|
 
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| EDITORIAL |
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| Year : 2016 | Volume
: 1
| Issue : 1 | Page : 2-4 |
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Rethinking Tilt Testing
Richard Sutton
Emeritus Professor of Clinical Cardiology, National Heart and Lung Institute, Imperial College, London, United Kingdom
| Date of Web Publication | 30-Sep-2016 |
Correspondence Address:
Richard Sutton
ICCH Building, St. Mary's Hospital Campus, 59-61 North Wharf Road London W2 1 LA
United Kingdom
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2352-4197.191478
Tilt was used physiologically, 1930s–1970s, becoming a clinical diagnostic test for syncope in 1980s. Tilt has been criticized recently for failing to discriminate between reflex and more sinister syncope. Studies on possible benefit of pacing for older reflex syncope patients (2012–2014) yielded unexpected results. Patients with electrocardiogram implantable loop recorder (ILR) documented asystole and negative tilt, despite history strongly suggestive of reflex syncope, did well with pacing having syncope recurrence similar to that in paced His-Purkinje disease, while those with identical ILR findings and positive tilt did little better than those without pacing. These findings prompted explanation. The hypothesis hinged on tilt revealing a hypotensive/vasodepressor tendency rather than defining vasovagal syncope. Support was drawn from literature demonstrating good test sensitivity and specificity but no clinical value in arrhythmic, unexplained, or structural cardiovascular disease syncope. Further, in carotid sinus syndrome, another reflex syncope, the same pattern of disappointing pacing results was seen when tilt was positive but lack of syncope when tilt was negative. Thus, rethinking tilt testing is required to portray it in reflex, arrhythmic, unexplained, and cardiovascular syncope as having value in demonstrating risk of recurrence rather than being diagnostic. Its value in diagnosis of orthostatic hypotension (immediate/delayed), psychogenic pseudosyncope, and postural orthostatic tachycardia remains important and unchanged. The hypothesis has additional implications for management of hypertensive patients with syncope where medication may exacerbate symptoms requiring reduction/discontinuation. Tilt testing has greater value now than that claimed at its 1986 introduction. Keywords: Cardioinhibition, pacing, syncope, tilt testing, vasodepression
How to cite this article:
Sutton R. Rethinking Tilt Testing. Int J Heart Rhythm 2016;1:2-4 |
| Background | |  |
Tilt or use of upright posture occurred first in physiological studies attempting to explain the vasovagal phenomenon.[1],[2] It is important to note that tilt in comparison with active standing avoids the use of the lower limb muscle pump, thus providing a greater circulatory stress than standing.[3] In recent years, epidemiological studies have shown [4] that approximately 40% of the population will have at least one syncope during life. The great majority of these episodes of syncope are reflex in nature. Thus, it can be assumed that a hypotensive/vasodepressive tendency exists in 40% of the population.
Tilt was introduced for clinical diagnosis of vasovagal syncope (VVS) in 1986[5] when three groups of subjects were studied: Patients with carotid sinus syndrome, patients with unexplained syncope (by currently available techniques – history, physical examination, electrocardiogram (ECG), echocardiography, ambulatory monitoring, and electrophysiological study), and age-matched controls. Tilt reproduced the patient's symptoms in the vast majority of both patient groups but was only positive in 10% of controls. This study proved to be very influential and tilt testing was taken up as a diagnostic test for VVS across the world.
With the passage of many years, tilt has been criticized for failing to provide discrimination between reflex (vasovagal) and other more sinister causes of syncope in individual patients. Perhaps the most notable of these criticisms came from the United Kingdom body, the National Institute of Clinical Excellence.[6] In arrhythmic syncope, both supraventricular tachycardias [7],[8] and ventricular tachycardias of channelopathies,[9] in unexplained syncope [10],[11] and in syncope caused by structural cardiovascular disease diagnostic discrimination [12],[13],[14] may be disappointing. Tilt testing was also criticized for lack of sensitivity and specificity. However, this criticism was ill-founded. In terms of sensitivity, reports indicate an adequate range of 65–92%[9],[10],[14],[15] and for specificity >85%[10],[13],[16] [Figure 1]. As shown in [Figure 1], the results in the mid-band (red) indicate the areas in which tilt testing has failed to deliver. | Figure 1: Published positivity rates of tilt testing in different populations. The upper band in black shows studies, which estimate the sensitivity of the test when the history strongly suggested vasovagal syncope. The middle band in red show studies of patients considered likely to have arrhythmia or structural heart disease as cause of syncope or unexplained syncope. The lower band in green reports studies using tilt testing in populations with no history of syncope yielding estimates of specificity. The drug challenge used or none (passive) is quoted in brackets and the references are given in subsequent brackets. Clom = Clomipramine, GTN = Glyceryl trinitrate.
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| New Data | | |
The ISSUE-3 study and its subsequent substudies [17],[18] have demonstrated a surprising finding. In reflex syncope of older patients whose ECG mechanism of syncope was demonstrated by inserted loop recorder did better with subsequent pacing if their tilt tests had been negative than if the tests were positive (VASIS 2B).[19] These results called for an explanation and Sutton and Brignole, 2014,[20] provided a hypothesis to explain the findings. They argued that tilt was merely demonstrating a hypotensive tendency, which was often masked by the intense cardioinhibition shown on the ECG during a spontaneous syncope. Intense bradycardia was a necessity, by protocol, for implanting a pacemaker in the ISSUE-3 study.[17] In their hypothesis,[20] Sutton and Brignole invoked data from studies of carotid sinus syndrome, a similar reflex syncope, where those who were tilt-positive had almost 3 times the likelihood of syncope recurrence in follow-up compared with those who were tilt-negative.[21],[22] Thus, the argument stated that tilt should, in future, be considered as a risk of recurrence stratification tool rather than as a means of diagnosis of reflex syncope.
A further implication is that the hypotensive/vasodepressive tendency revealed by tilt may be playing a role in arrhythmic, structural heart disease, and unexplained syncope. It is important as a possible cause of syncope in the individual patient, but it may not be the cause of the index syncope under investigation. Moreover, tilt positivity may reveal a more benign syncope than the index mechanism. Attempts to treat the tilt-induced syncope may, therefore, not address a dangerous alternative mechanism, such as ventricular tachycardia in a channelopathy, aortic stenosis, or hypertrophic cardiomyopathy.[9],[11],[14] This is the basis for the disappointing results of tilt testing in these conditions where the physician really needs help in determining the cause of syncope.
Tilt testing should be considered to have an important and unchanged role in the evaluation of orthostatic hypotension, postural orthostatic tachycardia, and psychogenic pseudosyncope.[23],[24]
Extension of the hypothesis of tilt revealing hypotensive/vasodepressive tendency is in the management of hypertension. All physicians with an interest in syncope have seen patients with a history of syncope in youth, develop hypertension in middle age requiring treatment and subsequently return with reflex syncope. The main implication is that in patients, such as these, treatment of hypertension requires particular care and if syncope occurs, medication levels will have to be reduced or even discontinued.[25],[26] We are currently encouraged to treat nonelderly hypertensives energetically with even lower blood pressure targets than before to avoid stroke. Tilt testing in patients in this age group may indicate which patients will tolerate high medication doses and which will not.
| Conclusions | | |
Tilt testing remains a valuable assessment tool in syncope. It should be considered diagnostic in orthostatic hypotension, postural orthostatic tachycardia, and psychogenic pseudosyncope in patients who present clinical pictures compatible with these conditions. However, tilt should not be considered diagnostic in patients with reflex syncope who receive a treatment such as permanent pacing rather the test should be considered a risk of recurrence stratification tool. In arrhythmic, structural heart disease and unexplained syncope tilt must be applied with caution bearing in mind that it may reveal a syncope which is not the prognostically important one. Finally, tilt may offer value in the pharmaceutical treatment of hypertension by anticipation of excessive hypotension during therapy.
Instead of less tilt testing, it appears that more is needed and it will have clinical value that was not considered when the test was introduced in 1986.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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| 14. | Ungar A, Sgobino P, Russo V, Vitale E, Sutton R, Melissano D, et al. Diagnosis of neurally mediated syncope at initial evaluation and with tilt table testing compared with that revealed by prolonged ECG monitoring. An analysis from the Third International Study on Syncope of Uncertain Etiology (ISSUE-3). Heart 2013;99:1825-31. |
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| 16. | Petersen ME, Williams TR, Gordon C, Chamberlain-Webber R, Sutton R. The normal response to prolonged passive head up tilt testing. Heart 2000;84:509-14. |
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| 20. | Sutton R, Brignole M. Twenty-eight years of research permit reinterpretation of tilt-testing: Hypotensive susceptibility rather than diagnosis. Eur Heart J 2014;35:2211-2. |
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| 23. | Nilsson D, Sutton R, Tas W, Burri P, Melander O, Fedorowski A. Orthostatic changes in hemodynamics and cardiovascular biomarkers in dysautonomic patients. PLoS One 2015;10:e0128962. |
| 24. | Tannemaat MR, van Niekerk J, Reijntjes RH, Thijs RD, Sutton R, van Dijk JG. The semiology of tilt-induced psychogenic pseudosyncope. Neurology 2013;81:752-8. |
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| 26. | Gaggioli G, Bottoni N, Mureddu R, Foglia-Manzillo G, Mascioli G, Bartoli P, et al. Effects of chronic vasodilator therapy to enhance susceptibility to vasovagal syncope during upright tilt testing. Am J Cardiol 1997;80:1092-4. |
[Figure 1]
| This article has been cited by | | 1 |
Underlying hemodynamic differences are associated with responses to tilt testing |
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