Menstrual Cycle Affects Renal-Adrenal and Hemodynamic Responses During Prolonged Standing in the Postural Orthostatic Tachycardia Syndrome

Fu, Qi; VanGundy, Tiffany B.; Shibata, Shigeki; Auchus, Richard J.; Williams, Gordon H.; Levine, Benjamin D.

doi:10.1161/hypertensionaha.110.151787

Cited by 53 publications

(53 citation statements)

References 49 publications

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“…Previous work from our laboratory has demonstrated that a smaller and less “distensible” heart in young women or in healthy individuals after bed rest deconditioning can result in a larger reduction in stroke volume during orthostasis as a function of the Frank-Starling mechanism, leading to an excessive increase in HR (50). Consistent with our previous preliminary observations reported in abstract format (51), upright stroke volume was markedly smaller in POTS patients than healthy controls in this study. The orthostatic tachycardia observed in these patients thus appeared to be a physiological compensatory response to the smaller stroke volume (51,52), which was attributable to cardiac atrophy and reduced blood volume.…”

Section: Discussionsupporting

confidence: 93%

Cardiac Origins of the Postural Orthostatic Tachycardia Syndrome

VanGundy

Galbreath

et al. 2010

Journal of the American College of Cardiology

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Objectives To test the hypothesis that a small heart coupled with reduced blood volume contributes to the Postural Tachycardia Syndrome (POTS), while exercise training improves this syndrome. Background Patients with POTS have marked increases in heart rate during orthostasis. However, the underlying mechanisms are unknown and the effective therapy is uncertain. Methods Twenty-seven POTS patients underwent autonomic function tests, cardiac MRI, and blood volume measurements. Twenty-five of them participated in a 3-mo specially designed exercise training program with 19 completing the program; these patients were reevaluated after training. Results were compared with those of 16 healthy controls. Results Upright heart rate and total peripheral resistance were greater, while stroke volume and cardiac output were smaller in patients than controls. Baroreflex function was similar between groups. Left ventricular mass (median [25%, 75%], 1.26 [1.12, 1.37] vs 1.45 [1.34, 1.57] g/kg; P<0.01) and blood volume (60 [54, 64] vs 71 [65, 78] ml/kg; P<0.01) were smaller in patients than controls. Exercise training increased left ventricular mass and blood volume by ~12% and ~7%, and decreased upright heart rate by 9 [1, 17] bpm. Ten out of 19 patients no longer met POTS criteria after training, while patients’ Quality of Life assessed by Short-Form 36 was improved in all patients after training. Conclusions Autonomic function was intact in POTS patients. The marked tachycardia during orthostasis was attributable to a small heart coupled with reduced blood volume. Exercise training improved or even cured this syndrome in the majority of patients. It seems reasonable to offer POTS a new name based on its underlying pathophysiology – “The Grinch Syndrome”, because in this famous children’s book by Dr. Seuss, the main character had a heart that was “two sizes too small.”

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Section: Discussionsupporting

confidence: 93%

Cardiac Origins of the Postural Orthostatic Tachycardia Syndrome

VanGundy

Galbreath

et al. 2010

Journal of the American College of Cardiology

Self Cite

273

292

View full text Add to dashboard Cite

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“…Also, we did not control for the phase of the menstrual cycle in which patients were evaluated. However, in a previous study, the menstrual cycle did not affect orthostatic HR responses, BV or PRA at 30 min on standing in POTS women [35]. Finally, a relatively small number of non-CFS–POTS patients were included in the BV assessments that may have introduced a type II error (false negative results).…”

Section: Discussionmentioning

confidence: 98%

Neurohumoral and haemodynamic profile in postural tachycardia and chronic fatigue syndromes

et al. 2011

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Several studies recognized an overlap between CFS (chronic fatigue syndrome) and POTS (postural tachycardia syndrome). We compared the autonomic and neurohormonal phenotype of POTS patients with CFS (CFS–POTS) to those without CFS (non-CFS–POTS), to determine whether CFS–POTS represents a unique clinical entity with a distinct pathophysiology. We recruited 58 patients with POTS, of which 47 were eligible to participate. A total of 93% of them reported severe fatigue [CIS (Checklist of Individual Strength), fatigue subscale >36], and 64% (n=30) fulfilled criteria for CFS (CFS–POTS). The prevalence of CFS symptoms (Centers for Disease Control and Prevention criteria) was greater in the CFS–POTS group, but the pattern of symptoms was similar in both groups. Physical functioning was low in both groups (RAND-36 Health Survey, 40±4 compared with 33±3; P=0.153), despite more severe fatigue in CFS–POTS patients (CIS fatigue subscale 51±1 compared with 43±3; P=0.016). CFS–POTS patients had greater orthostatic tachycardia than the non-CFS–POTS group (51±3 compared with 40±4 beats/min; P=0.030), greater low-frequency variability of BP (blood pressure; 6.3±0.7 compared with 4.8±1.0 mmHg2; P=0.019), greater BP recovery from early to late phase II of the Valsalva manoeuvre (18±3 compared with 11±2 mmHg; P=0.041) and a higher supine (1.5±0.2 compared with 1.0±0.3 ng/ml per·h; P=0.033) and upright (5.4±0.6 compared with 3.5±0.8 ng/ml per h; P=0.032) PRA (plasma renin activity). In conclusion, fatigue and CFS-defining symptoms are common in POTS patients. The majority of them met criteria for CFS. CFS–POTS patients have higher markers of sympathetic activation, but are part of the spectrum of POTS. Targeting this sympathetic activation should be considered in the treatment of these patients.

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“…The phase of the menstrual cycle can exert important effects on NO-dependent mechanisms. There is also evidence indicating differences in renin activity and serum aldosterone but not in CO, stroke volume, blood pressure, heart rate, or total peripheral resistance in the midluteal phase compared with the early follicular phase of the menstrual cycle in POTS (5).…”

Section: Limitationsmentioning

confidence: 99%

Ascorbate improves circulation in postural tachycardia syndrome

Stewart

Ocon

Medow

2011

American Journal of Physiology-Heart and Circulatory Physiology

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Stewart JM, Ocon AJ, Medow MS. Ascorbate improves circulation in postural tachycardia syndrome. Am J Physiol Heart Circ Physiol 301: H1033-H1042, 2011. First published May 27, 2011 doi:10.1152/ajpheart.00018.2011.-Low flow postural tachycardia syndrome (LFP) is associated with vasoconstriction, reduced cardiac output, increased plasma angiotensin II, reduced bioavailable nitric oxide (NO), and oxidative stress. We tested whether ascorbate would improve cutaneous NO and reduce vasoconstriction when delivered systemically. We used local cutaneous heating to 42°C and laser Doppler flowmetry to assess NO-dependent conductance (%CVCmax) to sodium ascorbate and the systemic hemodynamic response to ascorbic acid in 11 LFP patients and in 8 control subjects (aged 23 Ϯ 2 yr). We perfused intradermal microdialysis catheters with sodium ascorbate (10 mM) or Ringer solution. Predrug heat response was reduced in LFP, particularly the NO-dependent plateau phase (56 Ϯ 6 vs. 88 Ϯ 7%CVCmax). Ascorbate increased baseline skin flow in LFP and control subjects and increased the LFP plateau response (82 Ϯ 6 vs. 92 Ϯ 6 control). Systemic infusion experiments used Finometer and ModelFlow to estimate relative cardiac index (CI) and forearm and calf venous occlusion plethysmography to estimate blood flows, peripheral arterial and venous resistances, and capacitance before and after infusing ascorbic acid. CI increased 40% after ascorbate as did peripheral flows. Peripheral resistances were increased (nearly double control) and decreased by nearly 50% after ascorbate. Calf capacitance and venous resistance were decreased compared with control but normalized with ascorbate. These data provide experimental support for the concept that oxidative stress and reduced NO possibly contribute to vasoconstriction and venoconstriction of LFP. free radicals; vasoconstriction POSTURAL TACHYCARDIA SYNDROME (POTS) accounts for most cases of chronic orthostatic intolerance (21,28,39,47,48). POTS is defined by excessive increase in upright heart rate and symptoms of orthostatic intolerance (39) improving with recumbence. Our laboratory (42) has described a subset of POTS designated "low flow POTS" (LFP) in which there is marked upright tachycardia and circulatory insufficiency even while supine including resting tachycardia, decreased cardiac output (CO), and decreased regional blood flows with peripheral and cutaneous vasoconstriction, findings often ascribed to a hyperadrenergic state (1, 6). A consistent observation has been increased plasma angiotensin II (ANG II; Refs. 40,43,45), which can act locally to decrease bioavailable nitric oxide (NO) by superoxide scavenging to create peroxynitrite (36). ANG II also acts through reactive oxygen species (ROS; Ref. 35) to increase central and peripheral sympathetic activity (9, 52). Both increased ANG II due to deficient ACE2 and decreased bioavailable NO have been demonstrated in LFP during prior experiments using intradermal microdialysis techniques. Experiments made extensive use of the local vasodilator...

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Menstrual Cycle Affects Renal-Adrenal and Hemodynamic Responses During Prolonged Standing in the Postural Orthostatic Tachycardia Syndrome

Cited by 53 publications

References 49 publications

Cardiac Origins of the Postural Orthostatic Tachycardia Syndrome

Cardiac Origins of the Postural Orthostatic Tachycardia Syndrome

Neurohumoral and haemodynamic profile in postural tachycardia and chronic fatigue syndromes

Ascorbate improves circulation in postural tachycardia syndrome

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