MSA that direct patients with dysautonomia into the MSA group may be inappropriate.
Reimann et al (2010) stated that differential diagnosis of parkinsonian syndromes is a major challenge in movement disorders. Dysautonomia is a common feature but may vary in clinical severity and onset. These investigators attempted to find a pattern of autonomic abnormalities discriminative for patients with different parkinsonian syndromes. The cross-sectional study included 38 patients with MSA, 32 patients with progressive supranuclear palsy (PSP), 26 patients with idiopathic PD (IPD), and 27 age-matched healthy controls. Autonomic symptoms were evaluated by a standardized questionnaire. The performance of patients and controls was compared on 5 autonomic function tests: (i) deep breathing, (ii) Valsalva maneuvre, (iii) tilt-table testing, (iv) sympathetic skin response, (v) pupillography, as well as 24-hr ambulatory BP monitoring (ABPM). Disease severity was significantly lower in IPD than PSP and MSA. Except for pupillography, none of the laboratory autonomic tests distinguished one patient group from the other alone or in combination. The same was observed on the questionnaire. Receiver operating characteristic curve revealed discriminating performance of pupil diameter in darkness and nocturnal BP change. The composite score of urogenital and vasomotor domains significantly distinguished MSA from IPD patients but not from PSP. These findings supported the observation that even mild IPD is frequently indistinguishable from more severe MSA and PSP. Thus, clinical combination of motor and non-motor symptoms does not exclusively point at MSA. Pupillography, ABPM and the questionnaire may assist in delineating the 3 syndromes when applied in combination.
CPT Codes / HCPCS Codes / ICD-9 Codes
CPT codes covered if selection criteria are met:
ICD-9 codes covered if selection criteria are met:
Syncope and collapse
ICD-9 codes not covered for indications listed in the CPB (not all-inclusive):
332.0 - 332.1
Compression of the brain [Chiari type I-malformation (Chiari drop attacks)]
Other specified disorders of nervous system [multiple system atrophy]
Other specified idiopathic peripheral neuropathy [supranuclear palsy]
780.71 - 780.79
Malaise and fatigue
Long-term (current) use of other medications
Examination following completed treatment with high-risk medications, NEC
Other follow-up examination
Examination following combined treatment
Unspecified follow-up examination
The above policy is based on the following references:
Grubb BP, Kosinski D. Current trends in etiology, diagnosis, and management of neurocardiogenic syncope. Curr Opin Cardiol. 1996;11(1):32-41.
Morillo CA, Klein GJ, Gersh BJ. Can serial tilt testing be used to evaluate therapy in neurally mediated syncope? Am J Cardiol. 1996;77(7):521-523.
Ruiz GA, Scaglione J, Gonzalez-Zuelgaray J. Reproducibility of head-up tilt test in patients with syncope. Clin Cardiol. 1996;19(3):215-220.
Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for assessing syncope. American College of Cardiology. J Am Coll Cardiol. 1996;28(1):263-275.
Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope. Part 2: Unexplained syncope. Ann Intern Med. 1997;127(1):76-86.
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Rowe PC, Bou-Holaigah I, Kan JS, et al. Is neurally mediated hypotension an unrecognized cause of chronic fatigue? Lancet. 1995;345(8950):623-624.
Klonoff D. Chronic fatigue syndrome and neurally mediated hypotension. JAMA. 1996;275(5):359-360.
Morillo CA, Klein GJ, Gersh BJ. Can serial tilt testing be used to evaluate therapy in neurally mediated syncope? Am J Cardiol. 1996;77:521-523.
Wessely S. Is neurally mediated hypotension an unrecognized cause of chronic fatigue? Lancet. 1995;345:1112; discussion 1112-1113.
Baschetti R. Chronic fatigue syndrome and neurally mediated hypotension. JAMA. 1996;275(5):359; author reply 360.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope. Eur Heart J. 2001;22(15):1256-1306.
Luria DM, Shen WK. Syncope in the elderly: New trends in diagnostic approach and nonpharmacologic management. Am J Geriatr Cardiol. 2001;10(2):91-96.
Faddis MN, Rich MW. Pacing interventions for falls and syncope in the elderly. Clin Geriatr Med. 2002;18(2):279-294.
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Timoteo AT, Oliveira MM, Antunes E, et al. Tilt test in elderly patients with syncope of unknown etiology: Experience with pharmacological stimulation with nitroglycerin. Rev Port Cardiol. 2005;24(7-8):945-953.
Gierelak G, Makowski K, Guzik P, et al. Effects of therapy based on tilt testing results on the long-term outcome in patients with syncope. Kardiol Pol. 2005;63(7):1-16; discussion 17-19.
Steinberg LA, Knilans TK. Syncope in children: Diagnostic tests have a high cost and low yield. J Pediatr. 2005;146(3):355-358.
Miller TH, Kruse JE. Evaluation of syncope. Am Fam Physician. 2005;72(8):1492-1500.
Freeman R. Assessment of cardiovascular autonomic function. Clin Neurophysiol. 2006;117(4):716-730.
Vlahos AP, Tzoufi M, Katsouras CS, et al. Provocation of neurocardiogenic syncope during head-up tilt testing in children: Comparison between isoproterenol and nitroglycerin. Pediatrics. 2007;119(2):e419-e425.
Kirsch P, Mitro P, Mudrakova K, Valocik G. Diagnostic yield of adenosine and nitroglycerine stimulated tilt test in patients with unexplained syncope. Bratisl Lek Listy. 2007;108(6):259-264.
Edfors R, Erdal J, A-Rogvi-Hansen B. Tilt table testing in patients with suspected epilepsy. Acta Neurol Scand. 2008;117(5):354-358.
Mehlsen AB, Mehlsen J. Investigation in suspected syncope. A study of more than 1,174 consecutively referred patients. Ugeskr Laeger. 2008;170(9):723-727.
Straus D, Foster K, Zimmerman F, Frim D. Chiari drop attacks: Surgical decompression and the role of tilt table testing. Pediatr Neurosurg. 2009;45(5):384-389.
Riley DE, Chelimsky TC. Autonomic nervous system testing may not distinguish multiple system atrophy from Parkinson's disease. J Neurol Neurosurg Psychiatry. 2003;74(1):56-60.
Uno C, Fukuda C, Tanaka N, et al. Study of autonomic dysfunction in patients with obstructive sleep apnea syndrome to head-up tilt test. Rinsho Byori. 2009;57(12):1164-1169.
Oliveira MM, da Silva N, Timóteo AT, et al. Alterations in autonomic response head-up tilt testing in paroxysmal atrial fibrillation patients: A wavelet analysis. Rev Port Cardiol. 2009;28(3):243-257.
Reimann M, Schmidt C, Herting B, et al. Comprehensive autonomic assessment does not differentiate between Parkinson's disease, multiple system atrophy and progressive supranuclear palsy. J Neural Transm. 2010;117(1):69-76.
Arnold M. In adult patients presenting with syncope, how effective is tilt table testing in diagnosing psychogenic blackout? BestBETS Best Evidence Topics. July 21, 2011.
Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial, general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely responsible for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is subject to change.