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1 l (21.2 percent), cardiac (9.5 percent), and orthostatic (9.4 percent); for 36.6 percent the cause wa
4 ce data and prevalence estimates of impaired orthostatic blood pressure (BP) stabilization, initial o
6 drochloride, an alpha-agonist, could improve orthostatic BP by increasing vasomotor and venomotor ton
7 ed on the frequency of a 20 mm Hg or greater orthostatic BP decline during any of 8 postural change m
10 ume expansion prior to the application of an orthostatic challenge attenuates heat stress-induced red
18 upper GI cause associated with hypotension, orthostatic changes in heart rate [>20 beats per minute]
19 ed duration of sleep (47 [92%] vs 39 [71%]), orthostatic dizziness (42 [78%] vs 46 [81%]), depression
21 autonomic dysfunction (as assessed using the Orthostatic Grading Scale [OGS]) were significantly more
29 Patients with Parkinson's disease (PD) and orthostatic hypotension (OH) (PD+OH) or with pure autono
30 arkinsonism and non-motor features including orthostatic hypotension (OH) and cognitive impairment.
37 sed on HUT results, we divided patients into orthostatic hypotension (OH), postural tachycardia syndr
38 n the heart and other organs, manifesting as orthostatic hypotension (OH; also known as postural hypo
39 measured in patients with PD with or without orthostatic hypotension (PD+OH, PD-No-OH); in patients w
40 It might be possible to improve treatment of orthostatic hypotension acutely with water imbibation an
41 gns of sympathetic neurocirculatory failure (orthostatic hypotension and abnormal blood-pressure resp
42 Screening autonomic function tests indicated orthostatic hypotension and confirmed chronic autonomic
43 ide an explanation for the predisposition to orthostatic hypotension and intolerance in well-trained
47 betes increases the risk of hypertension and orthostatic hypotension and raises the risk of cardiovas
49 comes in patients with coexistent neurogenic orthostatic hypotension and supine hypertension, clinici
51 erapy in patients with coexistent neurogenic orthostatic hypotension and supine hypertension; and the
53 mediate benefits of treatment for neurogenic orthostatic hypotension and the long-term risks of supin
55 zation, initial orthostatic hypotension, and orthostatic hypotension based on beat-to-beat blood pres
56 thesis that short-term alcohol intake causes orthostatic hypotension because of an impairment in the
70 available concerning the predictive value of orthostatic hypotension on mortality in ambulatory elder
73 cterised by autonomic failure, manifested as orthostatic hypotension or urogenital dysfunction, with
76 or autonomic failure in Parkinson disease), orthostatic hypotension reflects sympathetic neurocircul
77 uncomplicated faint, situational syncope, or orthostatic hypotension should receive electrocardiograp
78 apeutic requirements for managing neurogenic orthostatic hypotension that manifests with falls or cog
81 t stroke, coronary heart disease and cancer, orthostatic hypotension was a significant independent pr
82 Program's fourth examination (1991 to 1993), orthostatic hypotension was assessed in relation to subs
85 ed mortality rates in those with and without orthostatic hypotension were 56.6 and 38.6 per 1000 pers
87 ous events, two of which (hallucinations and orthostatic hypotension) were deemed related to study dr
89 sed a significant increase in heart rate and orthostatic hypotension, and 20% of the nortriptyline-tr
90 imates of impaired BP stabilization, initial orthostatic hypotension, and orthostatic hypotension are
91 c blood pressure (BP) stabilization, initial orthostatic hypotension, and orthostatic hypotension bas
92 re likely to have mild cognitive impairment, orthostatic hypotension, and RBD at baseline, and at pro
93 ients with PD for mild cognitive impairment, orthostatic hypotension, and RBD even at baseline visits
95 and all with Parkinson's disease-associated orthostatic hypotension, have a loss of cardiac sympathe
96 The best cluster solution found was based on orthostatic hypotension, mild cognitive impairment, rapi
97 n, upper gastrointestinal tract dysfunction, orthostatic hypotension, sweating abnormalities, or erec
98 gene encoding alpha-synuclein, also features orthostatic hypotension, sympathetic neurocirculatory fa
99 e symptomatic autonomic failure (symptomatic orthostatic hypotension, urinary incontinence, or both)
100 There was no effect by center, severity of orthostatic hypotension, use of fludrocortisone or compr
101 sk factors were identified across 6 domains: orthostatic hypotension, visual impairment, impairment o
114 supine hypertension when treating neurogenic orthostatic hypotension; the effectiveness of nocturnal
115 Identification of the gene responsible for orthostatic hypotensive disorder in these families may a
121 heat stress augments and cooling attenuates orthostatic-induced decreases in stroke volume (SV) via
124 ed by tilt-table testing on 15 subjects with orthostatic intolerance (OI) and UARS, five normotensive
127 y are likely responsible for the symptoms of orthostatic intolerance across the menstrual cycle in wo
128 are probably responsible for the symptoms of orthostatic intolerance across the menstrual cycle in wo
132 Starling relationship, which contributes to orthostatic intolerance by causing an excessive reductio
133 s during head-up tilt (HUT) in patients with orthostatic intolerance during daily life, and to identi
145 ia syndrome (POTS) induces disabling chronic orthostatic intolerance notable for an excessive increas
146 repeated neurocardiogenic presyncope (NCS), orthostatic intolerance occurs without persistent sympat
149 ia syndrome (POTS) induces disabling chronic orthostatic intolerance with an excessive increase in he
150 re commonly used in the treatment of chronic orthostatic intolerance with postural tachycardia syndro
151 m onset (hazard ratio 1.67, P < 0.003); (iv) orthostatic intolerance within 1 year of symptom onset (
152 e hypothesized that patients with idiopathic orthostatic intolerance would have impaired cardiac vaga
153 rdiovascular adaptation to bed rest leads to orthostatic intolerance, characterized by an excessive f
154 by echocardiogram, weight loss > 10 pounds, orthostatic intolerance, fatigue) in combination were hi
155 uced red blood cell masses, hypovolaemia and orthostatic intolerance, marked by greater cardio-accele
157 (P< .001), primarily due to elevation of the orthostatic intolerance, secretomotor, upper gastrointes
169 ion between the chronic fatigue syndrome and orthostatic intolerance; however, treatment with the sal
172 e series documented mild ptosis and striking orthostatic reductions in intraocular pressure and mean
173 and forearm vascular resistance (FVR) during orthostatic stress achieved by stepwise increases in low
174 ing leads to a greater decrease in SV during orthostatic stress after bed rest than hypovolemia alone
175 re and the Starling curve was steeper during orthostatic stress after HDTBR than after hypovolemia.
176 ia, astronauts respond normally to simulated orthostatic stress and are able to maintain their arteri
177 cohol consumption elicits hypotension during orthostatic stress because of impairment of vasoconstric
178 y assessed the heart variability response to orthostatic stress during tilt table testing before and
186 easurements were made during supine rest and orthostatic stress, as simulated on Earth and in space b
197 to investigate the frequency and pattern of orthostatic symptoms during head-up tilt (HUT) in patien
199 and to identify the relationship between the orthostatic symptoms during HUT and autonomic parameters
202 yndrome (POTS) with exaggerated tachycardia, orthostatic symptoms, and "pooling" (which comprises acr
209 ow dose in standing heart rate (P<0.001) and orthostatic tachycardia (P<0.001), the improvement in sy
211 yndrome (POTS) is characterized by excessive orthostatic tachycardia and significant functional disab
212 of baroreflex afferents, a mild syndrome of orthostatic tachycardia or orthostatic intolerance may a
213 ced blood volume contributes to the postural orthostatic tachycardia syndrome (POTS) and that exercis
216 omponent of the pathogenesis of the postural orthostatic tachycardia syndrome (POTS), similar to phys
217 Fibroblasts from a patient with postural orthostatic tachycardia syndrome (POTS), who presented w
218 ropriate sinus tachycardia and from postural orthostatic tachycardia syndrome, with which overlap may
219 posture and may contribute to the subsequent orthostatic tachycardia that is the hallmark of this dis
221 iorated the heat stress-induced reduction in orthostatic tolerance (1110 +/- 69 CSI, P < 0.001).
223 negative pressure test to determine level of orthostatic tolerance (cumulative stress index, CSI), wo
226 neous adrenergic responses in women with low orthostatic tolerance (LT), whereas progesterone enhance
227 We examined two novel hypotheses: (1) that orthostatic tolerance (OT) would be prolonged when hyper
232 mpathetic tone in patients with NMS improves orthostatic tolerance and raises the possibility that th
234 mechanism may contribute to improvements in orthostatic tolerance during cold stress and orthostatic
235 dicate that midodrine significantly improves orthostatic tolerance during head-up tilt in patients wi
237 body mass index 22 +/- 1 kg m(-2)) or a high orthostatic tolerance group (HT, n = 7, 22 +/- 1 years o
238 and nonneural tissue, on blood pressure and orthostatic tolerance in 19 patients with severe NOH (8
243 rough an impedance threshold device (ITD) on orthostatic tolerance in patients with postural tachycar
246 ower stroke volume contribute to compromised orthostatic tolerance in women; this inability to vasoco
248 he hypothesis that individual variability in orthostatic tolerance is dependent on the degree of neur
250 ensated Fontan subjects demonstrate superior orthostatic tolerance resulting from decreased compartme
251 ardia syndrome (POTS) report fluctuations in orthostatic tolerance throughout the menstrual cycle.
253 jects (age, 40 +/- 10 years: mean +/- S.D.), orthostatic tolerance was assessed using graded lower-bo
255 tal conditions have the capacity to modulate orthostatic tolerance, where heat stress decreases and c
262 d heart rate responses to orthostasis in low orthostatic tolerant women, which is likely to be a comp
265 s, 86.8% of patients presented with isolated orthostatic tremor and 13.2% had additional neurological
266 inical and electrophysiological diagnosis of orthostatic tremor and a minimum follow-up of 5 years is
267 Although the essential clinical features of orthostatic tremor are well established, little is known
273 p, seven patients who initially had isolated orthostatic tremor later developed further neurological
275 postural muscle EMG signals in five primary orthostatic tremor patients and in two normal controls t
278 olated tongue tremor, Wilson's disease, slow orthostatic tremor, peripheral trauma-induced tremor, ta
283 limb blood flow ("high flow") and defective orthostatic vasoconstriction or decreased limb blood flo
284 We studied hemodynamic changes leading to orthostatic vasovagal presyncope to determine whether ch
291 story and physical examination that includes orthostatic vital signs measured in both recumbent and v
292 mistry, hematology, coagulation, urinalysis, orthostatic vital signs, WSF, or 12-lead ECG parameters.
293 ose and postdose safety assessments included orthostatic vital signs; 6-lead continuous telemetry mon
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