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1 ersensitivity, and the remaining 6 addressed vasovagal syncope.
2  (DDD-CLS) in patients with cardioinhibitory vasovagal syncope.
3 ce whether being on fludrocortisone prevents vasovagal syncope.
4 ation therapy, and the use of pacemakers for vasovagal syncope.
5 hanisms may also contribute to some cases of vasovagal syncope.
6 contributes to the occurrence of orthostatic vasovagal syncope.
7 sure reductions in patients with orthostatic vasovagal syncope.
8 he serotonin hypothesis of the physiology of vasovagal syncope.
9 ize cardiovascular profiles in patients with vasovagal syncope.
10 ad-up tilt test, confirming the diagnosis of vasovagal syncope.
11  of mechanisms, diagnosis, and management of vasovagal syncope.
12 ether plausible gene variants associate with vasovagal syncope.
13 lay a central role in the pathophysiology of vasovagal syncope.
14  nerve activity in patients with orthostatic vasovagal syncope.
15 hetic activity is frequently observed before vasovagal syncope.
16 aluating predisposition to neurocardiogenic (vasovagal) syncope.
17  to 4 toxicities included neutropenia (34%), vasovagal syncope (10%), hypertension (7%), nausea/vomit
18                                     Most had vasovagal syncope (227 [35%]); other causes included car
19 ervational cohort study of 153 patients with vasovagal syncope, 52 of whom received beta-blockers.
20 ilt in 25 healthy subjects with tilt-induced vasovagal syncope and 25 age-matched nonsyncopal control
21 iated syncope beyond patients with recurrent vasovagal syncope and asystole documented by implantable
22 toxicity was reversible ataxia at 114 mg/m2, vasovagal syncope and motor neuropathy at 88 mg/m2, and
23                                              Vasovagal syncope appears to have a benign prognosis.
24                 The triggering mechanisms of vasovagal syncope are complex.
25                                  Triggers of vasovagal syncope are likely to be protean, and many pot
26   The dynamic autonomic processes leading to vasovagal syncope are poorly understood.
27 es the proportion of patients with recurrent vasovagal syncope by at least 40%, representing a pre-sp
28 e objective was to investigate mechanisms of vasovagal syncope by identifying laboratory techniques t
29 at fludrocortisone reduced the likelihood of vasovagal syncope by the specified risk reduction of 40%
30 e >/=40 years with head-up tilt test-induced vasovagal syncope compared with sham pacing.
31 nce (TPR), in 163 patients with tilt-induced vasovagal syncope documented by continuous ECG and video
32 nomic dysregulation that predisposes them to vasovagal syncope during head-up tilt.
33                 Several studies suggest that vasovagal syncope has a genetic origin, but this is uncl
34  We determined whether beta-blockers prevent vasovagal syncope in an age-related fashion.
35          beta-blocker treatment may suppress vasovagal syncope in middle-aged patients aged >42 years
36 kers have little effectiveness in preventing vasovagal syncope in unselected populations, but they mi
37 ast 2 years and a positive cardioinhibitory (Vasovagal Syncope International Study types 2A and 2B) r
38                                              Vasovagal syncope is a common clinical syndrome that has
39              The population of patients with vasovagal syncope is highly heterogeneous.
40                                              Vasovagal syncope is preceded by a period of hyperpnea a
41 tients who have infrequent events or in whom vasovagal syncope is suspected.
42                                              Vasovagal syncope is the most common type of syncope and
43 ial of fludrocortisone for the prevention of vasovagal syncope; ISRCTN51802652; Prevention of Syncope
44 is was a prolonged QTc interval secondary to vasovagal syncope (n = 87; 30%), followed by a seemingly
45 ntricular tachycardia to the adolescent with vasovagal syncope, new and effective therapies have evol
46  (cardiac syncope), or other causes, such as vasovagal syncope or orthostatic hypotension.
47 t assessed the effects of fludrocortisone in vasovagal syncope over a 1-year treatment period.
48 and the effects of three drugs used to treat vasovagal syncope (propranolol, clonidine, and paroxetin
49 QTS and full diagnostic reversal or removal (vasovagal syncope, "pseudo"-positive genetic test result
50 ethods for risk stratification, treatment of vasovagal syncope, radiofrequency ablation for atrial fi
51                                    Pacing in vasovagal syncope remains controversial.
52 effect of alleles of serotonin signaling and vasovagal syncope, supporting the serotonin hypothesis o
53                                              Vasovagal syncope (VVS) is a common yet challenging cond
54  normal subjects and patients with recurrent vasovagal syncope (VVS) is unclear.
55 ), postural tachycardia syndrome (POTS), and vasovagal syncope (VVS), symptomatic excessive HR occurs
56 pontaneous recovery; the most common form is vasovagal syncope (VVS).
57 ) with those of 31 patients with established vasovagal syncope (VVS).
58        Prodromes (64 vs. 26%, P < 0.001) and vasovagal syncope (VVS, 59 vs. 19%, P < 0.001) were more
59                                              Vasovagal syncope was more common among the No-LQTS subs
60 diovascular control in the period leading to vasovagal syncope we monitored beat-to-beat blood pressu
61  2 major factors lowering BP in tilt-induced vasovagal syncope were reduced SV and cardioinhibition.