Neurocirculatory Abnormalities in Chronic Orthostatic Intolerance

Goldstein, David S.; Eldadah, Basil A.; Holmes, Courtney; Pechnik, Sandra; Moak, Jeffrey P.; Sharabi, Yehonatan

doi:10.1161/01.cir.0000155613.20376.ca

Cited by 39 publications

(32 citation statements)

References 47 publications

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“…It has been speculated that female sex hormones might modulate reflex neural or vascular properties, resulting in the greater incidence of orthostatic hypotension in young women (5,14,15,52,69). An additional indication of impaired orthostatic responses in women includes the observation that women have a greater propensity towards postural orthostatic tachycardia syndrome (18,60).…”

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confidence: 99%

Hemodynamics and brain blood flow during posture change in younger women and postmenopausal women compared with age-matched men

Edgell

Robertson

Hughson

2012

Journal of Applied Physiology

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Edgell H, Robertson AD, Hughson RL. Hemodynamics and brain blood flow during posture change in younger women and postmenopausal women compared with age-matched men. J Appl Physiol 112: 1482-1493, 2012. First published February 23, 2012 doi:10.1152/japplphysiol.01204.2011.-Increased incidence of orthostatic hypotension and presyncopal symptoms in young women could be related to hormonal factors that might be isolated by comparing cardiovascular and cerebrovascular responses to postural change in young and older men and women. Seven young women, 11 young men, 10 older women (Ͼ1 yr postmenopausal, no hormone therapy), and 9 older men participated in a supine-to-sit-to-stand test while measuring systemic hemodynamics, end-tidal PCO2, and blood flow velocity of the middle cerebral artery (MCA). Women had a greater reduction in stroke volume index compared with age-matched men (change from supine to standing: young women: Ϫ22.9 Ϯ 1.6 ml/m 2 ; young men: Ϫ14.4 Ϯ 2.4 ml/m 2 ; older women: Ϫ17.4 Ϯ 3.3 ml/m 2 ; older men: Ϫ13.8 Ϯ 2.2 ml/m 2 ). This was accompanied by offsetting changes in heart rate, particularly in young women, resulting in no age or sex differences in cardiac output index. Mean arterial pressure (MAP) was higher in older subjects and increased with movement to upright postures. Younger men and women had higher forearm vascular resistance that increased progressively in the upright posture compared with older men and women. There was no difference between sexes or ages in total peripheral resistance index. Women had higher MCA velocity, but both sexes had reduced MCA velocity while upright, which was a function of reduced blood pressure at the MCA and a significant reduction in end-tidal PCO2. The reductions in stroke volume index suggested impaired venous return in women, but augmented responses of heart rate and forearm vascular resistance protected MAP in younger women. Overall, these results showed significant sex and age-related differences, but compensatory mechanisms preserved MAP and MCA velocity in young women. cerebrovascular; sex; age; orthostatic ORTHOSTATIC HYPOTENSION (a condition that sometimes leads to fainting) is an important and sometimes dangerous condition that particularly affects young women during daily life, as reflected by admission to emergency rooms (51). It has been speculated that female sex hormones might modulate reflex neural or vascular properties, resulting in the greater incidence of orthostatic hypotension in young women (5,14,15,52,69). An additional indication of impaired orthostatic responses in women includes the observation that women have a greater propensity towards postural orthostatic tachycardia syndrome (18, 60).Contrary to observations for young women, clinical evidence supports the concept that orthostatic hypotension occurs less frequently in women ages 40 -60 yr (many of whom could be postmenopausal) (51). Investigations of men and women from 23-77 yr of age indicated that the heart rate response to tilt was reduced with aging, but vascular responses a...

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confidence: 99%

Hemodynamics and brain blood flow during posture change in younger women and postmenopausal women compared with age-matched men

Edgell

Robertson

Hughson

2012

Journal of Applied Physiology

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“…Many patients with POTS are so debilitated by their orthostatic symptoms, they are unable to work. 2 A number of different pathophysiologies underlie symptoms in subgroups of patients, [3][4][5][6][7][8][9][10][11][12][13][14] but the basis of POTS remains obscure in most afflicted individuals. Genes encoding the NE transporter (SLC6A2), 13 the ␤-1 15 and ␤-2 (G. Jacob, unpublished data, 2005) adrenergic receptors, and endothelin-1 (R. Winker, unpublished data, 2005) are associated with the development of POTS.…”

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Endothelial NO Synthase Polymorphisms and Postural Tachycardia Syndrome

et al. 2005

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Abstract-Postural tachycardia syndrome (POTS) is a heterogeneous disorder characterized by an excessive rise in heart rate and symptoms consistent with cerebral hypoperfusion in the upright position. NO produced by endothelial NO synthase is a significant factor in the regulation of blood flow. Genetic polymorphisms in the promoter region (T-786C) and exon 7 (E298D) of the NO synthase isoform 3 gene affect enzyme activity and have been associated with a number of cardiovascular diseases. Because some findings in POTS suggest aberrant NO-mediated functions, we postulated that the variant genotypes of these polymorphisms may increase the risk of developing POTS and correlate with more severe symptoms. We genotyped 136 patients with POTS (mean age 32.2Ϯ9.9 years; 46 men and 90 women) from Nashville, Tenn, and Vienna, Austria, and compared them with 191 healthy volunteers (mean age 29.1Ϯ8.0 years; 127 men and 64 women). Participants also underwent orthostatic testing with blood pressure, heart rate, and plasma norepinephrine measurements while supine and upright.

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“…As a result of autonomic dysfunction, patients with POTS demonstrate orthostatic tachycardia in the absence of orthostatic hypotension as well as increased sympathetic activity in the supine position [2][3]. POTS can be readily identified during head-up tilt-testing if a patient displays a heart rate increase of >30 beats/min and a maximum heart rate of >120 beat/min within the first minutes of upright posture in the absence of hypotension [1].…”

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confidence: 99%

Treatment questions in POTS with hypertension and syncope

Lelonek

Goch

2008

Open Medicine

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AbstractA 27-year old man experienced recurrent syncope with prodromal palpitations and resultant injury. The features of these episodes suggested a potentially neurally-mediated mechanism. Head-up tilt test revealed the postural orthostatic tachycardia syndrome (POTS). Within the first minutes of upright posture during the total head-up tilt testing, a heart rate increase of >30 beats/min and to a maximum of 150 beats/min was documented in the patient. At the end of passive tilting, the patient lost consciousness in the absence of hypotension while in sinus rhythm of 140 bpm. The 12-lead ECG and electrophysiological study showed no abnormalities. The patient received a beta-adrenergic blocker, a selective central imidazoline receptor agonist and psychiatric therapy, resulting in only a short-term improvement.

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Neurocirculatory Abnormalities in Chronic Orthostatic Intolerance

Abstract: Background-Chronic orthostatic intolerance (COI) occurs in postural tachycardia syndrome (POTS)

Cited by 39 publications

References 47 publications

Hemodynamics and brain blood flow during posture change in younger women and postmenopausal women compared with age-matched men

Hemodynamics and brain blood flow during posture change in younger women and postmenopausal women compared with age-matched men

Endothelial NO Synthase Polymorphisms and Postural Tachycardia Syndrome

Treatment questions in POTS with hypertension and syncope

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