Regular issueClinical: GeneralDesmopressin acutely decreases tachycardia and improves symptoms in the postural tachycardia syndrome
Introduction
Postural tachycardia syndrome (POTS) is a chronic disorder of the autonomic nervous system characterized by excessive increase in heart rate (HR) on standing in the absence of orthostatic hypotension. It is estimated to affect 500,000 patients in the United States alone,1 disproportionately affecting women of childbearing age.2 Symptoms may include palpitations, lightheadedness, and mental clouding.3 POTS is associated with significant functional deficits and diminished quality of life.4, 5
There are several likely pathophysiologic mechanisms that may contribute to the symptoms of POTS. These include increased sympathetic tone,2, 6 partial autonomic neuropathy,7 and low blood volume.8, 9 The treatment of low blood volume in patients with POTS is still evolving, and scant data exist to support it. Acutely, the rapid infusion of normal saline can reverse the orthostatic tachycardia.10 On a chronic basis, patients with POTS are often advised to follow a high sodium diet (200–300 mEq/d) with significant water intake, though there are no data as to the effectiveness of this approach. Another treatment option is fludrocortisone, a mineralocorticoid agonist, to augment sodium retention and secondarily increase blood volume,11 but the increase in blood volume is transient.12
Desmopressin (DDAVP) is a synthetic version of arginine vasopressin, a natural antidiuretic hormone, and is commonly used to treat enuresis in children. DDAVP promotes fluid retention by increasing water permeability in the distal tubule of the kidney.13 It elicits a greater antidiuretic response but a reduced effect on smooth muscle contraction and vasopressor properties when compared with vasopressin.13 Finally, DDAVP, unlike vasopressin, does not stimulate adrenocorticotropic hormone release or increase plasma cortisol concentrations.13 By enhancing fluid retention, DDAVP might promote acute blood volume expansion and reduce upright tachycardia. Therefore, we prospectively tested the hypothesis that DDAVP would decrease orthostatic tachycardia and improve symptoms in patients with POTS.
Section snippets
Subjects
Patients with POTS referred to the Vanderbilt University Autonomic Dysfunction Center between November 2003 and September 2008 were candidates for inclusion in this study. Patients met criteria for POTS3, 14, 15 in that they developed symptoms of orthostatic intolerance accompanied by a HR rise of ≥30 beats/min within 10 minutes of standing in the absence of orthostatic hypotension (a fall in blood pressure [BP] of >20/10 mm Hg). All patients had at least a 6-month history of symptoms in the
Patient characteristics
Study inclusion criteria were met by 30 subjects with POTS (26 women; 37 ± 12 years). All subjects underwent the paired administration of placebo and DDAVP.
The data from the baseline supine and standing study are presented in Table 1. The supine HR was 77 ± 13 beats/min, and BP was 110 ± 12/69 ± 11 mm Hg. The supine plasma norepinephrine and epinephrine values were within the normal range (norepinephrine <2.81 nmol/L [<475 pg/mL] and epinephrine <0.41 nmol/L [<75 pg/mL]), with the exception of
Discussion
POTS is a form of chronic orthostatic intolerance that leads to a significant decrease in quality of life.17 Excessive orthostatic tachycardia in response to standing up from a lying position is the most obvious physiologic abnormality in patients with POTS. One treatment strategy is to increase the circulating blood volume acutely.
We found that over 4 hours from the time of administration, DDAVP (1) significantly decreased the standing HR of patients with POTS, (2) significantly decreased
Conclusions
DDAVP is highly effective at acutely decreasing orthostatic tachycardia and standing tachycardia in patients with POTS, and this was associated with an improvement in symptom burden in these patients. Longer-term studies are needed to assess this therapy.
Acknowledgments
We thank our patients who participated in this project and recognize the highly professional care provided by the staff of the Elliot V. Newman Clinical Research Center.
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2023, Autonomic Neuroscience: Basic and ClinicalCitation Excerpt :Domains and symptoms included orthostatic intolerance (OI) (although OI domain symptoms varied somewhat between questionnaires), vasomotor, secretomotor, gastrointestinal, bladder, pupillomotor/vision, fatigue/sleep, mental clouding, head/neck/chest discomfort, perspiration, shortness of breath, tremulousness, nausea, palpitations, syncope and more (Table 2). Overall, the methodological quality score, using the Downs and Black quality assessment tool (Downs and Black, 1998) was high in 17 studies (Cortez et al., 2020; Rea et al., 2017; Johansson et al., 2021; Raj et al., 2005; Barbic et al., 2020; Benrud-Larson et al., 2003; Kharraziha et al., 2020; Kimpinski et al., 2010; Lee et al., 2017; Coffin et al., 2012; Green et al., 2014; Green et al., 2013; Kpaeyeh et al., 2014; Moon et al., 2018; Raj et al., 2009b; Smith et al., 2020; Garland et al., 2021), medium in 12 studies (Benrud-Larson et al., 2002; Dipaola et al., 2020; Fisher et al., 2020; Kimpinski et al., 2012; Lewis et al., 2013; McDonald et al., 2014; Moon et al., 2016; Ruska et al., 2018; Wells et al., 2020; Bourne et al., 2021; Mar et al., 2014; Nardone et al., 2020), and low in 0 studies (Table 3). The next part of the results is divided into two major sections.
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2021, Journal of the American College of CardiologyCitation Excerpt :Blood for aldosterone was collected in chilled vacuum tubes without preservative, and the serum was extracted and sent to the laboratory on ice. Patients were asked to report their standing symptom burden at the end of the stand portion of the posture study, using the Vanderbilt Orthostatic Symptoms Scale (VOSS) (16). They rated the severity of 9 symptoms (palpitations, lightheadedness, mental confusion, blurred vision, shortness of breath, tremulousness, chest discomfort, headache, and nausea) on a 0 to 10 scale (with 0 reflecting an absence of symptoms).
This study was supported in part by National Institutes of Health grants R01 HL102387, R01 HL071784, R01 NS055670, P01 HL56693, and UL1 RR024975 (Clinical and Translational Science Award) and the Paden Dysautonomia Center.