Original Article
The Neuropathic Postural Tachycardia Syndrome
N Engl J Med 2000; 343:1008-1014October 5, 2000
- Abstract
Background
The postural tachycardia syndrome is a common disorder that is characterized by chronic orthostatic symptoms and a dramatic increase in heart rate on standing, but that does not involve orthostatic hypotension. Several lines of evidence indicate that this disorder may result from sympathetic denervation of the legs.
Methods
We measured norepinephrine spillover (the rate of entry of norepinephrine into the venous circulation) in the arms and legs both before and in response to exposure to three stimuli (the cold pressor test, sodium nitroprusside infusion, and tyramine infusion) in 10 patients with the postural tachycardia syndrome and in 8 age- and sex-matched normal subjects.
Results
At base line, the mean (±SD) plasma norepinephrine concentration in the femoral vein was lower in the patients with the postural tachycardia syndrome than in the normal subjects (135±30 vs. 215±55 pg per milliliter [0.80±0.18 vs. 1.27±0.32 nmol per liter], P=0.001). Norepinephrine spillover in the arms increased to a similar extent in the two groups in response to each of the three stimuli, but the increases in the legs were smaller in the patients with the postural tachycardia syndrome than in the normal subjects (0.001±0.09 vs. 0.12±0.12 ng per minute per deciliter of tissue [0.006±0.53 vs. 0.71±0.71 nmol per minute per deciliter] with the cold pressor test, P=0.02; 0.02±0.07 vs. 0.23±0.17 ng per minute per deciliter [0.12±0.41 vs. 1.36±1.00 nmol per minute per deciliter] with nitroprusside infusion, P=0.01; and 0.008± 0.09 vs. 0.19±0.25 ng per minute per deciliter [0.05± 0.53 vs. 1.12±1.47 nmol per minute per deciliter] with tyramine infusion, P=0.04).
Conclusions
The neuropathic postural tachycardia syndrome results from partial sympathetic denervation, especially in the legs.
Media in This Article
Figure 2
Mean (+SD) Norepinephrine Clearance in the Arms and Legs in 10 Patients with the Postural Tachycardia Syndrome (Solid Bars) and 8 Normal Subjects (Hatched Bars) before the Cold Pressor Test, Nitroprusside Infusion, and Tyramine Infusion.Figure 1
Mean (+SD) Norepinephrine Spillover in the Arms and Legs in 10 Patients with the Postural Tachycardia Syndrome (Solid Bars) and 8 Normal Subjects (Hatched Bars) before the Cold Pressor Test, Nitroprusside Infusion, and Tyramine Infusion.Article Activity
- Article
The postural tachycardia syndrome is a chronic form of orthostatic intolerance that primarily affects young women. This disorder is characterized by symptoms (such as lightheadedness, dimming of vision, confusion, and anxiety) and signs (such as bluish-red skin in dependent limbs) that occur on standing and that are relieved by lying down or sitting.1,2 A remarkable physical finding is a dramatic increase in the heart rate that occurs on standing and that is not associated with a decrease in blood pressure.3 Patients with this syndrome frequently have high plasma catecholamine concentrations, a finding that suggests that the disorder is a primary hyperadrenergic condition.1,4-7 The syndrome, which has also been referred to as idiopathic orthostatic intolerance,8-11 has features in common with the mitral-valve prolapse syndrome,12 the hyperdynamic β-adrenergic circulatory state,13 and vasoregulatory asthenia.1
Patients with the postural tachycardia syndrome often have high plasma norepinephrine concentrations,14 hypovolemia,4,15 excessive pooling of the blood in the legs while standing,16 and exaggerated orthostatic hypovolemia.3,17,18 These findings help explain some of the clinical features of the disorder, but few studies have examined its pathophysiology. Several lines of evidence indicate that sympathetic denervation of the legs may be the underlying mechanism. The results of galvanic skin testing19,20 and quantitative testing of the sudomotor axon reflex suggest that autonomic denervation of the skin is present.21,22 The finding of hypersensitivity to infusion of norepinephrine into veins of the foot, despite high plasma catecholamine concentrations, suggests that denervation hypersensitivity of the veins of the legs is involved.18 Increased sensitivity to systemically administered phenylephrine and isoproterenol and resistance to the norepinephrine-releasing effects of tyramine9 are findings consistent with noradrenergic neuronal dysfunction, as is the short-term improvement in orthostatic symptoms after the administration of the α1-adrenergic–receptor agonist midodrine.8
To test the hypothesis that the postural tachycardia syndrome is caused by partial dysautonomia resulting in dysregulation of autonomic control of the cardiovascular system, we measured the spillover of norepinephrine (the rate of entry of norepinephrine into the venous circulation) in the arms and legs of patients with the postural tachycardia syndrome and in the arms and legs of normal subjects before and after exposure to several stimulators of sympathetic activation.
Methods
Study Population
Between February 1995 and September 1996, we studied 18 patients (16 women and 2 men) who had been referred to the Autonomic Dysfunction Center at Vanderbilt University (Nashville) for the evaluation and treatment of debilitating symptoms consistent with the postural tachycardia syndrome. Most of these patients underwent extensive testing, some of the results of which have been reported previously.8,9 Patients with systemic illnesses that might affect the autonomic nervous system were excluded.
All potentially eligible patients underwent a physical examination and were interviewed with use of a questionnaire to determine the type and extent of their symptoms. Patients were enrolled if they met the following criteria: an increase in the heart rate of at least 30 beats per minute (without a concomitant decrease in systolic blood pressure of more than 20 mm Hg or in diastolic pressure of more than 10 mm Hg) within five minutes after assuming a standing position on at least three separate occasions; a plasma norepinephrine concentration of at least 600 pg per milliliter (3.5 nmol per liter) on standing; and the presence of characteristic symptoms of the postural tachycardia syndrome for at least six months. The last 10 patients enrolled also underwent testing to assess norepinephrine spillover. We also studied 10 normal subjects (8 women and 2 men) matched for age and sex with the patients; 8 of the 10 normal subjects underwent norepinephrine-spillover testing. All the investigational procedures were approved by the Vanderbilt University institutional review board, and all the patients and normal subjects gave written informed consent before entering the study.
Experimental Design
All the patients and normal subjects were admitted to the General Clinical Research Center at Vanderbilt University and given a diet that contained 150 mmol of sodium and 70 mmol of potassium per day, no caffeine, and low levels of monoamines. All current medications were discontinued at least two weeks before admission, and smoking was not permitted during the study. After three days of this diet and an overnight rest in the supine position, blood was obtained for blood-volume measurements. Blood pressure, heart rate, and plasma catecholamine concentrations were measured with the subjects in the supine and upright positions. Blood volume was measured by a modification15 of the technique of Campbell et al.23 Plasma catecholamine concentrations were measured by high-performance liquid chromatography with electrochemical detection.24 Testing of autonomic function (the change in the heart rate in response to controlled ventilation and in response to hyperventilation, the change in the heart rate in response to the Valsalva maneuver, and the change in blood pressure in response to sustained handgrip exercise) was performed as previously described.25
On the following day, sympathetic-nerve function was tested (in 10 of the patients and in 8 of the normal subjects) by measuring the rate of entry of norepinephrine into the systemic circulation (systemic spillover) or into the local venous drainage (local spillover). Subjects were studied after an overnight rest in the supine position and an overnight fast. After catheterization of the brachial artery (for blood-pressure monitoring and blood sampling), the ipsilateral femoral vein (for blood sampling), and two large antecubital veins (one ipsilateral to the arterial line for blood sampling and one contralateral to the arterial catheter for the infusion of tritiated norepinephrine), the subjects rested for 30 minutes. Tritiated norepinephrine (sterile, pyrogen-free levo-[ring-2,5,6-3H]-norepinephrine [Dupont–New England Nuclear, Boston]) was then administered intravenously, first as a 25-μCi loading dose over a two-minute period and then at an infusion rate of 0.9 μCi per milliliter per minute.9 After 30 minutes, when a steady state had been attained, blood samples for the measurement of norepinephrine spillover were simultaneously obtained from the brachial artery, the femoral vein, and an antecubital vein. Blood flow in a forearm and leg was then measured by venous-occlusion air plethysmography.26,27
Norepinephrine spillover and other variables were measured during stimulation by three methods: immersion of the contralateral hand in ice water for at least one minute (the cold pressor test), infusion of sodium nitroprusside (at an initial rate of 0.1 μg per kilogram of body weight per minute in the arm contralateral to that in which blood flow was measured, with the rate increased until systolic blood pressure had decreased by approximately 20 mm Hg), and infusion of tyramine (0.25 mg per minute until systolic blood pressure had increased by approximately 25 mm Hg). Values for norepinephrine spillover were determined before and during exposure to each of these stimuli, and at least 20 minutes was allowed after each stimulus for recovery. The concentrations of 3H-norepinephrine in plasma were measured as previously described.9
Determination of Norepinephrine Kinetics
Norepinephrine kinetics were calculated by the one-compartment model of Esler et al.28 Systemic norepinephrine clearance (in liters per minute) was defined as the rate of infusion of [3H]norepinephrine (in disintegrations per minute [dpm]) divided by the arterial concentration of [3H]norepinephrine (in dpm per liter). Systemic norepinephrine spillover (in nanograms per minute) was calculated as systemic norepinephrine clearance multiplied by the arterial plasma concentration of norepinephrine (in nanograms per liter). The fractional extraction of [3H]norepinephrine (a unitless measure) in the arm or leg was calculated as (A*–V*)÷A*, where A* and V* are the arterial and venous concentrations of [3H]norepinephrine (in dpm per liter), respectively. Local norepinephrine spillover (in nanograms per minute per deciliter of tissue) in the arm or leg was calculated as ([V – A] + A[EF]) × PF, where V is the local venous plasma norepinephrine concentration (in nanograms per liter), A the arterial norepinephrine concentration (in nanograms per liter), EF the fractional extraction of norepinephrine, and PF the local plasma flow (calculated as the blood flow × [1 – hematocrit], expressed in milliliters per minute per deciliter of tissue). Local norepinephrine clearance (in liters per minute) was calculated as EF × PF. The term “spillover” is used, rather than “release,” because what was measured was not the norepinephrine released from the sympathetic neurons but, more accurately, the norepinephrine that escaped from the synaptic and neuronal pools into the circulation.
Statistical Analysis
The results are expressed as means ±SD. Paired and unpaired t-tests were used for comparisons between groups and within each group before and after exposure to the various stimuli. One-way analysis of variance for repeated measures was used to assess the effect of time on each of the variables. Data were analyzed with Quattro Pro software, version 7 (Corel, Jericho, N.Y.) and GraphPad Prism software, version 2.0 (GraphPad Software, San Diego, Calif.). All P values are two-sided.
Results
Characteristics of the Study Population
The blood pressure in the supine and upright positions and the heart rate in the supine position were similar in the patients with the postural tachycardia syndrome and the normal subjects (Table 1Table 1
Characteristics of the Patients with the Postural Tachycardia Syndrome and the Normal Subjects.). The mean heart rate in the upright position was 113±13 beats per minute in the patients and 82±7 beats per minute in the normal subjects. In the supine position, the mean plasma norepinephrine and epinephrine concentrations were similar in the two groups, but in the upright position, the plasma norepinephrine concentration was substantially higher in the patients than in the normal subjects (840±500 vs. 430±80 pg per milliliter [5.0±3.0 vs. 2.5±0.5 nmol per liter], P=0.02), as was the plasma epinephrine concentration (80±42 vs. 47±30 pg per milliliter [0.44±0.23 vs. 0.26±0.16 nmol per liter], P=0.04). Lightheadedness or dizziness and exercise intolerance were the symptoms most frequently reported by the patients (Table 1). Most of the patients could not precisely identify the point in time at which their symptoms had begun, but the mean estimated time of onset was about 2.5 years (range, 8 months to 7 years) before the beginning of the study.The autonomic-function tests revealed normal parasympathetic control of the heart rate in both the patients and the normal subjects (sinus arrhythmia ratio, 1.5±0.2 and 1.4±0.1, respectively; Valsalva ratio, 2.0±0.3 and 1.9±0.4, respectively). The increase in blood pressure during sustained handgrip exercise was higher in the patients than in the normal subjects (15±7 vs. 9±5 mm Hg, P=0.02). The increase in heart rate with hyperventilation was also greater in the patients than in the normal subjects (21±5 vs. 4±1 beats per minute, P=0.01).
Local and Systemic Spillover and Clearance of Norepinephrine
Local and systemic norepinephrine spillover was measured in 10 of the 18 patients (8 women and 2 men) and in 8 of the 10 normal subjects (6 women and 2 men). At base line, the mean norepinephrine concentration in the femoral vein was significantly lower in the patients than in the normal subjects (Table 2Table 2
Effects of Exposure to Three Stimuli of the Sympathetic Nervous System in 10 Patients with the Postural Tachycardia Syndrome and 8 Normal Subjects.). Systolic blood pressure increased by a similar amount in the two groups during the cold pressor test and decreased by a similar amount during nitroprusside infusion. During nitroprusside infusion, the heart rate increased in both groups, but the increase was greater in the patients than in the normal subjects (27±6 vs. 12±5 beats per minute, P<0.001).There was no effect of time on any of the measured or calculated values (i.e., no significant change in base-line values). The fractional extraction of [3H]-norepinephrine before exposure to each of the three stimuli was similar in the patients and the normal subjects, both in the arms (55±13 and 56±14 percent in the two groups, respectively) and in the legs (56±10 and 55±9 percent, respectively).
Norepinephrine spillover before exposure to each of the three stimuli was lower in the patients than in the normal subjects, both in the arms and in the legs (Figure 1Figure 1
Mean (+SD) Norepinephrine Spillover in the Arms and Legs in 10 Patients with the Postural Tachycardia Syndrome (Solid Bars) and 8 Normal Subjects (Hatched Bars) before the Cold Pressor Test, Nitroprusside Infusion, and Tyramine Infusion.). In the arms, before exposure to each of the stimuli, norepinephrine clearance was similar in the two groups, but in the legs it was lower in the patients than in the normal subjects (Figure 2Figure 2Mean (+SD) Norepinephrine Clearance in the Arms and Legs in 10 Patients with the Postural Tachycardia Syndrome (Solid Bars) and 8 Normal Subjects (Hatched Bars) before the Cold Pressor Test, Nitroprusside Infusion, and Tyramine Infusion.). During exposure to each of the three stimuli, norepinephrine spillover in the arms increased by a similar amount in the two groups, but in the legs the increases were significantly smaller in the patients than in the normal subjects (0.001±0.09 vs. 0.12±0.12 ng per minute per deciliter [0.006±0.53 vs. 0.71±0.71 nmol per minute per deciliter] with the cold pressor test, P=0.02; 0.02±0.07 vs. 0.23±0.17 ng per minute per deciliter [0.12±0.41 vs. 1.36±1.00 nmol per minute per deciliter] with nitroprusside infusion, P=0.01; and 0.008±0.09 vs. 0.19±0.25 ng per minute per deciliter [0.05±0.53 vs. 1.12±1.47 nmol per minute per deciliter] with tyramine infusion, P=0.04) (Figure 3Figure 3
Mean (+SD) Increase in Norepinephrine Spillover in the Arms and Legs in 10 Patients with the Postural Tachycardia Syndrome (Solid Bars) and 8 Normal Subjects (Hatched Bars) during the Cold Pressor Test, Nitroprusside Infusion, and Tyramine Infusion.). The increase in norepinephrine clearance in the arms was similar in the patients and the normal subjects, but in the legs the norepinephrine clearance tended to increase less in the patients than in the normal subjects (data not shown). During cold pressor testing and nitroprusside infusion, the fractional extraction of norepinephrine in the legs did not change significantly in either group. With tyramine infusion, the fractional extraction of norepinephrine decreased to 46±3 percent in the normal subjects but did not change in the patients (P=0.04).Discussion
The postural tachycardia syndrome is characterized by orthostatic symptoms and tachycardia without orthostatic hypotension. The nonspecific nature of the symptoms and the absence of orthostatic hypotension have probably resulted in a lack of recognition of this syndrome by both clinicians and investigators. Poorly defined diagnostic criteria and the likelihood of multiple causes have made it difficult to clarify the underlying pathophysiology. In the current study, we used stringent criteria to obtain as homogeneous a study group as possible. Only patients with an increase in the heart rate of at least 30 beats per minute on standing and a plasma norepinephrine concentration of at least 600 pg per milliliter on standing were included in the study.
Several previous investigations have provided clues that patients with the postural tachycardia syndrome have peripheral autonomic dysfunction. Streeten et al. found that patients with orthostatic tachycardia had excessive venous pooling in the legs while standing and suggested that denervation of the legs was a mechanism of the syndrome.16 This hypothesis was supported by the finding of hypersensitivity to infusion of norepinephrine into the veins of the foot, despite high plasma catecholamine concentrations.18 Other investigators studying patients with a similar syndrome observed prolonged latency of plantar autonomic surface potentials during galvanic skin testing,19,20 as well as greater impairment of sweating in the legs than in the arms.21 Previously, we found that patients with the postural tachycardia syndrome were twice as sensitive as normal subjects to the hypertensive effect of the α1-adrenergic–receptor agonist phenylephrine9 and had short-term improvement in orthostatic tachycardia and orthostatic symptoms with the administration of the oral α1-adrenergic–receptor agonist midodrine8; these findings suggest that dysfunction of the peripheral autonomic neurons of the cardiovascular system may contribute to the pathophysiology of the postural tachycardia syndrome. Dysfunction of these nerves, if present, should become apparent when they are activated.
In the current study, we measured the responses to three distinct stimuli of the sympathetic nervous system. The cold pressor test — a nonspecific, painful stimulus — activates the sympathetic nervous system centrally, increasing blood pressure and muscle sympathetic-nerve activity.29 Nitroprusside induces hypotension, which in turn causes baroreflex-mediated increases in plasma catecholamine concentrations and muscle sympathetic-nerve activity.30 Tyramine is taken up into the sympathetic neurons and causes the release of norepinephrine.31,32 These stimuli, each of which causes sympathetic activation by a different mechanism, increased norepinephrine spillover in the arms of both the patients with the postural tachycardia syndrome and the normal subjects, with similar increases in the two groups, but failed to increase norepinephrine spillover in the legs of the patients. Moreover, approximately 35 percent more tyramine was required in the patients than in the normal subjects to achieve similar pressor responses. These findings suggest that in the legs of patients with the postural tachycardia syndrome, neuronal stores of norepi-nephrine are low, norepinephrine release is impaired, or the uptake of tyramine is impaired.33 The results of the current study support the hypothesis that partial autonomic dysfunction that is more pronounced in the legs than in the arms can cause the postural tachycardia syndrome.
In the absence of stimulation, systemic norepinephrine spillover in these patients was normal despite the impaired spillover in the legs. This finding may be explained by the activation of intact sympathetic neurons in other organs (such as the mesentery), a process that contributes more than one third of the systemic spillover in normal subjects.34 The reduced clearance of norepinephrine in the legs, without a similar reduction in the arms, may result from impairment of norepinephrine-reuptake mechanisms due to isolated damage to nerve terminals in the legs. Hypovolemia, shown previously to be present in patients with this syndrome,4 may result in a reduction in local blood flow and a subsequent reduction in norepinephrine spillover.35 Changes in capillary permeability in the limbs,36 the possibility of which is not addressed by assessments of spillover, may also contribute to the observed alterations in norepinephrine spillover and clearance. However, our data strongly implicate impaired noradrenergic function in the legs as the cause of a neuropathic form of the postural tachycardia syndrome.
The dysautonomia associated with the neuropathic postural tachycardia syndrome suggests that its treatment should be similar to that of pure autonomic failure, which results from nearly complete peripheral autonomic neuropathy.37,38 Autonomic failure is treated by increasing blood volume through greater intake of fluids and salt and administration of the mineralocorticoid agonist fludrocortisone39 and by minimizing orthostatic pooling of the blood in the lower body with compression garments to increase extravascular hydrostatic pressure40 or with short-acting vasoconstrictors to increase intravascular pressure.41-43 Indeed, volume loading,8 administration of an α1-adrenergic–receptor agonist,8 and compression of the legs16 in patients with the postural tachycardia syndrome have been shown to decrease the severity of orthostatic tachycardia. Regular exercise, by increasing intravascular volume,44 would probably also be beneficial. However, the long-term effects of these measures have not been determined.
Supported in part by grants (HL-56693 and RR-00095) from the National Institutes of Health, by a grant (NAS 9-19483) from the National Aeronautics and Space Administration, and by the Nathan Blaser Shy–Drager Research Program of Vanderbilt University.
Source Information
From the Jacob Recanati Autonomic Dysfunction Center and the Department of Internal Medicine C, Rambam Medical Center, Haifa, Israel (G.J.); and the Autonomic Dysfunction Center and the Departments of Medicine (F.C., J.R.S., R.M.R., M.W., M.S., I.B., A.E., B.B., D.R.), Pharmacology (D.R.), and Neurology (D.R.), Vanderbilt University, Nashville.
Address reprint requests to Dr. David Robertson at the Autonomic Dysfunction Center, AA3228 MCN, Vanderbilt University, Nashville, TN 37232-2195, or at david.robertson@mcmail.vanderbilt.edu.
- References
References
1
Wooley CF . Where are the diseases of yesteryear? DaCosta's syndrome, soldiers heart, the effort syndrome, neurocirculatory asthenia -- and the mitral valve prolapse syndrome. Circulation 1976;53:749-751
Web of Science | Medline2
Low PA ,Opfer-Gehrking TL ,Textor SC , et al. Postural tachycardia syndrome (POTS). Neurology 1995;45:Suppl 5:S19-S25
Web of Science | Medline3
Jacob G ,Ertl AC ,Shannon JR ,Robertson RM ,Robertson D . Idiopathic orthostatic tachycardia: the role of dynamic orthostatic hypovolemia and norepinephrine. Circulation 1996;94:Suppl I:I-627 abstract.4
Fouad FM ,Tadena-Thome L ,Bravo EL ,Tarazi RC . Idiopathic hypovolemia. Ann Intern Med 1986;104:298-303
Web of Science | Medline5
Frohlich ED ,Tarazi RC ,Dustan HP . Hyperdynamic beta-adrenergic circulatory state: increased beta-receptor responsiveness. Arch Intern Med 1969;123:1-7
CrossRef | Web of Science | Medline6
Shannon JR ,Jordan J ,Black BK ,Diedrich A ,Biaggioni I ,Robertson D . Sympathetic support of the circulation in idiopathic orthostatic intolerance. Circulation 1998;98:Suppl I:I-336 abstract.7
Narkiewicz K ,Somers VK . Chronic orthostatic intolerance: part of a spectrum of dysfunction in orthostatic cardiovascular homeostasis? Circulation 1998;98:2105-2107
Web of Science | Medline8
Jacob G ,Shannon JR ,Black B , et al. Effects of volume loading and pressor agents in idiopathic orthostatic tachycardia. Circulation 1997;96:575-580
Web of Science | Medline9
Jacob G ,Shannon JR ,Costa F , et al. Abnormal norepinephrine clearance and adrenergic receptor sensitivity in idiopathic orthostatic intolerance. Circulation 1999;99:1706-1712
Web of Science | Medline10
Jordan J ,Shannon JR ,Black BK ,Paranjape SY ,Barwise J ,Robertson D . Raised cerebrovascular resistance in idiopathic orthostatic intolerance: evidence for sympathetic vasoconstriction. Hypertension 1998;32:699-704
Web of Science | Medline11
Shannon JR ,Flattem NL ,Jordan J , et al. Orthostatic intolerance and tachycardia associated with norepinephrine-transporter deficiency. N Engl J Med 2000;342:541-549
Full Text | Web of Science | Medline12
Boudoulas H ,Reynolds JC ,Mazzaferri E ,Wooley CF . Metabolic studies in mitral valve prolapse syndrome: a neuroendocrine-cardiovascular process. Circulation 1980;61:1200-1205
Web of Science | Medline13
Frohlich ED ,Dustan HP ,Page IH . Hyperdynamic beta-adrenergic circulatory state. Arch Intern Med 1966;117:614-619
CrossRef | Web of Science | Medline14
Pasternac A ,Tubau JF ,Puddu PE ,Krol RB ,de Champlain J . Increased plasma catecholamine levels in patients with symptomatic mitral valve prolapse. Am J Med 1982;73:783-790
CrossRef | Web of Science | Medline15
Jacob G ,Robertson D ,Mosqueda-Garcia R ,Ertl AC ,Robertson RM ,Biaggioni I . Hypovolemia in syncope and orthostatic intolerance role of the renin-angiotensin system. Am J Med 1997;103:128-133
CrossRef | Web of Science | Medline16
Streeten DH ,Anderson GH Jr ,Richardson R ,Thomas FD . Abnormal orthostatic changes in blood pressure and heart rate in subjects with intact sympathetic nervous function: evidence for excessive venous pooling. J Lab Clin Med 1988;111:326-335
Medline17
Gruchalla R . Southwestern Internal Medicine Conference: masocytosis: developments during the past decade. Am J Med Sci 1995;309:328-338
CrossRef | Web of Science | Medline18
Streeten DH . Pathogenesis of hyperadrenergic orthostatic hypotension: evidence of disordered venous innervation exclusively in the lower limbs. J Clin Invest 1990;86:1582-1588
CrossRef | Web of Science | Medline19
Hoeldtke RD ,Dworkin GE ,Gaspar SR ,Israel BC . Sympathotonic orthostatic hypotension: a report of four cases. Neurology 1989;39:34-40
Web of Science | Medline20
Hoeldtke RD ,Davis KM . The orthostatic tachycardia syndrome: evaluation of autonomic function and treatment with octreotide and ergot alkaloids. J Clin Endocrinol Metab 1991;73:132-139
CrossRef | Web of Science | Medline21
Low PA ,Caskey PE ,Tuck RR ,Fealey RD ,Dyck PJ . Quantitative sudomotor axon reflex test in normal and neuropathic subjects. Ann Neurol 1983;14:573-580
CrossRef | Web of Science | Medline22
Schondorf R ,Low PA . Idiopathic postural orthostatic tachycardia syndrome: an attenuated form of acute pandysautonomia? Neurology 1993;43:132-137
Web of Science | Medline23
Campbell TJ ,Frohman B ,Reeve EB . A simple, rapid, and accurate method of extracting T-1824 from plasma, adapted to the routine measurement of blood volume. J Lab Clin Med 1958;52:768-777
Medline24
Goldstein DS ,Eisenhofer G ,Stull R ,Folio CJ ,Keiser HR ,Kopin IJ . Plasma dihydroxyphenylglycol and the intraneuronal disposition of norepinephrine in humans. J Clin Invest 1988;81:213-220
CrossRef | Web of Science | Medline25
Mosqueda-Garcia R. Evaluation of the autonomic nervous system: In: Robertson D, Biaggioni I, eds. Disorders of the autonomic nervous system. London: Harwood Academic, 1995:25-59.
26
Siggaard-Andersen J . Venous occlusion plethysmography on the calf: evaluation of diagnosis and results in vascular surgery. Dan Med Bull 1970;17:Suppl I:1-68
Medline27
Vissing SF ,Scherrer U ,Victor RG . Relation between sympathetic outflow and vascular resistance in the calf during perturbations in central venous pressure: evidence for cardiopulmonary afferent regulation of calf vascular resistance in humans. Circ Res 1989;65:1710-1717
Web of Science | Medline28
Esler M ,Jennings G ,Lambert G ,Meredith I ,Horne M ,Eisenhofer G . Overflow of catecholamine neurotransmitters to the circulation: source, fate, and functions. Physiol Rev 1990;70:963-985
Web of Science | Medline29
Scriven AJ ,Brown MJ ,Murphy MB ,Dollery CT . Changes in blood pressure and plasma catecholamines caused by tyramine and cold exposure. J Cardiovasc Pharmacol 1984;6:954-960
CrossRef | Web of Science | Medline30
Rea RF ,Eckberg DL ,Fritsch JM ,Goldstein DS . Relation of plasma norepinephrine and sympathetic traffic during hypotension in humans. Am J Physiol 1990;258:R982-R986
Web of Science | Medline31
Rapoport RM ,Takimoto GS ,Cho AK . Compartmental analysis of tyramine-induced norepinephrine depletion. Pharmacology 1981;23:235-242
CrossRef | Web of Science32
Schafers RF ,Poller U ,Ponicke K , et al. Influence of adrenoceptor and muscarinic receptor blockade on the cardiovascular effects of exogenous noradrenaline and of endogenous noradrenaline released by infused tyramine. Naunyn Schmiedebergs Arch Pharmacol 1997;355:239-249
CrossRef | Web of Science | Medline33
Scriven AJ ,Dollery CT ,Murphy MB ,Macquin I ,Brown MJ . Blood pressure and plasma norepinephrine concentrations after endogenous norepinephrine release by tyramine. Clin Pharmacol Ther 1983;33:710-716
CrossRef | Web of Science | Medline34
Aneman A ,Eisenhofer G ,Olbe L , et al. Sympathetic discharge to mesenteric organs and the liver: evidence for substantial mesenteric organ norepinephrine spillover. J Clin Invest 1996;97:1640-1646
CrossRef | Web of Science | Medline35
Grossman E ,Chang PC ,Hoffman A ,Tamrat M ,Kopin IJ ,Goldstein DS . Tracer norepinephrine kinetics: dependence on regional blood flow and the site of infusion. Am J Physiol 1991;260:R946-R952
Web of Science | Medline36
Cousineau D ,Rose CP ,Goresky CA . Plasma expansion effect on cardiac capillary and adrenergic exchange in intact dogs. J Appl Physiol 1986;60:147-153
Web of Science | Medline37
Hague K ,Lento P ,Morgello S ,Caro S ,Kaufmann H . The distribution of Lewy bodies in pure autonomic failure: autopsy findings and review of the literature. Acta Neuropathol (Berl) 1997;94:192-196
CrossRef | Web of Science | Medline38
Kanda T ,Tomimitsu H ,Yokota T ,Ohkoshi N ,Hayashi M ,Mizusawa H . Unmyelinated nerve fibers in sural nerve in pure autonomic failure. Ann Neurol 1998;43:267-271
CrossRef | Web of Science | Medline39
Hickler RB ,Thompson GR ,Fox LM ,Hamlin JT III . Successful treatment of orthostatic hypotension with 9-alpha-fluorohydrocortisone. N Engl J Med 1959;261:788-791
Full Text | Web of Science | Medline40
Bradbury S ,Eggleston C . Postural hypotension: an autopsy upon a case. Am Heart J 1927;3:105-106
CrossRef | Web of Science41
Onrot J ,Goldberg MR ,Hollister AS ,Biaggioni I ,Robertson RM ,Robertson D . Management of chronic orthostatic hypotension. Am J Med 1986;80:454-464
CrossRef | Web of Science | Medline42
Jordan J ,Shannon JR ,Biaggioni I ,Norman R ,Black BK ,Robertson D . Contrasting actions of pressor agents in severe autonomic failure. Am J Med 1998;105:116-124
CrossRef | Web of Science | Medline43
Fouad-Tarazi FM ,Okabe M ,Goren H . Alpha sympathomimetic treatment of autonomic insufficiency with orthostatic hypotension. Am J Med 1995;99:604-610
CrossRef | Web of Science | Medline44
Convertino VA ,Brock PJ ,Keil LC ,Bernauer EM ,Greenleaf JE . Exercise training-induced hypervolemia: role of plasma albumin, renin, and vasopressin. J Appl Physiol 1980;48:665-669
Web of Science | Medline
- Citing Articles (76)
Citing Articles
1
Phillip A. Low, Paola Sandroni. 2012. Postural Tachycardia Syndrome (POTS). , 517-519.
CrossRef2
Satish R. Raj. 2012. Mechanisms of Postural Tachycardia Syndrome. , 521-523.
CrossRef3
Robert Hoeldtke. 2012. Somatostatin Agonists. , 645-648.
CrossRef4
Giris Jacob, Blair P. Grubb. 2012. Joint Hypermobility Syndrome and Dysautonomia. , 535-537.
CrossRef5
Julian Stewart. 2012. Symptoms and Signs of Postural Tachycardia Syndrome (POTS). , 525-528.
CrossRef6
Luis E. Okamoto, Satish R. Raj, Italo Biaggioni. 2012. Chronic Fatigue Syndrome and the Autonomic Nervous System. , 531-534.
CrossRef7
Christopher J. Mathias, David A. Low, Valeria Iodice, Andrew P. Owens, Mojca Kirbis, Rodney Grahame. (2011) Postural tachycardia syndrome—current experience and concepts. Nature Reviews Neurology
CrossRef8
Joanne L. Thanavaro, Kristin L. Thanavaro. (2011) Postural orthostatic tachycardia syndrome: Diagnosis and treatment. Heart & Lung: The Journal of Acute and Critical Care 40:6, 554-560
CrossRef9
Ya-Ju Lin, Helen L. Po, Hung-Yi Hsu, Chih-Ping Chung, Wen-Yung Sheng, Han-Hwa Hu. (2011) Transcranial Doppler Studies on Cerebral Autoregulation Suggest Prolonged Cerebral Vasoconstriction in a Subgroup of Patients with Orthostatic Intolerance. Ultrasound in Medicine & Biology 37:10, 1554-1560
CrossRef10
Jennifer A. Rabbitts, Cornelius B. Groenewald, Adam K. Jacob, Phillip A. Low, Timothy B. Curry. (2011) Postural orthostatic tachycardia syndrome and general anesthesia: a series of 13 cases. Journal of Clinical Anesthesia 23:5, 384-392
CrossRef11
KHALIL KANJWAL, MUJEEB SHEIKH, BEVERLY KARABIN, YOUSUF KANJWAL, BLAIR P. GRUBB. (2011) Neurocardiogenic Syncope Coexisting with Postural Orthostatic Tachycardia Syndrome in Patients Suffering from Orthostatic Intolerance: A Combined form of Autonomic Dysfunction. Pacing and Clinical Electrophysiology 34:5, 549-554
CrossRef12
2011. Active Supraventricular Arrhythmias. , 93-180.
CrossRef13
Hossam I. Mustafa, Emily M. Garland, Italo Biaggioni, Bonnie K. Black, William D. Dupont, David Robertson, Satish R. Raj. (2011) Abnormalities of angiotensin regulation in postural tachycardia syndrome. Heart Rhythm 8:3, 422-428
CrossRef14
Koichi Mizumaki. (2011) Postural Orthostatic Tachycardia Syndrome (POTS). Journal of Arrhythmia 27:4, 289-306
CrossRef15
Kunihisa Miwa, Masatoshi Fujita. (2011) Small Heart With Low Cardiac Output for Orthostatic Intolerance in Patients With Chronic Fatigue Syndrome. Clinical Cardiologyn/a-n/a
CrossRef16
David S. Goldstein. (2010) Catecholamines 101. Clinical Autonomic Research 20:6, 331-352
CrossRef17
Anita Korsós, László Rudas, Éva Zöllei. (2010) Egyszerű vízi csoda. Orvosi Hetilap 151:46, 1904-1907
CrossRef18
David S. Goldstein. (2010) Neurocardiology: Therapeutic Implications for Cardiovascular Disease. Cardiovascular Therapeuticsno-no
CrossRef19
Khalil Kanjwal, Beverly Karabin, Mujeeb Sheikh, Yousuf Kanjwal, Blair P. Grubb. (2010) New onset postural orthostatic tachycardia syndrome following ablation of AV node reentrant tachycardia. Journal of Interventional Cardiac Electrophysiology 29:1, 53-56
CrossRef20
Karl R Davis. (2010) The clinical assessment of orthostatic hypotension. Reviews in Clinical Gerontology 20:03, 171-182
CrossRef21
Amanda Catherine Peltier, Emily Garland, Satish R. Raj, Kyoko Sato, Bonnie Black, Yanna Song, Lily Wang, Italo Biaggioni, Andre Diedrich, David Robertson. (2010) Distal sudomotor findings in postural tachycardia syndrome. Clinical Autonomic Research 20:2, 93-99
CrossRef22
G. J. Taborsky, Q. Mei, D. J. Hackney, D. P. Figlewicz, R. LeBoeuf, T. O. Mundinger. (2009) Loss of islet sympathetic nerves and impairment of glucagon secretion in the NOD mouse: relationship to invasive insulitis. Diabetologia 52:12, 2602-2611
CrossRef23
Raffaello Furlan, Franca Barbic, Francesco Casella, Giorgio Severgnini, Luca Zenoni, Angelo Mercieri, Ruggero Mangili, Giorgio Costantino, Alberto Porta. (2009) Neural autonomic control in orthostatic intolerance. Respiratory Physiology & Neurobiology 169, S17-S20
CrossRef24
S. Carew, J. Cooke, M. O'Connor, T. Donnelly, A. Costelloe, C. Sheehy, D. Lyons. (2009) What is the optimal duration of tilt testing for the assessment of patients with suspected postural tachycardia syndrome?. Europace 11:5, 635-637
CrossRef25
Julian M. Stewart. (2009) Postural Tachycardia Syndrome and Reflex Syncope: Similarities and Differences. The Journal of Pediatrics 154:4, 481-485
CrossRef26
PHILLIP A. LOW, PAOLA SANDRONI, MICHAEL JOYNER, WIN-KUANG SHEN. (2009) Postural Tachycardia Syndrome (POTS). Journal of Cardiovascular Electrophysiology 20:3, 352-358
CrossRef27
Ho. Benjelloun, Ha. Benjelloun, S. Aboudrar, L. Coghlan, M. Benomar. (2009) Réflexes autonomiques cardiovasculaires dans le syndrome de tachycardie orthostatique idiopathique. Annales de Cardiologie et d'Angéiologie 58:1, 20-26
CrossRef28
S. Carew, M. O. Connor, J. Cooke, R. Conway, C. Sheehy, A. Costelloe, D. Lyons. (2008) A review of postural orthostatic tachycardia syndrome. Europace 11:1, 18-25
CrossRef29
Michael R. Hainstock, Nancy E. Gruchala, Nadia Fike, Ricardo A. Samson, Scott E. Klewer, Brent J. Barber. (2008) Postural Orthostatic Tachycardia in a Teenager with Klinefelter Syndrome. Congenital Heart Disease 3:6, 440-442
CrossRef30
T.L. Jones, C. Ng. (2008) Anaesthesia for caesarean section in a patient with Ehlers-Danlos syndrome associated with postural orthostatic tachycardia syndrome. International Journal of Obstetric Anesthesia 17:4, 365-369
CrossRef31
Thomas O. Mundinger, Qi Mei, Gerald J. Taborsky. (2008) Impaired activation of celiac ganglion neurons in vivo after damage to their sympathetic nerve terminals. Journal of Neuroscience Research 86:9, 1981-1993
CrossRef32
Ryan M Antiel, Justin M Risma, Rayna M Grothe, Chad K Brands, Philip R Fischer. (2008) Orthostatic Intolerance and Gastrointestinal Motility in Adolescents With Nausea and Abdominal Pain. Journal of Pediatric Gastroenterology and Nutrition 46:3, 285-288
CrossRef33
(2008) CrossRef Listing of Deleted DOIs. CrossRef Listing of Deleted DOIs
CrossRef34
2008. Sinus Rhythms. , 327-344.
CrossRef35
Annelinde Terlou, Kathy Ruble, Anne F. Stapert, Ho-Choong Chang, Peter C. Rowe, Cindy L. Schwartz. (2007) Orthostatic intolerance in survivors of childhood cancer. European Journal of Cancer 43:18, 2685-2690
CrossRef36
J. D. Pandian, K. Dalton, R. D. Henderson, P. A. McCombe. (2007) Postural orthostatic tachycardia syndrome: an underrecognized disorder. Internal Medicine Journal 37:8, 529-535
CrossRef37
Satish R. Raj, David Robertson. (2007) Blood Volume Perturbations in the Postural Tachycardia Syndrome. The American Journal of the Medical Sciences 334:1, 57-60
CrossRef38
Istvan Bonyhay, Roy Freeman. (2007) Sympathetic neural activity, sex dimorphism, and postural tachycardia syndrome. Annals of Neurology 61:4, 332-339
CrossRef39
Marvin S. Medow, Julian M. Stewart. (2007) The Postural Tachycardia Syndrome. Cardiology in Review 15:2, 67-75
CrossRef40
Mark J. Thieben, Paola Sandroni, David M. Sletten, Lisa M. Benrud-Larson, Robert D. Fealey, Steven Vernino, Phillip A. Low, Vanda A. Lennon, Win-Kuang Shen. (2007) Postural Orthostatic Tachycardia Syndrome: The Mayo Clinic Experience. Mayo Clinic Proceedings 82:3, 308-313
CrossRef41
M. J. Thieben, P. Sandroni, D. M. Sletten, L. M. Benrud-Larson, R. D. Fealey, S. Vernino, P. A. Low, V. A. Lennon, W.-K. Shen. (2007) Postural Orthostatic Tachycardia Syndrome: The Mayo Clinic Experience. Mayo Clinic Proceedings 82:3, 308-313
CrossRef42
Adrian H. Shandling, Daniel Rieders, Daniel M. Bethencourt. (2007) Thoracoscopic Microwave Epicardial Ablation: Feasibility for the Treatment of Idiopathic Sinus Node Tachycardia. The Annals of Thoracic Surgery 83:1, 300-302
CrossRef43
E. Carvajal Roca, I. Torró Doménech, E. Lurbe Ferrer. (2006) Hipertensión arterial episódica asociada al síndrome de taquicardia postural ortostática. Anales de Pediatría 65:5, 496-499
CrossRef44
Wolfgang Singer, Tonette L. Opfer-Gehrking, Kim K. Nickander, Stacy M. Hines, Phillip A. Low. (2006) Acetylcholinesterase Inhibition in Patients With Orthostatic Intolerance. Journal of Clinical Neurophysiology 23:5, 477-482
CrossRef45
David S. Goldstein. (2006) L-Dihydroxyphenylserine (L-DOPS): A Norepinephrine Prodrug. Cardiovascular Drug Reviews 24:3-4, 189-203
CrossRef46
Joshua Fessel, David Robertson. (2006) Orthostatic hypertension: when pressor reflexes overcompensate. Nature Clinical Practice Nephrology 2:8, 424-431
CrossRef47
Jochanan E. Naschitz, Renata Mussafia-Priselac, Yulia Kovalev, Natalia Zaigraykin, Gleb Slobodin, Nizar Elias, Itzhak Rosner. (2006) Patterns of Hypocapnia on Tilt in Patients with Fibromyalgia, Chronic Fatigue Syndrome, Nonspecific Dizziness, and Neurally Mediated Syncope. The American Journal of the Medical Sciences 331:6, 295-303
CrossRef48
Nancy R Keller, David Robertson. (2006) Familial orthostatic tachycardia. Current Opinion in Cardiology 21:3, 173-179
CrossRef49
Nehama Zuckerman-Levin, Oren Zinder, Avital Greenberg, Moshe Levin, Giris Jacob, Ze'ev Hochberg. (2006) Physiological and catecholamine response to sympathetic stimulation in turner syndrome. Clinical Endocrinology 64:4, 410-415
CrossRef50
Roy Freeman. (2006) Assessment of cardiovascular autonomic function. Clinical Neurophysiology 117:4, 716-730
CrossRef51
PETER A. BRADY, PHILLIP A. LOW, WIN K. SHEN. (2005) Inappropriate Sinus Tachycardia, Postural Orthostatic Tachycardia Syndrome, and Overlapping Syndromes. Pacing and Clinical Electrophysiology 28:10, 1112-1121
CrossRef52
ROLF R. DIEHL. (2005) Continuous Progression of Orthostatic Tachycardia as a Further Feature of the Postural Tachycardia Syndrome. Pacing and Clinical Electrophysiology 28:9, 975-979
CrossRef53
Shamil Yusuf, A. John Camm. (2005) Deciphering the sinus tachycardias. Clinical Cardiology 28:6, 267-276
CrossRef54
Terrence D. Lagerlund, Phillip A. Low, Vera Novak, Peter Novak, Stacy M. Hines, Benjamin McPhee, Neil E. Busacker. (2005) Spectral analysis of slow modulation of EEG amplitude and cardiovascular variables in subjects with postural tachycardia syndrome. Autonomic Neuroscience 117:2, 132-142
CrossRef55
Shamil Yusuf, A John Camm. (2005) The sinus tachycardias. Nature Clinical Practice Cardiovascular Medicine 2:1, 44-52
CrossRef56
Salvatore M. Romano, Chiara Lazzeri, Marco Chiostri, Gian Franco Gensini, Franco Franchi. (2004) Beat-to-beat analysis of pressure wave morphology for pre-symptomatic detection of orthostatic intolerance during head-up tilt. Journal of the American College of Cardiology 44:9, 1891-1897
CrossRef57
Christopher J. Mathias. (2004) Role of autonomic evaluation in the diagnosis and management of syncope. Clinical Autonomic Research 14:S1, i45-i54
CrossRef58
Terhi Saisto, Risto Kaaja, Satu Helske, Olavi Ylikorkala, Erja Halmesmaki. (2004) Norepinephrine, adrenocorticotropin, cortisol and beta-endorphin in women suffering from fear of labor: responses to the cold pressor test during and after pregnancy. Acta Obstetricia et Gynecologica Scandinavica 83:1, 19-26
CrossRef59
M. Yousuf Kanjwal, Daniel J. Kosinski, Blair P. Grubb. (2003) Treatment of postural orthostatic tachycardia syndrome and inappropriate sinus tachycardia. Current Cardiology Reports 5:5, 402-406
CrossRef60
YOUSUF KANJWAL, DAN KOSINSKI, BLAIR P. GRUBB. (2003) The Postural Orthostatic Tachycardia Syndrome:. Definitions, Diagnosis, and Management. Pacing and Clinical Electrophysiology 26:8, 1747-1757
CrossRef61
Phillip A. Low, Steven Vernino, Guillermo Suarez. (2003) Autonomic dysfunction in peripheral nerve disease. Muscle & Nerve 27:6, 646-661
CrossRef62
W Singer. (2003) Heart rate-dependent electrocardiogram abnormalities in patients with postural tachycardia syndrome. Autonomic Neuroscience 103:1-2, 106-113
CrossRef63
William H. Frishman, Victor Azer, Domenic Sica. (2003) Drug Treatment of Orthostatic Hypotension and Vasovagal Syncope. Heart Disease 5:1, 49-64
CrossRef64
Thomas D. Sabin. (2003) AN APPROACH TO CHRONIC FATIGUE SYNDROME IN ADULTS. The Neurologist 9:1, 28-34
CrossRef65
EMILY M. GARLAND, MAUREEN K. HAHN, TERRY P. KETCH, NANCY R. KELLER, CHUN-HYUNG KIM, KWANG-SOO KIM, ITALO BIAGGIONI, JOHN R. SHANNON, RANDY D. BLAKELY, DAVID ROBERTSON. (2002) Genetic Basis of Clinical Catecholamine Disorders. Annals of the New York Academy of Sciences 971:1, 506-514
CrossRef66
M Custaud. (2002) Orthostatic tolerance and spontaneous baroreflex sensitivity in men versus women after 7 days of head-down bed rest. Autonomic Neuroscience 100:1-2, 66-76
CrossRef67
Horacio Kaufmann, Kirsty Bhattacharya. (2002) Diagnosis and Treatment of Neurally Mediated Syncope. The Neurologist 8:3, 175-185
CrossRef68
W. Singer, W.-K. Shen, T. L. Opfer-Gehrking, B. R. McPhee, M. J. Hilz, P. A. Low. (2002) Evidence of an Intrinsic Sinus Node Abnormality in Patients With Postural Tachycardia Syndrome. Mayo Clinic Proceedings 77:3, 246-252
CrossRef69
ANTONIO G. HERMOSILLO, MANLIO F. M??RQUEZ, KATHRINE J??UREGUI-RENAUD, MANUEL C??RDENAS. (2001) Orthostatic Hypotension, 2001. Cardiology in Review 9:6, 339-347
CrossRef70
Phillip A. Low, Ronald Schondorf, Teresa A. Rummans. (2001) Why do patients have orthostatic symptoms in POTS?. Clinical Autonomic Research 11:4, 223-224
CrossRef71
Martín Nogués, Ricardo Delorme, Daniela Saadia, Kirsten Heidel, Eduardo Benarroch. (2001) Postural tachycardia syndrome in syringomyelia: Response to fludrocortisone and β-blockers. Clinical Autonomic Research 11:4, 265-267
CrossRef72
R Furlan. (2001) Orthostatic intolerance: different abnormalities in the neural sympathetic response to a gravitational stimulus. Autonomic Neuroscience 90:1-2, 83-88
CrossRef73
D. Robertson, J.R. Shannon, J. Jordan, T.L. Davis, A. Diedrich, G. Jacob, E. Garland, T. Tellioglu, I. Biaggioni. (2001) Multiple system atrophy: new developments in pathophysiology and therapy. Parkinsonism & Related Disorders 7:3, 257-260
CrossRef74
T Tellioglu. (2001) Orthostatic Intolerance in Behcet's Disease. Autonomic Neuroscience 89:1-2, 96-99
CrossRef75
RONALD SCHONDORF, JULIE BENOIT, REUBEN STEIN. (2001) Cerebral Autoregulation in Orthostatic Intolerance. Annals of the New York Academy of Sciences 940:1, 514-526
CrossRef76
DAVID ROBERTSON, NANCY FLATTEM, TAHIR TELLIOGLU, ROBERT CARSON, EMILY GARLAND, JOHN R. SHANNON, JENS JORDAN, GIRIS JACOB, RANDY D. BLAKELY, ITALO BIAGGIONI. (2001) Familial Orthostatic Tachycardia Due to Norepinephrine Transporter Deficiency. Annals of the New York Academy of Sciences 940:1, 527-544
CrossRef
