Research in Review

• Postural Orthostatic Tachycardia Syndrome: Dental Treatment Considerations
• Increased hydration alone does not improve orthostatic tolerance in patients with neurocardiogenic syncope
• Postural orthostatic tachycardia syndrome: the Mayo clinic experience
• Postural orthostatic tachycardia syndrome: an under-recognized disorder
• The postural tachycardia syndrome
• Sympathetic neural activity, sex dimorphism, and postural tachycardia syndrome

Read the full text publication “Postural Orthostatic Tachycardia Syndrome: Dental Treatment Considerations” by John K. Brooks, DDS and Laurie A. P. Francis, RDH at: http://jada.ada.org/cgi/reprint/137/4/488.pdf

Increased hydration alone does not improve orthostatic tolerance in patients with neurocardiogenic syncope.

Bellard E, Fortrat JO, Custaud MA, Victor J, Greenleaf J, Leftheriotis G. Clin Auton Res. 2007 Apr;17(2):99-105. Epub 2007 Apr 25.

Laboratoire de Physiology, UMR CNRS 6214 Inserm 771, Faculte de Medecine d'Angers rue Haute de Reculee, 49035, Angers, France, jofortrat@chu-angers.fr.

In patients with neurocardiogenic syncope, the beneficial effects of increased daily fluid intake, without an accompanying high dose of salt, are unknown. Our aim was to (1) determine whether plasma volume was low in patients with recurrent neurocardiogenic syncope, and (2) determine how recommendation about increased daily fluid intake, without an accompanying high dose of sodium, effects plasma volume and if this potential therapy improves orthostatic tolerance. Eighty-six patients with neurocardiogenic syncope were recruited in a prospective randomized open study. After an initial head-up tilt test, patients were randomly assigned to either the hydration supplementation group (1500 ml of water + 1500 mg of NaCl/day) or the no treatment (control) group. After ten days a second head-up tilt test was performed. Plasma volume, osmolality, and total body water were measured at baseline, and heart rate, arterial blood pressure, and cardiac transthoracic impedance were monitored during tilting. Hydration treatment did not affect the number of positive tilt tests (52% initial day, 54% after treatment, NS). In both groups, the overall number of positive tilt tests decreased between the initial and final head-up tilt test. There was no association between low plasma volume and positive tilt test. Patients with the lowest plasma volume were equally distributed in both positive and negative tilt response groups. An increased daily intake of fluid, without an accompanying high dose of salt, had no measurable beneficial effect on tolerance to head-up tilting in patients with neurocardiogenic syncope. Moreover in this patient group there was no association between a low plasma volume and a reduced tolerance to orthostatic stress.

PMID: 17464552

Postural orthostatic tachycardia syndrome: the Mayo clinic experience.

Thieben MJ, Sandroni P, Sletten DM, Benrud-Larson LM, Fealey RD, Vernino S, Lennon VA, Shen WK, Low PA. Mayo Clin Proc. 2007 Mar;82(3):308-13.

OBJECTIVE: To evaluate the prevalence and pathogenetic mechanisms of postural orthostatic tachycardia syndrome (POTS). PATIENTS AND

METHODS: We reviewed the medical records of patients with POTS seen at the Mayo Clinic in Rochester, Minn, from January 1, 1993, through December 31, 2003. All patients were required to have had a full autonomic reflex screen. The results of the following additional tests were evaluated: thermoregulatory sweat test, plasma catecholamine measurement, serum ganglionic (a3) acetylcholine receptor antibody detection, and 24-hour urinary sodium measurement.

RESULTS: We identified 152 patients (86.8% female; mean +/- SD age, 30.2+/-10.3 years) with a mean duration of symptoms of 4.1 years. The mean orthostatic heart rate increment was 44 beats/min. Half the patients had sudomotor abnormalities (apparent on both the quantitative sudomotor axon reflex test and thermoregulatory sweat test), and 34.9% had significant adrenergic impairment, indicating that at least half of the patients had a neuropathic pattern of POTS. In 13.8% of patients, onset was subacute, and ganglionic acetylcholine receptor antibody was detected in 14.6%, suggesting an autoimmune origin in at least 1 in 7 patients. Hyperadrenergic status was documented in 29.0% of patients (standing plasma norepinephrine level 2600 pg/mL), and at least 28.9% were presumably hypovolemic (24-hour urinary sodium level <100 mEq/24h). The lack of correlation between urinary sodium and standing norepinephrine levels suggests that mechanisms other than hypovolemia accounted for the hyperadrenergic state.

CONCLUSION: Our findings suggest a neuropathic basis for at least half the cases of POTS and that a substantial percentage of cases may be autoimmune. Hyperadrenergic and hypovolemic correlates are likely compensatory or exacerbating.

PMID: 17352367

Full text: http://www.mayoclinicproceedings.com/pdf%2F8203%2F8203a5.pdf

Postural orthostatic tachycardia syndrome: an under-recognized disorder.

Pandian JD, Dalton K, Henderson RD, McCombe PA. Intern Med J. 2007 Apr 19.
Department of Neurology, Royal Brisbane and Women's Hospital, Brisbane, Queensland, Australia.

Background: Postural orthostatic tachycardia syndrome (POTS), a clinical syndrome of orthostatic intolerance characterized by excessive tachycardia and symptoms of cerebral hypoperfusion on standing, is not well recognized in Australia. The aim was to study the clinical symptomatology, results of autonomic testing and outcome in patients with POTS.

Methods: Sixteen subjects from a tertiary referral centre who met the criteria for POTS were studied between January 2003 and January 2006. Ten of these patients consented to be interviewed using a validated autonomic symptom questionnaire. Heart rate responses to deep breathing and the Valsalva manoeuvre were measured using Colin BP-508 machine (WR Medical Electronic Co., Stillwater, MN, USA). Tilt studies were carried out for 10 min to 80 degrees of head-up tilting. Patient outcome was assessed as functionally normal, able to stand 30 min without symptoms, able to work and carry out recreational activities or worse on follow up. Results: The mean age of 10 subjects was 24.9 +/- 6.8 years, six being women. The mean duration of symptoms was 70.7 months (range 3-228 months). The common presenting orthostatic symptoms were light-headedness (100%), palpitations (90%), pallor (90%), weakness (80%) and clammy skin (80%). The mean heart rate increment during the tilt study was 51.7 +/- 14.3 b.p.m. The mean duration of follow up was 8.9 months (range 1-16 months). Only five patients were functioning normally at the follow-up visit.

Conclusion: POTS is an underrecognized but persistent autonomic disorder in young patients with a variety of symptoms and variable outcome.

PMID: 17445012

The postural tachycardia syndrome.

Medow MS, Stewart JM. Cardiol Rev. 2007 Mar-Apr;15(2):67-75.

Department of Pediatrics, New York Medical College, Valhalla, New York 10598, USA. Marvin_Medow@nymc.edu

Postural tachycardia syndrome (POTS) is a disorder of unknown etiology, and patients with this condition exhibit orthostatic intolerance (OI) and excessive tachycardia. Excessive tachycardia with POTS has been defined as a rapid (within 10 minutes) increase in heart rate by more than 30 beats per minute or a heart rate that exceeds 120 beats per minute. Patients with POTS can experience difficulty with daily routines such as housework, shopping, eating, and attending work or school. The possibility exists that all forms of OI, including POTS, result from central hypovolemia even without tachycardia. The clinical findings of POTS are observed in an increasing number of patients who are usually female and aged 15 to 50 years. Adults with POTS do not have hypotension, whereas children may exhibit hypotension. Many patients with POTS are intolerant of exercise. "Idiopathic" POTS must be distinguished from other conditions that can reduce venous return to the heart and produce similar signs and symptoms such as dehydration, anemia, or hyperthyroidism. Therapies for POTS are directed at relieving the central hypovolemia or at compensating for the circulatory dysfunctions that may cause this disorder. Treatments have resulted in varying degrees of success and are often used in combination with each other.

PMID: 17303993

Sympathetic neural activity, sex dimorphism, and postural tachycardia syndrome.

Bonyhay I, Freeman R. Ann Neurol. 2007 Apr;61(4):332-9.
Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.

OBJECTIVE: To elucidate the mechanisms whereby postural tachycardia syndrome (POTS) patients maintain orthostatic blood pressure and explain the greater prevalence of female cases in POTS cohorts.

METHODS: We investigated muscle sympathetic nerve (MSN) discharge characteristics in 12 female POTS patients and in 9 male and 12 female control subjects using the burst amplitude distribution and the relative contribution of burst frequency and burst amplitude.

RESULTS: At rest, burst distribution was shifted toward larger amplitudes in POTS patients (p < 0.005), consistent with increased sympathetic activity. During hypotension, the distribution shifted toward larger amplitude bursts in control subjects (p < 0.001), whereas it did not change in POTS patients. Total MSN activity increase to hypotension did not differ between subject groups, but the relative contribution of burst frequency change to the total activity increase was greater in POTS patients than in female (p < 0.05) and male (p < 0.001) control subjects. In contrast, the relative contribution of burst amplitude change to total MSN activity increase was greater in male compared with female control subjects (p < 0.05) and POTS patients (p < 0.001).

INTERPRETATION: At rest, the burst amplitude distribution was consistent with increased sympathetic activity in POTS and did not change in response to hypotension. In response to hypotension, burst frequency makes a proportionally greater contribution to the increase in total MSN activity in POTS patients compared with female control subjects, and female compared with male control subjects. These physiological differences in MSN discharge characteristics, in the setting of sympathetic fiber loss associated with POTS, may contribute to the predisposition to and greater prevalence of POTS in female individuals.

PMID: 17358006

Editor's Note: I asked our medical advisor, Dr. Blitshteyn, for clarification of the above article. Here is what she had to say:

Basically, the authors of this article studied muscle sympathetic nerve activity, which is defined by 2 parameters: 1) burst frequency and 2) burst amplitude. Their findings are that:

• POTS patients have increased burst amplitude at rest, consistent with increased muscle sympathetic nerve activity at rest.
• in response to hypotension, the burst frequency contributed more to the increased sympathetic activity in POTS patient than to the same response in women without POTS
• furthermore, the burst frequency contributed more to women without POTS than to men without POTS

Essentially, the normal physiology of men and women differ in the parameters of their sympathetic activity in response to hypotention. Therefore, physiologically, women appear to be more predisposed than men to POTS.

Research abstracts obtained from PubMed.

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