Postural Orthostatic Tachycardia Syndrome

In the paper

“direct testing of autonomic function in this patient population is often normal/appropriate for the hemodynamic stress (4).”

What the sources say

• Supported

  In the Discussion (‘POTS and “deconditioning”’), the authors say they comprehensively assessed autonomic function in all their patients and found no evidence of abnormalities. They also describe the orthostatic tachycardia as a physiological compensatory response to smaller stroke volume; the Results (‘Autonomic function’) report comparable baroreflex, cold-pressor, and handgrip responses in patients and controls. (LLM, conf=0.92)

  cites [4] Fu, 2010, Cardiac origins of the postural orthostatic tachycardia syndrome, J Am Coll Cardiol source

In the paper

“The pathophysiological mechanisms underlying POTS are thought to be heterogeneous (15).”

What the sources say

• Supported

  The introductory passage explicitly says that POTS is pathophysiologically heterogeneous. The Conclusions and Perspective section also describes multiple interacting pathophysiologic mechanisms, matching the citing sentence. (LLM, conf=0.95)

  cites [15] Benarroch, 2012, Postural tachycardia syndrome: a heterogeneous and multifactorial disorder, Mayo Clin Proc source

In the paper

“in patients under 20 years of age, the HR increment with upright posture should exceed 40 beats/min in order to be considered clinically significant (1,3).”

What the sources say

• Partly supported

  The POTS Definition (Section 1; page not provided) gives a heart-rate increase of ≥40 beats/min on standing for individuals aged 12–19. The claim broadens that age range to everyone under 20 and says the increase must exceed 40, whereas the source includes exactly 40. It also presents the threshold as a general measure of clinical significance rather than one criterion of POTS. (LLM, conf=0.88)

  cites [1] Sheldon, 2015, 2015 Heart Rhythm Society expert consensus statement on the diagnosis and treatment of postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope, Heart Rhythm sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [3] Freeman, 2011, Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome, Auton Neurosci source

In the paper

“Figure 2B shows the tight relationship between stroke volume and HR in men, healthy women, and women with POTS (4,12).”

What the sources say

• Partly supported

  The Discussion (page not provided) links smaller stroke volume to higher heart rate in POTS patients and describes a similar mechanism in young women. It does not establish a tight stroke-volume–heart-rate relationship across all three groups. The Methods (page not provided) report only one healthy male control, so the claim about men is not supported by this study. (LLM, conf=0.84)

  cites [4] Fu, 2010, Cardiac origins of the postural orthostatic tachycardia syndrome, J Am Coll Cardiol sourceExperimental — accuracy not yet measured
• Partly supported

  The ‘Responses during upright tilt’ section reports that heart rate increased while stroke volume decreased in healthy men and women. It does not establish a tight stroke-volume–heart-rate relationship, and the ‘Study limitations’ section says all subjects were healthy, so the claim about women with POTS is not supported by this paper. (LLM, conf=0.82)

  cites [12] Fu, 2009, Menstrual cycle effects on sympathetic neural responses to upright tilt, J Physiol sourceExperimental — accuracy not yet measured

In the paper

“Since the inception of space missions, a postflight orthostatic intolerance on return to Earth has been noted following both short-and long-term flights, especially in women astronauts.”

What the sources say

• ?Not checked — no full text of the sourcecites [16] Fritsch-Yelle, 1996, Subnormal norepinephrine release relates to presyncope in astronauts after spaceflight, J Appl Physiol (1985) source
• ?Not checked — no full text of the sourcecites [17] Buckey, 1996, Orthostatic intolerance after spaceflight, J Appl Physiol (1985) source
• Partly supported

  The Discussion states that orthostatic intolerance has been observed after both short- and long-duration missions since the inception of the manned space program. It does not say it occurs especially in women; the Methods (Subjects) report that this study included only six male crew members. No page number is available for these passages. (LLM, conf=0.90)

  cites [18] Levine, 2002, Human muscle sympathetic neural and haemodynamic responses to tilt following spaceflight, J Physiol sourceExperimental — accuracy not yet measured

In the paper

“One feature that appears to be universally present in all POTS is cardiovascular deconditioning, a specific biological process characterized by cardiac atrophy and hypovolemia (4).”

What the sources say

• Partly supported

  The Discussion reports smaller left ventricular mass and lower blood volume in the patients studied, and describes deconditioning in terms of cardiac atrophy and hypovolemia. It does not establish that deconditioning is universally present in all people with POTS; the Discussion instead says that almost all of its patients had a history of physical inactivity and notes that POTS may have heterogeneous mechanisms. Page numbers are unavailable in our copy. (LLM, conf=0.88)

  cites [4] Fu, 2010, Cardiac origins of the postural orthostatic tachycardia syndrome, J Am Coll Cardiol sourceExperimental — accuracy not yet measured

In the paper

“Even after brief trips, approximately one-fourth to two-thirds of astronauts cannot stand for even 10 min upon return to earth (16)(17)(18).”

What the sources say

• ?Not checked — no full text of the sourcecites [16] Fritsch-Yelle, 1996, Subnormal norepinephrine release relates to presyncope in astronauts after spaceflight, J Appl Physiol (1985) source
• ?Not checked — no full text of the sourcecites [17] Buckey, 1996, Orthostatic intolerance after spaceflight, J Appl Physiol (1985) source
• Supported

  The paper states that, depending on the type and duration of orthostatic stress, one-quarter to two-thirds of crew members returning from brief (8–14 day) missions could not remain standing for 10 minutes (passage [4], labeled Abstract). This is a report of earlier studies, not a result from the paper’s own six-person cohort; all six completed 10 minutes of postflight tilt (Results, passage [7]). (LLM, conf=0.94)

  cites [18] Levine, 2002, Human muscle sympathetic neural and haemodynamic responses to tilt following spaceflight, J Physiol source

In the paper

“Some have inappropriately low plasma renin activity and aldosterone levels resulting in inadequate renal sodium retention (42,44).”

What the sources say

• ?Could not verify

  The Introduction describes hypovolemia in a low-flow POTS subgroup and says increased angiotensin II was not accounted for by changes in renin. Neither it nor the other passages found by searching for renin, aldosterone, and sodium retention addresses inappropriately low plasma renin activity and aldosterone causing inadequate renal sodium retention. Page numbers were not available in our copy. (LLM, conf=0.76)

  cites [42] Stewart, 2009, Defects in cutaneous angiotensin-converting enzyme 2 and angiotensin-(1-7) production in postural tachycardia syndrome, Hypertension sourceExperimental — accuracy not yet measured
• Supported

  The 'Pathophysiology of POTS' section describes low blood and plasma volumes alongside inappropriately low renin and aldosterone levels. The volume-loading section explains that an aldosterone agonist promotes sodium and water retention, supporting the stated link to inadequate retention. The copy provides no page numbers for these sections. (LLM, conf=0.90)

  cites [44] Mar, 2014, Neuronal and hormonal perturbations in postural tachycardia syndrome, Front Physiol source

In the paper

“More common than genetic NET deficiency is NET blockade from pharmacological agents, such as NE reuptake inhibitors (e.g., bupropion), tricyclic antidepressants (e.g., nortriptyline), and other sympathomimetic drugs (e.g., methylphenidate) (15).”

What the sources say

• Partly supported

  The ARTICLE HIGHLIGHTS passage says that increased norepinephrine levels more commonly reflect pharmacological NET blockade than the genetic NET deficiency described in a case. It names tricyclic antidepressants, selective NET inhibitors, and amphetamine-like drugs including methylphenidate, but does not name bupropion or nortriptyline as the citing sentence does. (LLM, conf=0.85)

  cites [15] Benarroch, 2012, Postural tachycardia syndrome: a heterogeneous and multifactorial disorder, Mayo Clin Proc sourceExperimental — accuracy not yet measured

In the paper

“Another large subgroup within the POTS population is the so-called hyperadrenergic subtype, with features that may correspond to 30% to 60% of POTS patients (6,36,37).”

What the sources say

• ?Not checked — no full text of the sourcecites [6] Thieben, 2007, Postural orthostatic tachycardia syndrome: the Mayo clinic experience, Mayo Clin Proc source
• Partly supported

  The Hyperadrenergic POTS section reports elevated norepinephrine in 29.0% of patients tested, and the HUT and Evaluation of Adrenergic Function section says about half have a hyperadrenergic response. These figures support the claim that hyperadrenergic features occur in a substantial subgroup, but the paper does not establish a 30%–60% prevalence for the subtype, which it defines using both a blood-pressure rise and elevated norepinephrine. (LLM, conf=0.84)

  cites [36] Low, 2009, Postural tachycardia syndrome (POTS), J Cardiovasc Electrophysiol sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [37] Benarroch, 2014, The clinical approach to autonomic failure in neurological disorders, Nat Rev Neurol source

In the paper

“These observations led to the concept that peripheral sympathetic denervation might lead to impaired vasoconstriction and increased venous pooling in lower extremities (34).”

What the sources say

• Supported

  The Discussion (page not available in our copy) proposes that anatomical or functional denervation confined to lower-limb veins causes excessive venous pooling in these patients. This supports the claimed concept of impaired physiological venous constriction; the paper also notes that the denervated foot veins were unusually responsive to infused norepinephrine, not less responsive to it. (LLM, conf=0.90)

  cites [34] Streeten, 1990, Pathogenesis of hyperadrenergic orthostatic hypotension. Evidence of disordered venous innervation exclusively in the lower limbs, J Clin Invest source

In the paper

“These patients have elevated standing plasma norepinephrine (NE) levels (>600 pg/ml), reflecting an exaggerated sympathetic response (6,36),”

What the sources say

• ?Not checked — no full text of the sourcecites [6] Thieben, 2007, Postural orthostatic tachycardia syndrome: the Mayo clinic experience, Mayo Clin Proc source
• Supported

  The Hyperadrenergic POTS section defines the subtype by elevated orthostatic plasma norepinephrine (≥600 pg/mL) and describes a major role for orthostatic sympathetic activation. The HUT and Evaluation of Adrenergic Function section also calls standing norepinephrine above 600 pg/mL a hyperadrenergic response. (LLM, conf=0.94)

  cites [36] Low, 2009, Postural tachycardia syndrome (POTS), J Cardiovasc Electrophysiol source

In the paper

“There also appear to be some fluctuations in the renin-angiotensin-aldosterone system during different phases of the menstrual cycle that affect the orthostatic hemodynamic response in POTS (45).”

What the sources say

• Supported

  The Abstract reports lower renin activity and aldosterone in the early-follicular than mid-luteal phase during standing in women with POTS, alongside differences in cardiac output, stroke volume, and peripheral resistance. The Discussion (Menstrual Cycle Effects in POTS Women) suggests that lower RAAS activation may account for the phase-dependent hemodynamic responses. The citing sentence's tentative wording matches that interpretation. (LLM, conf=0.94)

  cites [45] Fu, 2010, Menstrual cycle affects renal-adrenal and hemodynamic responses during prolonged standing in the postural orthostatic tachycardia syndrome, Hypertension source

In the paper

“Others have elevated plasma angiotensin II levels suggesting inadequate angiotensin-converting enzyme 2 activity (42,44).”

What the sources say

• Supported

  The Introduction reports increased plasma angiotensin II in the low-flow POTS subgroup. The Discussion’s Perspectives section reports blunted ACE2 activity and identifies ACE2 as a pathway for angiotensin II degradation, supporting the proposed connection. No page numbers are available in our copy. (LLM, conf=0.92)

  cites [42] Stewart, 2009, Defects in cutaneous angiotensin-converting enzyme 2 and angiotensin-(1-7) production in postural tachycardia syndrome, Hypertension source
• Supported

  The Angiotensin II section reports elevated plasma Ang-II in some POTS patients. The ACE2 section reports that POTS patients with elevated systemic Ang-II had a significantly lower Ang(1-7):Ang-II ratio, used as a surrogate for functional ACE2 activity. This supports the claim’s cautious wording; page numbers were not provided. (LLM, conf=0.92)

  cites [44] Mar, 2014, Neuronal and hormonal perturbations in postural tachycardia syndrome, Front Physiol source

In the paper

“Women with POTS often report fluctuations in the severity of POTS symptoms throughout their menstrual cycle, with worsening during either the pre-menstrual or early follicular phase when both estrogen and progesterone levels are dropping or low (6,9,45,51).”

What the sources say

• ?Not checked — no full text of the sourcecites [6] Thieben, 2007, Postural orthostatic tachycardia syndrome: the Mayo clinic experience, Mayo Clin Proc source
• ?Not checked — no full text of the sourcecites [9] Raj, 2006, The postural tachycardia syndrome (POTS): pathophysiology, diagnosis & management, Indian Pacing Electrophysiol J
• Partly supported

  Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [45] Fu, 2010, Menstrual cycle affects renal-adrenal and hemodynamic responses during prolonged standing in the postural orthostatic tachycardia syndrome, Hypertension sourceExperimental — accuracy not yet measured

In the paper

“Many studies have demonstrated that prolonged bedrest or microgravity exposure can result in a POTS-like syndrome characterized by a tachycardic orthostatic intolerance even in previously healthy and active individuals (17,18,25,27,57-60).”

What the sources say

• ?Not checked — no full text of the sourcecites [17] Buckey, 1996, Orthostatic intolerance after spaceflight, J Appl Physiol (1985) source
• Partly supported

  The Discussion (page not provided) reports greater tachycardia after spaceflight and describes earlier studies in which astronauts could not remain standing for 10 minutes. It also notes increased heart rates after head-down bed rest, but does not establish bed-rest-induced orthostatic intolerance or characterize the response as a POTS-like syndrome in previously healthy, active individuals. None of this study’s astronauts experienced presyncope during postflight tilt. (LLM, conf=0.85)

  cites [18] Levine, 2002, Human muscle sympathetic neural and haemodynamic responses to tilt following spaceflight, J Physiol sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [25] Perhonen, 2001, Cardiac atrophy after bed rest and spaceflight, J Appl Physiol (1985) source

In the paper

“When plasma volume, blood volume, and supine hemodynamics were measured in a cohort of POTS patients and controls, no variations were noted while comparing the mid-luteal phase to the early-follicular phase (45).”

What the sources say

• Supported

  The Results (EFP versus MLP; page not provided) state that plasma and blood volume were not significantly affected by menstrual phase in either group. The same section says the menstrual cycle did not influence supine hemodynamics in POTS women or controls. This supports the claimed comparison, though 'no variations' should be understood as no statistically significant differences. (LLM, conf=0.94)

  cites [45] Fu, 2010, Menstrual cycle affects renal-adrenal and hemodynamic responses during prolonged standing in the postural orthostatic tachycardia syndrome, Hypertension source

In the paper

“These findings suggest that the orthostatic tachycardia in POTS is a physiological compensatory response to the smaller stroke volume (61,62) in the setting of cardiac atrophy and reduced blood volume (Figure 2B).”

What the sources say

• Partly supported

  The Results report that heart rate rose while stroke volume fell during upright tilt, and the Discussion links falling stroke volume to sympathetic activation. However, the study involved healthy individuals; it does not establish that tachycardia in POTS compensates for smaller stroke volume. The citation is attached to the smaller-stroke-volume explanation, not specifically to the cardiac-atrophy and reduced-blood-volume phrase. (LLM, conf=0.85)

  cites [61] Fu, 2006, Vasomotor sympathetic neural control is maintained during sustained upright posture in humans, J Physiol sourceExperimental — accuracy not yet measured
• Supported

  In “Is the rise in heart rate with POTS really ‘excessive?’”, the paper reports lower stroke volume and higher heart rate in POTS patients despite similar cardiac output. “Is POTS psychogenic?” calls the tachycardia during venous pooling a compensatory physiological response, and the interim summary links these responses to small hearts and low plasma volumes. These passages support the citing sentence’s hedged interpretation. (LLM, conf=0.91)

  cites [62] Joyner, 2008, POTS versus deconditioning: the same or different?, Clin Auton Res source

In the paper

“When the 10-min criterion for upright position was applied to these data, HUT and the active stand test were comparable (95).”

What the sources say

• Partly supported

  The Results section, “Diagnostic Characteristics of the 30 bpm Criterion” (page unavailable), reports comparable sensitivity at 10 minutes: 93% for tilt and 87% for standing. But specificity was substantially lower for tilt (40% versus 67%), so the tests were not comparable on both diagnostic measures under that criterion. (LLM, conf=0.88)

  cites [95] Plash, 2013, Diagnosing postural tachycardia syndrome: comparison of tilt testing compared with standing haemodynamics, Clin Sci (Lond) sourceExperimental — accuracy not yet measured

In the paper

“Orthostatic intolerance has been reported to occur more frequently in patients with chronic pelvic pain, including interstitial cystitis, bladder pain syndrome, and myofascial pelvic pain (92).”

What the sources say

• Supported

  The Discussion reports orthostatic intolerance in 19% of participants with IC/BPS, 29% with myofascial pelvic pain, and 37% with both, versus 0% of healthy participants. The study enrolled adult women; page numbers are not supplied in our copy. (LLM, conf=0.93)

  cites [92] Chelimsky, 2016, Autonomic testing in women with chronic pelvic pain, J Urol source

In the paper

“a potential etiology for this link is less refreshing sleep due to increased sympathetic activation (84).”

What the sources say

• Partly supported

  The Polysomnogram Correlations section (page not provided) proposes that increased sympathetic activity may reduce sleep efficiency and lead to less restful sleep. But the reported link is with the change in heart rate from supine to standing, not supine heart rate itself. (LLM, conf=0.86)

  cites [84] Bagai, 2016, Objective sleep assessments in patients with postural tachycardia syndrome using overnight polysomnograms, J Clin Sleep Med sourceExperimental — accuracy not yet measured

In the paper

“as such, they may exist along the same clinical spectrum (82).”

What the sources say

• Supported

  The Discussion concludes that CFS in patients with POTS seems to be part of the POTS spectrum, rather than a separate clinical entity. This supports the citing sentence’s hedged description of a shared clinical spectrum. (LLM, conf=0.92)

  cites [82] Okamoto, 2012, Neurohumoral and haemodynamic profile in postural tachycardia and chronic fatigue syndromes, Clin Sci (Lond) source

In the paper

“When the active stand test was compared with passive HUT, orthostatic tachycardia was noted to be greater with HUT than with the active stand test in both POTS patients and healthy controls.”

What the sources say

• Supported

  The Results section (‘Orthostatic HR Responses to Passive Tilt and Active Stand’) reports greater heart-rate increases with passive tilt than active standing in both POTS patients and healthy controls from 10 through 30 minutes. It notes that the differences at 5 minutes were not statistically significant for either group. (LLM, conf=0.94)

  cites [95] Plash, 2013, Diagnosing postural tachycardia syndrome: comparison of tilt testing compared with standing haemodynamics, Clin Sci (Lond) source

In the paper

“Orthostatic tachycardia is more pronounced in the morning, and the active stand test (or HUT) should be performed in the morning when possible (93).”

What the sources say

• Supported

  The Discussion states that orthostatic tachycardia was significantly higher first thing in the morning than in the evening, in both POTS patients and healthy controls. The Results likewise report a larger morning increase in heart rate on standing. (LLM, conf=0.94)

  cites [93] Brewster, 2012, Diurnal variability in orthostatic tachycardia: implications for the postural tachycardia syndrome, Clin Sci (Lond) source

In the paper

“In a retrospective study looking at GI transit in patients with POTS, two-thirds had abnormal gastric emptying.”

What the sources say

• Supported

  The Methods describe a retrospective review of records for patients with POTS who underwent gastrointestinal transit assessment. The Discussion reports that two-thirds of the patients with POTS and GI symptoms had abnormal gastric emptying; that proportion refers to this selected group, not all patients with POTS. (LLM, conf=0.91)

  cites [87] Loavenbruck, 2015, Disturbances of gastrointestinal transit and autonomic functions in postural orthostatic tachycardia syndrome, Neurogastroenterol Motil source

In the paper

“Lower urinary tract symptoms, including increased daytime frequency, urgency, and nocturia have been reported at higher frequencies in POTS (90).”

What the sources say

• Partly supported

  The Results report that 13 of 19 women with POTS met criteria for probable overactive bladder and identify nocturia, frequency, and urgency as bothersome symptoms. The paper does not establish that each symptom occurs more frequently in POTS than in a comparison group, or separately quantify increased daytime frequency. (LLM, conf=0.86)

  cites [90] Kaufman, 2017, Overactive bladder and autonomic dysfunction: lower urinary tract symptoms in females with postural tachycardia syndrome, Neurourol Urodyn sourceExperimental — accuracy not yet measured

In the paper

“Research has demonstrated that physical reconditioning with a short-term (3 month) progressive exercise training program leads to improvement or remission of POTS in the majority of patients (4,64).”

What the sources say

• Supported

  The Results (Exercise training effects) report that 10 of 19 patients who completed the three-month program no longer met POTS criteria, and that quality of life improved significantly after training in all patients. The Discussion (Exercise training for POTS) likewise describes improved quality of life, including among patients whose orthostatic tachycardia persisted. The majority finding applies to program completers; the paper also notes that increased salt and water intake and other advice may have contributed to symptom improvements. (LLM, conf=0.90)

  cites [4] Fu, 2010, Cardiac origins of the postural orthostatic tachycardia syndrome, J Am Coll Cardiol source
• ?Not checked — no full text of the sourcecites [64] George, 2016, The international POTS registry: Evaluating the efficacy of an exercise training intervention in a community setting, Heart Rhythm source

In the paper

“A negative correlation between supine HR and sleep efficiency has been noted;”

What the sources say

• Partly supported

  The 'Correlation between Polysomnogram Data and Autonomic Data' section reports negative correlations between sleep efficiency and maximal standing HR and the change in HR from supine to standing in POTS patients. It does not report a negative correlation with supine HR itself; the claim substitutes a different HR measure. (LLM, conf=0.87)

  cites [84] Bagai, 2016, Objective sleep assessments in patients with postural tachycardia syndrome using overnight polysomnograms, J Clin Sleep Med sourceExperimental — accuracy not yet measured

In the paper

“Several other studies have implicated dysmotility at different levels of the GI tract (duodenal, gastric) in POTS (87)(88)(89).”

What the sources say

• Partly supported

  The Discussion reports abnormal gastric emptying in two-thirds of patients with POTS and GI symptoms, supporting the gastric part of the cited sentence. Although the paper also evaluated small-bowel transit, the passages do not establish duodenal dysmotility specifically. (LLM, conf=0.82)

  cites [87] Loavenbruck, 2015, Disturbances of gastrointestinal transit and autonomic functions in postural orthostatic tachycardia syndrome, Neurogastroenterol Motil sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [88] Moak, 2016, Antroduodenal manometry is abnormal in children presenting with orthostatic intolerance and gastrointestinal symptoms, J Pediatr Gastroenterol Nutr source
• ?Not checked — no full text of the sourcecites [89] Wang, 2015, Gastrointestinal dysfunction in postural tachycardia syndrome, J Neurol Sci source

In the paper

“Behavioral and cognitive therapy has been used to obtain long-term control of symptoms, particularly when anxiety, hypervigilance, or catastrophizing behaviors are present (15).”

What the sources say

• Partly supported

  In “Why Are Some Patients With POTS So Difficult to Treat?” (page not supplied), the paper identifies somatic hypervigilance as a factor in persistent symptoms and says behavioral-cognitive approaches are more likely than pharmacotherapy to improve quality of life. It does not report that therapy has been used to achieve long-term symptom control or specifically identify catastrophizing behaviors. (LLM, conf=0.86)

  cites [15] Benarroch, 2012, Postural tachycardia syndrome: a heterogeneous and multifactorial disorder, Mayo Clin Proc sourceExperimental — accuracy not yet measured

In the paper

“A small study evaluating this showed that modafinil did not significantly worsen standing HR or orthostatic symptoms in POTS (115).”

What the sources say

• Supported

  The Abstract Conclusions state that modafinil did not significantly worsen standing HR or acute orthostatic symptoms in POTS patients compared with placebo. The Results report 54 participants and no significant difference in standing HR or symptom burden over four hours, supporting the description of a small study. (LLM, conf=0.95)

  cites [115] Kpaeyeh, 2014, Hemodynamic profiles and tolerability of modafinil in the treatment of postural tachycardia syndrome: a randomized, placebo-controlled trial, J Clin Psychopharmacol source

In the paper

“In limited studies, ivabradine has also been shown to reduce HR in POTS (112,113).”

What the sources say

• Partly supported

  The Results report that patients taking ivabradine experienced fewer episodes of palpitations and tachycardia, and the Discussion describes reduced patient-perceived tachycardia in 55% of POTS patients. The study relied on symptom reports rather than measured heart-rate changes, so it does not establish the claimed reduction in HR directly. (LLM, conf=0.84)

  cites [112] McDonald, 2011, Single centre experience of ivabradine in postural orthostatic tachycardia syndrome, Europace sourceExperimental — accuracy not yet measured
• Supported

  The Abstract Results report that ivabradine slowed heart rate in POTS patients at rest and during head-up tilt. The Abstract Methods identify this as a small, open-label trial of eight patients without a placebo control, consistent with the citing sentence’s qualification that the studies are limited. (LLM, conf=0.94)

  cites [113] Barzilai, 2015, The effect of ivabradine on the heart rate and sympathovagal balance in postural tachycardia syndrome patients, Rambam Maimonides Med J source

In the paper

“Patients with hyperadrenergic POTS or significant hypertensive responses during tilt may respond to phenobarbital 15 mg in the morning and 60 mg at night (36).”

What the sources say

• Partly supported

  The Management > Hyperadrenergic POTS passage says that some patients with autonomic instability and unstable hypertensive responses to tilt respond to oral phenobarbital, beginning with 60 mg at night and 15 mg in the morning. It does not extend that treatment response to hyperadrenergic POTS patients generally; it describes a particularly difficult subset. (LLM, conf=0.82)

  cites [36] Low, 2009, Postural tachycardia syndrome (POTS), J Cardiovasc Electrophysiol sourceExperimental — accuracy not yet measured

In the paper

“They have not been shown to reduce tachycardia in POTS (110).”

What the sources say

• Partly supported

  The Discussion conclusion reports that acute sertraline did not significantly reduce heart rate in POTS patients. The study tested one SSRI over a short period, and the Discussion says longer-duration studies are needed; it does not establish the broader claim for SSRIs generally or chronic use. (LLM, conf=0.87)

  cites [110] Mar, 2014, Acute hemodynamic effects of a selective serotonin reuptake inhibitor in postural tachycardia syndrome: a randomized, crossover trial, J Psychopharmacol sourceExperimental — accuracy not yet measured

In the paper

“This has more recently been expanded to explain some of the symptoms and comorbid conditions associated with POTS(79).”

What the sources say

• Supported

  The Discussion (page unavailable) links somatic hypervigilance in PoTS to the persistence and broader range of its symptoms. It also describes sensitivity to physical and cognitive symptoms as related to anxiety and depression, and suggests that hypervigilance may help maintain affective symptoms. This supports the claim’s qualified explanation of some PoTS symptoms and comorbid conditions. (LLM, conf=0.87)

  cites [79] Owens, 2017, The genesis and presentation of anxiety in disorders of autonomic overexcitation, Auton Neurosci source

In the paper

“Several recent studies have shown that these comorbidities occur in increased frequency with each other regardless of whether a patient has POTS, suggesting that POTS is simply another comorbid condition rather than the cause of these other conditions(69).”

What the sources say

• Supported

  The Discussion states that patients with and without tilt-table-defined POTS share similar comorbidities and concludes that POTS appears to be another independent comorbid condition rather than the cause of the others. The Abstract Conclusions make the same point for children and young adults with functional disorders. Page numbers are not provided in our copy. (LLM, conf=0.94)

  cites [69] Chelimsky, 2015, Comorbid conditions do not differ in children and young adults with functional disorders with or without postural tachycardia syndrome, J Pediatr source

In the paper

“Several recent studies have shown that these comorbidities occur in increased frequency with each other regardless of whether a patient has POTS, suggesting that POTS is simply another comorbid condition rather than the cause of these other conditions(69).”

What the sources say

• Partly supported

  The Results and Discussion (page unavailable) find similar comorbidity burdens with and without POTS and report associations among some conditions, particularly fibromyalgia and hypermobility. The paper says this pattern suggests POTS is another comorbid condition rather than the cause of the others. It does not show that all the comorbidities occur together at increased frequency; the Discussion calls the fibromyalgia–hypermobility link the only reliable association found in the study. (LLM, conf=0.84)

  cites [69] Chelimsky, 2015, Comorbid conditions do not differ in children and young adults with functional disorders with or without postural tachycardia syndrome, J Pediatr sourceExperimental — accuracy not yet measured

In the paper

“These are numerous and include chronic fatigue, dizziness, syncope, migraines, functional GI disorders, chronic nausea, fibromyalgia, and joint hypermobility among others(68).”

What the sources say

• Partly supported

  The POTS sections on typical presentations and GI physiology (page unavailable) describe fatigue, dizziness, nausea, migraine-like headaches, functional GI symptoms, and joint hypermobility; the recovery section also lists fainting among POTS symptoms. But the recovery section calls fibromyalgia a syndrome with features similar to POTS, not a frequent POTS comorbidity. The source also describes several listed items as symptoms rather than separate comorbid conditions. (LLM, conf=0.88)

  cites [68] Kizilbash, 2014, Adolescent fatigue, POTS, and recovery: a guide for clinicians, Curr Probl Pediatr Adolesc Health Care sourceExperimental — accuracy not yet measured

In the paper

“with an average HR increment of 44.2 Æ 13.2 beats/min from supine to upright (6)”

What the sources say

• ?Not checked — no full text of the sourcecites [6] Thieben, 2007, Postural orthostatic tachycardia syndrome: the Mayo clinic experience, Mayo Clin Proc source

In the paper

“Under thermal stress, cutaneous vasodilation increases blood flow to the skin and redirects up to 50% to 70% of resting cardiac output to the skin to maintain core temperature (14).”

What the sources say

• Not checked yetcites [14] Rowell, 1986, Circulatory adjustments to dynamic exercise and heat stress: competing controls

In the paper

“Cardiovascular deconditioning can occur rapidly, within 20 h of bedrest (27);”

What the sources say

• ?Not checked — no full text of the sourcecites [27] Gaffney, 1985, Cardiovascular deconditioning produced by 20 hours of bedrest with head-down tilt (-5 degrees) in middle-aged healthy men, Am J Cardiol source

In the paper

“like with spaceflight, women, the predominant group afflicted by POTS, appear to be more susceptible (16,28,29).”

What the sources say

• ?Not checked — no full text of the sourcecites [16] Fritsch-Yelle, 1996, Subnormal norepinephrine release relates to presyncope in astronauts after spaceflight, J Appl Physiol (1985) source
• ?Not checked — no full text of the sourcecites [28] Waters, 2002, Postspaceflight orthostatic hypotension occurs mostly in women and is predicted by low vascular resistance, J Appl Physiol (1985) source
• ?Not checked — no full text of the sourcecites [29] Fu, 2010, Why do young women (donors) faint?, Transfusion source

In the paper

“These same mechanisms described in space flight have also been seen following prolonged bedrest deconditioning (23,(25)(26)(27).”

What the sources say

• ?Not checked — no full text of the sourcecites [23] Levine, 1997, Cardiac atrophy after bed-rest deconditioning: a nonneural mechanism for orthostatic intolerance, Circulation source
• ?Not checked — no full text of the sourcecites [25] Perhonen, 2001, Cardiac atrophy after bed rest and spaceflight, J Appl Physiol (1985) source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [26] Raj

In the paper

“In one study, >50% of POTS patients (6) were noted to have loss of sweat function in distal lower extremities (32), measured as impaired sweat volume on quantitative sudomotor axon reflex testing (32) or reduced intraepidermal C-fiber density on skin biopsy (33).”

What the sources say

• ?Not checked — no full text of the sourcecites [6] Thieben, 2007, Postural orthostatic tachycardia syndrome: the Mayo clinic experience, Mayo Clin Proc source
• ?Not checked — no full text of the sourcecites [32] Raj, 2007, Blood volume perturbations in the postural tachycardia syndrome, Am J Med Sci source
• ?Not checked — no full text of the sourcecites [33] Haensch, 2014, Small-fiber neuropathy with cardiac denervation in postural tachycardia syndrome, Muscle Nerve source

In the paper

“physiological cardiac atrophy in response to bedrest deconditioning, like its converse, physiological hypertrophy in response to exercise training, is a universal response to cardiac unloading, and by itself, is not pathological.”

In the paper

“in susceptible patients, even mild post-bedrest orthostatic intolerance may lead to a “downward spiral” of further bedrest deconditioning and worsening orthostatic intolerance that can be quite debilitating.”

In the paper

“A single case of POTS with elevated standing NE levels was found to have a mutation in NET, encoded by the SLC6A2 gene, causing loss of function;”

In the paper

“Stimulant-induced tachycardia has been known to closely mimic POTS (41),”

What the sources say

• ?Not checked — no full text of the sourcecites [41] Cheshire, 2016, Stimulant medication and postural orthostatic tachycardia syndrome: a tale of two cases, Clin Auton Res source

In the paper

“An autoimmune basis for POTS has been suggested on the basis of some of the clinical associations, including subacute onset in the setting of stress or viral illness, and the occasional association of POTS with a personal or family history of systemic autoimmune disorders such as Sjogren's syndrome.”

In the paper

“When sodium intake is controlled, urine sodium excretion can be used as a surrogate for hypovolemia, and approximately 30% of POTS patients have evidence of hypovolemia based on <100 mEq of urinary sodium excretion in 24 h (6).”

What the sources say

• ?Not checked — no full text of the sourcecites [6] Thieben, 2007, Postural orthostatic tachycardia syndrome: the Mayo clinic experience, Mayo Clin Proc source

In the paper

“Intolerance to orthostasis tends to be more significant in young women compared with their male counterparts (29).”

What the sources say

• ?Not checked — no full text of the sourcecites [29] Fu, 2010, Why do young women (donors) faint?, Transfusion source

In the paper

“Thus far, however, none of the autoantibody associations have been convincingly proven to be pathophysiologically or diagnostically important.”

In the paper

“More focused studies attempting to tie genetic variations in the SLC6A2 gene to elevated NE levels, however, have been inconclusive (39,40).”

What the sources say

• ?Not checked — no full text of the sourcecites [39] Ivancsits, 2003, Orthostatic intolerance is not necessarily related to a specific mutation (Ala457Pro) in the human norepinephrine transporter gene, Am J Med Sci source
• ?Not checked — no full text of the sourcecites [40] Bayles, 2012, Epigenetic modification of the norepinephrine transporter gene in postural tachycardia syndrome, Arterioscler Thromb Vasc Biol source

In the paper

“Orthostatic HR increments have been shown to be larger in the morning than in the afternoon (55).”

What the sources say

• ?Not checked — no full text of the sourcecites [55] Moon, 2016, The complexity of diagnosing postural orthostatic tachycardia syndrome: influence of the diurnal variability, J Am Soc Hypertens source

In the paper

“However, unlike in POTS, these paroxysmal symptoms are not positional.”

In the paper

“Reconditioning via exercise may not improve all symptoms (101).”

What the sources say

• ?Not checked — no full text of the sourcecites [101] Galbreath, 2011, Effects of exercise training on arterial-cardiac baroreflex function in POTS, Clin Auton Res source

In the paper

“This is felt to be a reflection of exaggerated sympathetic neuronal activation (97).”

What the sources say

• ?Not checked — no full text of the sourcecites [97] Raj, 2013, Postural tachycardia syndrome (POTS), Circulation source

In the paper

“Furthermore, cardiac arrhythmias following isoproterenol administration have been reported (96).”

What the sources say

• ?Not checked — no full text of the sourcecites [96] Aerts, 2003, Nitrate stimulated tilt table testing: a review of the literature, Pacing Clin Electrophysiol source

In the paper

“In fact, there is no apparent difference in prevalence between the incidence of joint hypermobility in POTS patients and patients with other underlying chronic functional conditions.”

What the sources say

• ?Not checked — no full text of the sourcecites [71] Chelimsky, 2016, Benign joint hypermobility minimally impacts autonomic abnormalities in pediatric subjects with chronic functional pain disorders, J Pediatr source

In the paper

“This higher incidence of orthostatic intolerance may be related to perceptual amplification and hypervigilance, which have been well-described in pain conditions (77).”

What the sources say

• ?Not checked — no full text of the sourcecites [77] McDermid, 1996, Generalized hypervigilance in fibromyalgia: evidence of perceptual amplification, Pain source

In the paper

“When asked to quantify and qualify their symptoms, POTS patients score higher on fatigue scales than they do sleepiness scales,”

What the sources say

• ?Not checked — no full text of the sourcecites [86] Miglis, 2016, Sleep disorders in patients with postural tachycardia syndrome, Clin Auton Res source

In the paper

“Patients with MCAD may also demonstrate hyperadrenergic POTS features with testing, such as an exaggerated BP overshoot during recovery after the Valsalva maneuver (46).”

What the sources say

• ?Not checked — no full text of the sourcecites [46] Shibao, 2005, Hyperadrenergic postural tachycardia syndrome in mast cell activation disorders, Hypertension source

In the paper

“Physical maneuvers such as leg crossing, muscle tensing, and squatting have been shown to be effective in postponing and in some subjects preventing vasovagal syncope if used at the onset of prodromal symptoms (102,103).”

What the sources say

• ?Not checked — no full text of the sourcecites [102] Wieling, 2004, Nonpharmacological treatment of reflex syncope, Clin Auton Res source
• ?Not checked — no full text of the sourcecites [103] Krediet, 2002, Management of vasovagal syncope: controlling or aborting faints by leg crossing and muscle tensing, Circulation source

In the paper

“Chronic fatigue syndrome (CFS) and fibromyalgia are comorbidities frequently associated with POTS.”

In the paper

“As with other POTS triggers, this may in part be related to deconditioning, because a period of physical activity withdrawal and increased bedrest is typically recommended following a concussion.”

In the paper

“In a follow-up of a small number of patients who participated in the exercise program in a community setting, the effectiveness persisted for at least 1 year (64).”

What the sources say

• ?Not checked — no full text of the sourcecites [64] George, 2016, The international POTS registry: Evaluating the efficacy of an exercise training intervention in a community setting, Heart Rhythm source

In the paper

“Additionally, medication effects of stimulant medications such as amphetamines have been reported as mimicking the tachycardia of POTS (41).”

What the sources say

• ?Not checked — no full text of the sourcecites [41] Cheshire, 2016, Stimulant medication and postural orthostatic tachycardia syndrome: a tale of two cases, Clin Auton Res source

In the paper

“Some patients with MCAD and associated POTS anecdotally responded to H 1 and H 2 histamine receptor blockers, the sympatholytic alphamethyldopa, or both (46).”

What the sources say

• ?Not checked — no full text of the sourcecites [46] Shibao, 2005, Hyperadrenergic postural tachycardia syndrome in mast cell activation disorders, Hypertension source

In the paper

“Additionally, there are data that support the efficacy of biobehavioral treatments to reduce headache, abdominal pain, and fibromyalgia in the child and adolescent populations (117);”

What the sources say

• ?Not checked — no full text of the sourcecites [117] Palermo, 2010, Randomized controlled trials of psychological therapies for management of chronic pain in children and adolescents: an updated meta-analytic review, Pain source

In the paper

“Of note, in the same series, beta-blockers triggered episodes of worsening symptoms in several patients and should be used with caution if MCAD is suspected.”

What the sources say

• ?Not checked — no full text of the sourcecites [46] Shibao, 2005, Hyperadrenergic postural tachycardia syndrome in mast cell activation disorders, Hypertension source