Positive Head-up Tilt Table Test Research Articles

An association between anxiety and neurocardiogenic syncope during head-up tilt table testing.

To study the association between anxiety and neurocardiogenic syncope as determined by head-up tilt table testing (HUT) in men and women with presyncope or syncope, patients with unexplained syncope or presyncope undergoing HUT were asked to complete the Burns Anxiety Inventory (BAI), a validated inventory of 33 questions with responses graded from 0 to 3. HUT consisted of a 30-minute tilt to 60 degrees, which if negative, was repeated with an isoproterenol infusion. A positive HUT was defined as symptomatic hypotension and/or bradycardia. Of the 66 patients who completed the BAI and underwent HUT, 33 were men and 33 were women. The mean age was 57 +/- 18 years (17-91 years). Patients with a positive HUT had a higher BAI score than those with a negative HUT (22 +/- 12 vs 14 +/- 13, P = 0.017). This association was stronger in women with a BAI score of 24 +/- 11 in those with a positive HUT versus 13 +/- 8 in those with a negative HUT (P = 0.005). In contrast, the mean BAI score for men with a positive HUT was 19 +/- 13, as compared to 15 +/- 16 for a negative HUT (P = 0.5). In conclusion, the present study demonstrates a statistical association between anxiety (as determined by BAI) and HUT result. Gender-based analysis revealed a more statistically significant relationship between anxiety and HUT outcome for women as compared to men.

Early Heart Rate Variations During Head-up Tilt Table Testing as a Predictor of Outcome of the Test

Head-up tilt table testing (HUTT) is a useful tool for the diagnosis of unknown origin of syncope. A setback is its duration. This study tries to establish a specific parameter that, according to the heart rate elevation in the test's initial phase, allows a reliable prediction of its outcome. In a prospective study, every patient being under unknown syncope workup was included. A two-phase 20-minute tilt table test was performed. The initial phase was passive, and the second required pharmacological stimulation with isoproterenol. The basal and 5- and 10-minute heart rate values of the passive phase were measured and compared within the group and against negative tests. During a 1-year period, 115 HUTT were performed: 88 were positive and 27 negative. The negative HUTT patients had an increase in HR of 5.05 (+/- 13.5) beats/min at 5 minutes, and 5.79 (+/- 12.9) beats/min at 10 minutes (P = 0.2). Those with a positive HUTT had an increase of 9.05 (+/- 14.5) beats/min at 5 minutes, and of 10 (+/- 13.4) beats/min at 10 minutes (P < 0.001). There were no significant changes in HR when comparing positive to negative HUTT. There is no specific number that allows predication of outcome early in HUTT. Within the group, variations are important. Only a group tendency can be established, which strongly correlates with the results obtained during the test.

Driving safety among patients with neurocardiogenic (vasovagal) syncope.

Neurocardiogenic syncope is one of the most common causes of syncope. However, the important issue of driving related injury due to syncope in this population is not well defined. Risk of injury due to syncope while driving and driving behavior was evaluated in 155 consecutive patients (92 women and 63 men; mean age 49 +/- 19 years) with history of syncope in whom hypotension and syncope or presyncope could be provoked during head-up tilt testing. Patients with syncope and positive head-up tilt table test were treated with pharmacological therapy. All participants were asked to fill out a detailed questionnaire regarding any driving related injuries and their driving behavior before tilt table testing and during follow-up. Prior to head-up tilt testing two patients had syncope while driving, and one of these patients had syncope related injury during driving. The mean duration of syncopal episodes was 50 +/- 14 months (range 12-72 months). Of the 155 patients, 52 (34%) had no warning prior to syncope, while 103 (6%) had warning symptoms such as dizziness prior to their clinical syncope. Following a diagnosis of neurocardiogenic syncope established by head-up tilt testing, six patients stopped driving on their own. During a median follow-up of 22 months recurrent syncope occurred in five (3.2%) patients. No patient had syncope or injury during driving. In conclusion, syncope and injury while driving in patients with neurocardiogenic syncope is rare. The precise mechanism of this is unclear but may be related to posture during driving. Consensus among the medical community will be needed to provide specific guidelines in these patients.

Positive head-up tilt table test in patients with the long QT syndrome.

Syncope in patients with the long QT syndrome is commonly attributed to a ventricular arrhythmia (torsades de pointes). The susceptibility of patients with the long QT syndrome (LQTS) to neurally mediated syncope is currently unknown. Head-up tilt table testing (70 degrees) was performed in six patients with the long QT syndrome and a history of syncope. All patients had syncope with a mixed response. The RR interval was significantly decreased 2 min before the onset of syncope (980 +/- 125 ms vs 630 +/- 91 ms, P=0.003), and significantly increased during syncope (983.17 +/- 224.71; P=0.006). Non-significant changes in QT intervals were observed. Baseline QT was 513 +/- 86 ms and decreased to 450 +/- 59 ms 2 min before the onset of syncope (P=0.11). Although not statistically significant, QT intervals during syncope were longer than at 2 min before syncope (485 +/- 85 ms vs 450 +/- 59 ms; P=0.29). Our results suggest that patients with the LQTS are susceptible to neurally mediated syncope. Whether this susceptibility differs from control populations remains unresolved. From a clinical standpoint, neurocardiogenic syncope should be considered a diagnostic alternative in patients with LQTS.

Efficacy and Safety of Clonazepam in Refractory Neurally Mediated Syncope

Neurally mediated syncope is a complex syndrome that is often difficult to manage using currently available treatment strategies. The efficacy and safety of clonazepam was evaluated in 35 patients with refractory neurally mediated syncope. All patients had syncope (n = 33) or disabling presyncope (n = 2) and a positive head-up tilt table test (HUTT) despite treatment with one or more of the following therapies: beta-blocker, high-salt diet, fludrocortisone, elastic compression stockings, and disopyramide. Clonazepam was initiated at 0.5 mg/day and titrated in 0.25-0.5 mg/day increments for symptom control. Early (first 8 weeks) symptomatic response was achieved in 31 of 35 (89%) patients. Early HUTT reverted to negative in 29 of 35 (83%) patients. Two patients discontinued clonazepam during early follow-up due to side effects. Thirty-three patients received long-term clonazepam therapy. Twenty-five patients had late HUTT with 21 remaining negative. Of the eight patients who did not have late HUTT, one patient discontinued clonazepam prior to HUTT due to side effects. Seven patients refused late HUTT. All seven patients achieved symptomatic control on clonazepam with two requiring dose titration. Of the 21 patients with a negative late HUTT, 18 achieved symptomatic control with two of these patients requiring dose titration. Two patients who had only partial symptom control despite dose titration achieved total symptomatic control with the addition of disopyramide and beta-blockers. Two patients with a negative late HUTT discontinued clonazepam due to side effects. One patient had been symptomatically controlled while the other had recurrent symptoms with dose limiting side effects occurring after clonazepam dose titration. In the 4 patients with a positive late HUTT, 2 patients were symptomatically controlled, 1 patients required combination therapy with a beta-blocker to achieve symptomatic control, and 1 patient discontinued therapy due to side effects. Overall, 29 of 35 (83%) patients continue to receive clonazepam with symptom control. Based on intention-to-treat HUTT results, 21 of 35 (60%) patients were responders. Four patients required clonazepam dose titration and three required combination therapy with clonazepam plus disopyramide and/or a beta-blocker to achieve control. Clonazepam was discontinued in 6 patients, 5 for side effects and 1 following a transient ischemic attack. Clonazepam appears to be an effective therapeutic alternative in patients with refractory neurally mediated syncope. Based on our preliminary findings, a placebo controlled evaluation of clonazepam in neurally mediated syncope is warranted.

Efficacy of pindolol for treatment of vasovagal syncope

The purpose of this study was to evaluate the efficacy, safety, and tolerance of pindolol as initial therapy for vasovagal syncope. Head-up tilt table testing (HUT) was performed on 192 patients for syncope or near-syncope of unknown cause. Forty-four (23%) patients had a positive HUT for vasovagal syncope, and 28 (64%) received oral pindolol as initial therapy. Three patients were lost to follow-up; of the remaining 25 patients (mean age 60 ± 22 years), 15 were women, 14 had syncope, and 11 had near-syncope. At 14 ± 6 months' follow-up, 16 (64%) patients were without recurrence or side effects from pindolol. Of the 9 patients who stopped taking pindolol, 3 were switched to another regimen for recurrent symptoms, 2 stopped because of side effects, and 4 did not comply with the regimen. In conclusion, pindolol appears to be safe and effective as initial treatment for vasovagal syncope.