Renin-Aldosterone Paradox and Perturbed Blood Volume Regulation Underlying Postural Tachycardia Syndrome

Raj, Satish R.; Biaggioni, Italo; Yamhure, Paula C.; Black, Bonnie K.; Paranjape, Sachin Y.; Byrne, Daniel W.; Robertson, David

doi:10.1161/01.cir.0000160356.97313.5d

Cited by 244 publications

(230 citation statements)

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“…Supine CBV is reduced in some patients with POTS 31, 34, 35, 36. This is striking in those patients with evidence for increased supine sympathoexcitation 37.…”

Section: Discussionmentioning

confidence: 95%

Postural Hyperventilation as a Cause of Postural Tachycardia Syndrome: Increased Systemic Vascular Resistance and Decreased Cardiac Output When Upright in All Postural Tachycardia Syndrome Variants

Stewart

Pianosi

Shaban

et al. 2018

JAHA

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BackgroundPostural tachycardia syndrome (POTS) is a heterogeneous condition. We stratified patients previously evaluated for POTS on the basis of supine resting cardiac output (CO) or with the complaint of platypnea or “shortness of breath” during orthostasis. We hypothesize that postural hyperventilation is one cause of POTS and that hyperventilation‐associated POTS occurs when initial reduction in CO is sufficiently large. We also propose that circulatory abnormalities normalize with restoration of CO 2.Methods and ResultsFifty‐eight enrollees with POTS were compared with 16 healthy volunteer controls. Low CO in POTS was defined by a resting supine CO <4 L/min. Patients with shortness of breath had hyperventilation with end tidal CO 2 <30 Torr during head‐up tilt table testing. There were no differences in height or weight between control patients and patients with POTS or differences between the POTS groups. Beat‐to‐beat blood pressure was measured by photoplethysmography, and CO was measured by ModelFlow. Systemic vascular resistance was defined as mean arterial blood pressure/CO. End tidal CO 2 and cerebral blood flow velocity of the middle cerebral artery were only reduced during head‐up tilt in the hyperventilation group, whereas blood pressure was increased compared with control. We corrected the reduced end tidal CO 2 in hyperventilation by addition of exogenous CO 2 into a rebreathing apparatus. With added CO 2, heart rate, blood pressure, CO, and systemic vascular resistance in hyperventilation became similar to control.ConclusionsWe conclude that all POTS is related to decreased CO, decreased central blood volume, and increased systemic vascular resistance and that a variant of POTS is consequent to postural hyperventilation.

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“…Supine CBV is reduced in some patients with POTS 31, 34, 35, 36. This is striking in those patients with evidence for increased supine sympathoexcitation 37.…”

Section: Discussionmentioning

confidence: 95%

Postural Hyperventilation as a Cause of Postural Tachycardia Syndrome: Increased Systemic Vascular Resistance and Decreased Cardiac Output When Upright in All Postural Tachycardia Syndrome Variants

Stewart

Pianosi

Shaban

et al. 2018

JAHA

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“…3 Onset of POTS occurs predominantly between the ages of 15 and 50 years, 4 with a female predominance. 1,2,[5][6][7] The female-to-male ratio has been reported to be as high as 5:1. 8 Given the female predominance and the occurrence of POTS during the childbearing years, the effects of this disorder on pregnancy is often raised in clinical practice.…”

confidence: 99%

Effect of Pregnancy on Postural Tachycardia Syndrome

Kimpinski

Iodice

Sandroni

et al. 2010

Mayo Clinic Proceedings

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P ostural tachycardia syndrome (POTS) is defined as the development of orthostatic symptoms associated with an increase in heart rate (HR) greater than 30 beats/min. More severe cases are associated with a standing HR increase greater than 120 beats/min. 1 Orthostatic symptoms most often include light-headedness, palpitations, presyncope, and exacerbations with heat or exercise. 2 Overall, the prognosis of POTS has been reported to be favorable in follow-up studies, with 80% of patients reporting improvement and 60% becoming functionally normal. 3 Onset of POTS occurs predominantly between the ages of 15 and 50 years, 4 with a female predominance. 1,2,[5][6][7] The female-to-male ratio has been reported to be as high as 5:1. 8 Given the female predominance and the occurrence of POTS during the childbearing years, the effects of this disorder on pregnancy is often raised in clinical practice.ObjECTIvES: To compare the clinical presentation, autonomic dysfunction, and pregnancy outcomes in parous and nulliparous women with postural tachycardia syndrome (POTS) and in women with POTS before and after pregnancy. PATIENTS AND METHODS:This study consists of women who had at least 1 pregnancy during which time they met criteria for POTS between May 1993 and July 2009. All patients underwent standard autonomic testing. POTS was defined as a heart rate (HR) increase of greater than 30 beats/min on head-up tilt (HUT) with symptoms of orthostatic intolerance. Patients' charts were reviewed retrospectively to determine pregnancy outcomes. RESULTS:Clinical characteristics related to POTS did not differ between parous and nulliparous women except for disease duration (parous, 3.7±2.6; nulliparous, 2.1±2.2; P<.001). Autonomic dysfunction did not differ between groups (change in HR on HUT: parous, 42.6±12.0 beats/min; nulliparous, 41.3±10.6 beats/min; P=.39). Of 116 total pregnancies, adverse pregnancy outcomes were reported in 9% and maternal complications in 1%. No complication was related to POTS. There was a trend toward modest improvement in autonomic dysfunction before and after pregnancy (change in HR on HUT: before pregnancy, 38.1±22.7 beats/min; after pregnancy, 21.9±14.9 beats/min; P=.07). CONCLUSION:The long-term impact of pregnancy on POTS does not appear to be clinically important. However, there does appear to be a trend toward improvement in the short-term postpartum period. Adverse pregnancy events were similar to those seen in the general public and do not present a barrier to women with POTS who want to have children.Mayo Clin Proc. 2010;85(7):639-644 CASS = composite autonomic severity score; HR = heart rate; HUT = head-up tilt; OI = orthostatic intolerance; POTS = postural tachycardia syndrome; TST = thermoregulatory sweat test However, until recently published data have been minimal. A recent study in 22 women indicated that, although the effect on symptoms related to POTS during pregnancy varied, the actual pregnancy was not affected. 9 The objectives of this study were as follows: (1) to determine whether ...

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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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confidence: 99%

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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Renin-Aldosterone Paradox and Perturbed Blood Volume Regulation Underlying Postural Tachycardia Syndrome

Cited by 244 publications

References 40 publications

Postural Hyperventilation as a Cause of Postural Tachycardia Syndrome: Increased Systemic Vascular Resistance and Decreased Cardiac Output When Upright in All Postural Tachycardia Syndrome Variants

Postural Hyperventilation as a Cause of Postural Tachycardia Syndrome: Increased Systemic Vascular Resistance and Decreased Cardiac Output When Upright in All Postural Tachycardia Syndrome Variants

Effect of Pregnancy on Postural Tachycardia Syndrome

Endothelial NO Synthase Polymorphisms and Postural Tachycardia Syndrome

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