Research in Review

• Experimental induction of panic-like symptoms in patients with postural tachycardia syndrome
• Treatment of postural tachycardia syndrome: a comparison of octreotide and midodrine
• Acute effects of low and moderate doses of alcohol on coordinate motor and autonomic nervous function in a group of healthy Hans
• Oesophageal acid exposure and altered neurocardiac function in patients with GERD and idiopathic cardiac dysrhythmias
• Norepinephrine transporter inhibition prevents tilt-induced pre-syncope

Clin Auton Res. 2006 Aug 16

Experimental induction of panic-like symptoms in patients with postural tachycardia syndrome.

Khurana, R. K.

Division of Neurology, The Union Memorial Hospital, 201 East University Parkway, Baltimore, MD, 21218, USA, ramesh.khurana@medstar.net.

Patients with postural tachycardia syndrome (POTS) might be misdiagnosed with panic disorder due to shared clinical features. The first aim of our study was to investigate the relationship between symptoms of POTS and panic disorder. The second aim was to delineate clinical features distinguishing symptoms of POTS from panic disorder. A total of 11 patients with POTS and 11 control subjects participated in an IRB-approved, prospective, placebo-controlled study. The experimentally induced panic-like symptoms of POTS were systematically studied using the Acute Panic Inventory (API) questionnaire. The participants answered the questionnaire after each placebo infusion and after each of the three provoking stimuli: head-up tilt test (HUT), isoproterenol infusion (ISI), and sodium lactate infusion (SLI). API responses were summed for each subject at each time point of administration. Individual API symptoms and summed responses were analyzed for statistical significance. All patients with POTS developed symptoms of orthostatic intolerance during HUT. Pharmacologically induced symptoms subjectively mimicked spontaneous symptoms in 5 of 11 patients during ISI and in none of 11 patients during SLI. In contrast, API scores in these patients reached panic threshold in 0 of 11 following HUT, in 4 of 11 following ISI and in 4 of 11 following SLI. Individual symptoms analysis revealed that significant increase in scores was limited to the somatic symptoms of palpitations, dyspnea, and twitching or trembling. In conclusion, the symptoms of POTS are phenomenologically different and clinically distinguishable from panic disorder symptoms.

PMID: 16915526

Clin Auton Res. 2006 Oct 11;

Treatment of postural tachycardia syndrome: a comparison of octreotide and midodrine.

Hoeldtke RD, Bryner KD, Hoeldtke ME, Hobbs G.

Dept. of Medicine, West Virginia University, One Medical Center Drive, PO Box 9159, Morgantown, WV, 26506-9159, USA, rhoeldtke@hsc.wvu.edu.

We assessed the potency of octreotide and midodrine, and their combination, in the treatment of the postural tachycardia syndrome (POTS) and orthostatic intolerance (OI). Nine patients with POTS and six patients with OI stood for up to 1 hour while their HR and BP were monitored. Patients received on separate days, midodrine 10 mg 1 hour before testing, octreotide 0.9 microg/kg 8 minutes before testing or combination therapy. Standing time in the patients with POTS was 41.2 +/- 8.4 minutes and not improved by midodrine or octreotide, but increased to 56.3 +/- 2.7 (P < 0.01) minutes following combination therapy. The standing heart rate in POTS, 114 +/- 0.7 bpm, was suppressed by midodrine 92.8 +/- 0.7 (P < 0.001), octreotide 90.6 +/- 0.78 (P < 0.001), and combination therapy 84.7 +/- 0.7 (P < 0.001). Combination therapy was better than monotherapy (P < 0.001) but only for the first 10 minutes of standing.Standing time of 36.3 +/- 3.5 minutes in the patients with OI improved with midodrine, octreotide and combination therapy (55.5 +/- 3.1, 56.5 +/- 3.5, and 56.6 +/- 3.3, respectively, P < 0.05 for each). Standing heart rate in OI was 100 +/- .76 bpm; following midodrine it was 80.3 +/- .69 (P < 0.05), following octreotide it was 84.8 +/- .86, and following combination therapy it was 71.2 +/- .9 (P < 0.01). The RR interval versus time area under the curve (The Orthostatic Index) was 21.1 +/- 4 in patients with OI. After midodrine it was 41.4 +/- 3.5 (P < 0.01), after octreotide 40.3 +/- 3.8 (P < 0.01) and after the combination it was 47.3 +/- 4.6 (P < 0.001).Midodrine and octreotide suppressed tachycardia in POTS and improved standing times in OI. The two drugs had similar potencies; combination therapy was not significantly better than monotherapy.

PMID: 17036177

Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2006 Jun;23(3):635-9.

Acute effects of low and moderate doses of alcohol on coordinate motor and autonomic nervous function in a group of healthy Hans.

Li X, Deng S, Xie Z.

College of Basic Medicine, Chongqing Medical University, Chongqing 400016, China.

The autonomic nervous function, blood pressure, coordinate motor and blood alcohol Concentration (BAG) of twenty-one healthy Han volunteers were examined before and after alcohol intake. The purpose was to assess the acute effects of low and moderate doses of alcohol on their coordinate motor and autonomic nervous function. The results showed that after alcohol intake the subjects' heart rate increased and the total power value (TPV) decreased significantly. After the intake of alcohol at low dose, the parasympathetic nervous function of the subjects lying supine was inhibited significantly. After the intake of alcohol at moderate dose, both the parasympathetic and the sympathetic nervous functions were inhibited. After the intake of alcohol at low dose, both the systolic pressure and the diastolic pressure of the subjects standing up-right were decreased and the diastolic pressure of those lying supine were also decreased. After the intake of alcohol at moderate dose, the systolic and diastolic pressures of the subjects, either lying supine or standing up-right, were decreased. Some subjects showed ataxia after the intake of alcohol at low dose ,and some showed aggravated ataxia after intake of alcohol at moderate dose of alcohol. There was no relationship of BAG with the degree of changes in autonomic nervous function, blood pressure and ataxia. The results indicated that ataxia was induced to come on and the autonomic nervous function was inhibited in some subjects who had taken low and moderate doses of alcohol, and the cardiovascular regulation was affected too. These suggested that the increase of alcohol intake is adverse to human body's adaptation to the sharp change of circumstance.

PMID: 16856405

Aliment Pharmacol Ther. 2006 Jul 15;24(2):361-70.

Oesophageal acid exposure and altered neurocardiac function in patients with GERD and idiopathic cardiac dysrhythmias.

Cuomo R, DE Giorgi F, Adinolfi L, Sarnelli G, Loffredo F, Efficie E, Verde C, Savarese MF, Usai P, Budillon G.

Department of Clinical and Experimental Medicine, Gastroenterology, University 'Federico II', Naples, Italy.

Oesophageal sensory stimuli alter neurocardiac function through autonomic reflexes. To evaluate in patients with idiopathic supraventricular cardiac dysrhythmias and gastro-oesophageal reflux disease (GERD) whether GE reflux alters neurocardiac function and the effect of acid suppression on cardiac symptoms. Thirty-two patients (13 females and 19 males; age: 20-69 years) with dysrhythmias plus GERD, and nine patients (five females and four males; age: 43-58 years) with GERD only, underwent simultaneous 24-h pH-metry and ECG monitoring. Power spectrum analysis of heart rate variability (PSHRV) was obtained with both its low frequency (LF, sympathetic modulation) and high frequency (HF, vagal modulation) components. Hourly mean oesophageal pH and LF/HF ratio were correlated. A 3 months full-dosage PPI therapy (esomeprazole 40 mg/day) was prescribed. In 18 (56%) of the 32 patients with dysrhythmia and in none with GERD only, a significant (P < 0.05) correlation between oesophageal pH and LF/HF ratio (oesophagus-heart correlation) was observed. A significant reduction of cardiac symptoms after PPI therapy was observed only in these patients (13/16 vs. 4/11, P < 0.01). This study has identified a subgroup of dysrhythmic patients in whom the oesophageal acid stimulus elicited cardiac autonomic reflexes. In these patients acid suppression seems to improve GERD and cardiac symptoms.

PMID: 16842463

J Am Coll Cardiol. 2006 Aug 1;48(3):516-22. Epub 2006 Jul 12.

Norepinephrine transporter inhibition prevents tilt-induced pre-syncope.

Schroeder C, Birkenfeld AL, Mayer AF, Tank J, Diedrich A, Luft FC, Jordan J.

Franz-Volhard Clinical Research Center, Medical Faculty of the Charite and HELIOS Klinikum, Berlin, Germany.

OBJECTIVES: We tested the hypothesis that pharmacological norepinephrine reuptake transporter (NET) inhibition delays the onset of head-up tilt-induced presyncope in healthy subjects.

BACKGROUND: Treatment of neurally mediated syncope is unsatisfactory. In a previous study in a small number of healthy subjects, pharmacologic NET inhibition delayed the onset of head-up tilt-induced pre-syncope.

METHODS: We combined data sets from 3 substudies comprising 51 healthy subjects without a history of syncope. In a double-blind, randomized, cross-over fashion, subjects underwent 2 head-up tilt tests, once with placebo and once with a NET inhibitor (sibutramine or reboxetine). Tilt testing was prematurely ended when pre-syncopal symptoms such as dizziness, nausea, or visual disturbances occurred together with a decrease in blood pressure and/or heart rate.

RESULTS: The mean tolerated tilt test duration was 29 +/- 2 min with placebo and 35 +/- 1 min with NET inhibition (p = 0.001). The odds ratio for premature abortion of head-up tilt testing was 0.22 (95% confidence interval 0.09 to 0.55, p < 0.001) in favor of NET inhibition. Norepinephrine reuptake transporter inhibition elicited a pressor response and increased upright heart rate.

CONCLUSIONS: In healthy subjects, NET inhibition prevents tilt-induced neurally mediated (pre)syncope. Therefore, NET inhibition may be a worthwhile target of drug intervention for larger trials in highly symptomatic patients with neurally mediated syncope.

PMID: 16875978

Research abstracts obtained from PubMed.

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