Heart Rate Increases in Tilt Test
To the Editor:
Mallat and colleagues have recently reported the predictive value of an early rise in heart rate during a Westminster tilt test (Circulation. 1997;96:581–584). They used a selected patient population and made an interesting observation that a rise in heart rate of >18 bpm almost invariably predicted those patients who would subsequently have a positive test. This observation is consistent with the current theories of the mechanism of syncope.
In our center, we use the Westminster protocol for tilt testing and have reviewed the last 110 documented cases studied in our laboratory. We applied Mallat’s criteria to the 28 positive and 76 negative tests, excluding 6 patients with permanent pacemakers. This produced 16 false-negative and 19 false-positive results, which gives a sensitivity of 43% and a specificity of 39%.
We were therefore disappointed that our findings appear to contrast sharply with those reported. Clearly unlike Mallat’s study, our patients were not a selected population, but if such criteria are to be clinically useful, they need to be generally applicable. Exclusion of 40% of the population because of comorbidity significantly limits such criteria. However, using Mallat’s exclusion criteria, the sensitivity and specificity were still unacceptably low at 50% and 40%, respectively.
One does have to question the suggested clinical relevance of such an observation: is the tilt test to be abandoned after 6 minutes of tilt? Although the test is laborious, is the clinician to terminate the test early when, by Mallat’s figures, there is the potential to make a false-negative result in 1 in 8 patients? We cannot agree that it is tenable to reduce a test that lasts over an hour by 20 minutes at the expense of missing or misdiagnosing a significant number of patients.
Mallat does confine his conclusions to patients who do not go on to develop syncope and hence avoids his 1-in-8 false-negative rate. However, this has the consequence of the clinician not knowing which patients can have the tilt test curtailed until after the first 26 minutes of the test. Pragmatically, this means that increasing the number of patients in a given clinical session is not possible.
Finally, our data do not confirm their observations and suggest a high false-positive rate. We would be interested to hear the experience of other centers.
We appreciate the opportunity to reply to Dr Newby and colleagues. We think that their interpretation of our results is confusing. First, they understood that the main observation of our study (Circulation. 1997;96:581–584) was that “a rise in heart rate of >18 bpm almost invariably predicted … a positive test.” However, our observation was that a rise in heart rate (HR) of ≤18 bpm (after strict application of our inclusion criteria) during the first 6 minutes of tilt has a high predictive value for a negative tilt test. The 2 assertions are not equivalent, and definitions for false-negative and false-positive results would be different. In their interpretation, a false-positive result is a negative tilt test after a rise in HR >18 bpm. However, in our study, a false-positive result is a positive tilt test with a rise of HR of ≤18 bpm. Second, given the number of positive and negative tests and the number of false-negative and false-positive results in their retrospective study, the reported values of sensitivity or specificity are incorrect. Third, according to our criteria, false-negative results could not be missed, as we did not propose to abandon the tilt test when the increase in HR is >18 bpm.
The results of the retrospective analysis by Newby et al differ from ours. Unfortunately, several issues are not clarified. For example, we do not know from their letter whether they included patients with recurrent vasovagal syncope, whether they are confident that relatively stable continuous measurements of HR were obtained in all their patients, or whether the increase in HR (as defined in our study) was measured in a blinded manner. In addition, although they excluded patients with comorbidity, we do not know whether patients with drug use have also been excluded from their analysis. Most importantly, we do not know how many patients with positive tilt tests showed a trend for decreased HR or blood pressure during the early tilt. As mentioned in our study, such patients were excluded because of a high probability for a positive tilt. Indeed, all patients with these characteristics had positive tilt tests in our study (with a rise in HR of ≤18 bpm). The proportion of such patients may be highly variable. In the absence of more information from Newby et al, we cannot comment further on their results.
Our study was conducted in a single center and included a relatively limited number of patients. However, the results were striking and are still reproducible in our center. We are eager to know whether they are reproducible in a multicenter study including a large population of selected patients using our strict inclusion and exclusion criteria. Meanwhile, standard protocols should be the rule.
- Copyright © 1998 by American Heart Association