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Previous Volume 343:1008-1014 October 5, 2000 Number 14 Next

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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.

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{at}mcmail.vanderbilt.edu.

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