This Article Full Text Full Text (PDF) All Versions of this Article: 111/7/839    most recent 01.CIR.0000155613.20376.CAv1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Goldstein, D. S. Articles by Sharabi, Y. Search for Related Content PubMed PubMed Citation Articles by Goldstein, D. S. Articles by Sharabi, Y. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB EPINEPHRINE Medline Plus Health Information Fainting Related Collections Biochemistry and metabolism Other diagnostic testing Autonomic, reflex, and neurohumoral control of circulation Other Vascular biology

(Circulation. 2005;111:839-845.)
© 2005 American Heart Association, Inc.

Arrhythmia/Electrophysiology

Neurocirculatory Abnormalities in Chronic Orthostatic Intolerance

David S. Goldstein, MD, PhD; Basil Eldadah, MD, PhD; Courtney Holmes, CMT; Sandra Pechnik, RN; Jeffrey Moak, MD; Yehonatan Sharabi, MD

From the Clinical Neurocardiology Section, NINDS, National Institutes of Health, Bethesda, Md

Correspondence to Dr David S. Goldstein, Bldg 10, Room 6N252, 10 Center Dr, MSC-1620, Bethesda, MD 20892-1620. E-mail goldsteind{at}ninds.nih.gov

Received June 16, 2004; revision received November 2, 2004; accepted November 5, 2004.

Background— Chronic orthostatic intolerance (COI) occurs in postural tachycardia syndrome (POTS) and in some individuals with repeated neurocardiogenic syncope/presyncope (NCS), without POTS. This study addressed whether patients with COI and POTS or NCS have neurocirculatory abnormalities during supine rest.

Methods and Results— Adult patients referred for COI who had POTS (n=90, mean±SEM age 40±1 years, 86% women) or NCS (n=36, 41±2 years old, 78% women) underwent measurements of plasma levels of catecholamines and forearm hemodynamics. Comparison data were obtained from 32 age- and gender-matched normal volunteers (39±2 years old, 81% women). The POTS group had a relatively fast mean heart rate (79±2 bpm) during supine rest compared with the NCS group (69±1.6 bpm, P=0.03) and normal volunteers (66±3 bpm, P=0.0004). The POTS group also had higher mean arterial norepinephrine (1.61±0.11 nmol/L, n=37) and epinephrine (0.39±0.03 nmol/L, n=37) concentrations than the NCS group (1.03±0.12 nmol/L, n=20, P=0.0012; 0.21±0.03 nmol/L, n=20, P=0.0005) and normal volunteers (1.13±0.11 nmol/L, n=20, P=0.006; 0.17±0.03 nmol/L, n=15, P=0.0001). The NCS group had higher mean forearm vascular resistance (52±6 U) than the POTS group (36±2 U, P=0.003).

Conclusions— Overall, POTS features increased heart rate and sympathetic nervous and adrenomedullary hormonal system outflows during supine rest. Increased sympathetic outflow may contribute to the relative tachycardia in POTS. NCS features forearm vasoconstriction during supine rest but not sympathoneural or adrenomedullary activation.

Key Words: syncope • nervous system, sympathetic • tachycardia • norepinephrine • epinephrine

This article has been cited by other articles:

				J. P. MOAK, D. S. GOLDSTEIN, B. A. ELDADAH, A. SALEEM, C. HOLMES, S. PECHNIK, and Y. SHARABI Supine low-frequency power of heart rate variability reflects baroreflex function, not cardiac sympathetic innervation* Cleveland Clinic Journal of Medicine, April 1, 2009; 76(Suppl_2): S51 - S59. [Abstract] [Full Text] [PDF]

				D. S. Goldstein and C. Holmes Neuronal Source of Plasma Dopamine Clin. Chem., November 1, 2008; 54(11): 1864 - 1871. [Abstract] [Full Text] [PDF]

				E. M. Garland, S. R. Raj, B. K. Black, P. A. Harris, and D. Robertson The hemodynamic and neurohumoral phenotype of postural tachycardia syndrome Neurology, August 21, 2007; 69(8): 790 - 798. [Abstract] [Full Text] [PDF]

				E. M. Garland, B. K. Black, P. A. Harris, and D. Robertson Dopamine-beta-hydroxylase in postural tachycardia syndrome Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H684 - H690. [Abstract] [Full Text] [PDF]

				A K Agarwal, R Garg, A Ritch, and P Sarkar Postural orthostatic tachycardia syndrome Postgrad. Med. J., July 1, 2007; 83(981): 478 - 480. [Abstract] [Full Text] [PDF]

				G. Jacob, E. M. Garland, F. Costa, C. M. Stein, H.-G. Xie, R. M. Robertson, I. Biaggioni, and D. Robertson {beta}2-Adrenoceptor Genotype and Function Affect Hemodynamic Profile Heterogeneity in Postural Tachycardia Syndrome Hypertension, March 1, 2006; 47(3): 421 - 427. [Abstract] [Full Text] [PDF]

				E. M. Garland, R. Winker, S. M. Williams, L. Jiang, K. Stanton, D. W. Byrne, I. Biaggioni, I. Cascorbi, J. A. Phillips III, P. A. Harris, et al. Endothelial NO Synthase Polymorphisms and Postural Tachycardia Syndrome Hypertension, November 1, 2005; 46(5): 1103 - 1110. [Abstract] [Full Text] [PDF]

				R. Schondorf, J. Benoit, and R. Stein Cerebral autoregulation is preserved in postural tachycardia syndrome J Appl Physiol, September 1, 2005; 99(3): 828 - 835. [Abstract] [Full Text] [PDF]

				K. Jáuregui-Renaud, J. A. G. Hermosillo, J. L. Jardón, M. F. Márquez, A. Kostine, M. A. Silva, and M. Cárdenas Cerebral blood flow during supine rest and the first minute of head-up tilt in patients with orthostatic intolerance Europace, January 1, 2005; 7(5): 460 - 464. [Abstract] [Full Text] [PDF]