[Head-up tilt test in vasovagal syncope: for which purposes? for whom?].

30 Vasovagal syncope is a disorder that has been known for years since its clinical characteristics were masterfully described by Sir Thomas Lewis at the beginning of the 20th century.1 Traditionally, the criteria used to establish the diagnosis of a vasovagal origin in patients with syncopal episodes was based only on the presence of triggering circumstances and typical prodromic symptoms. In 1986, Kenny et al2 published an article in which they proposed the use of the tilt-table test (TTT) as a diagnostic tool to establish vasovagal origin in patients with syncope of unknown cause. After this publication, interest in the condition increased considerably and the number of publications dealing with vasovagal syncope and the TTT increased spectacularly. Fifteen years after this first publication, it is interesting to critically review what the TTT has contributed to our knowledge of the vasovagal syncope, as well as its limitations. TTT can be considered an experimental model that makes it possible to induce, in a relatively controlled way, vasovagal responses in susceptible patients. This has made it possible to better understand various aspects of the pathophysiological mechanisms involved in vasovagal syncope, such as the behavior of the vascular tree, changes in volemia, myocardial contractility disorders preceding the episode, variations in cathecholamine secretion, and modifications in the variability of heart rate or sympathetic traffic, among others. Likewise, by observing the behavior of the heart rate and blood pressure during TTT, different patterns have been characterized, which has allowed vasovagal responses to be classified.3 Therefore, the use of TTT has undoubtedly contributed in an important way to improving our knowledge of the pathophysiological mechanisms and clinical characterization of vasovagal syncope. However, the use of TTT as a diagnostic tool has some limitations. The first of them is related to the fact that it has not been possible to establish a uniform protocol. As a consequence, a large variety of protocols exist,4 making it difficult to compare results between different series. Another problem resides in the difficulty of establishing the diagnostic reliability of the test, because it is essential to first know its specificity and sensitivity. The specificity of most protocols has been established easily by analyzing the rate of positive responses in healthy persons without a history of syncope and it has been found to be relatively high. However, the sensitivity is not known because no «gold standard» exists against which test results can be compared. Therefore, the presence of a positive response to TTT in patients without heart disease and with a normal ECG, or in patients with heart disease in which a cardiogenic cause of the syncopal episodes has been reasonably excluded, can be considered diagnostic of a vasovagal origin. This has made it possible to diagnose vasovagal syncope in patients with abrupt syncopal episodes in the absence of any apparent trigger. Nevertheless, the absence of a positive response to TTT, especially in patients without heart disease and with a normal ECG, does not allow a vasovagal cause to be excluded. Although various studies have tried to evaluate if TTT could be used as a predictor of the recurrence or severity of syncopal episodes, no variable related with the test has been found to be capable of predicting the evolution during follow-up. Sheldon et al5 analyzed a series of variables including both clinical and TTT data, and found that only the combination of the number of previous syncopes and the duration of the syncopal history was predictive of recurrences during follow-up. Likewise, Malik et al6 reported that the presence of a new syncopal episode in the first month after TTT was also predictive of recurrence. In all the ED I TO R I A L S