ライフサイエンスコーパス: vasovagal syncope

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1 ation therapy, and the use of pacemakers for vasovagal syncope.

2 hanisms may also contribute to some cases of vasovagal syncope.

3 contributes to the occurrence of orthostatic vasovagal syncope.

4 sure reductions in patients with orthostatic vasovagal syncope.

5 ersensitivity, and the remaining 6 addressed vasovagal syncope.

6 ize cardiovascular profiles in patients with vasovagal syncope.

7 ad-up tilt test, confirming the diagnosis of vasovagal syncope.

8 (DDD-CLS) in patients with cardioinhibitory vasovagal syncope.

9 of mechanisms, diagnosis, and management of vasovagal syncope.

10 lay a central role in the pathophysiology of vasovagal syncope.

11 nerve activity in patients with orthostatic vasovagal syncope.

12 hetic activity is frequently observed before vasovagal syncope.

13 ce whether being on fludrocortisone prevents vasovagal syncope.

14 aluating predisposition to neurocardiogenic (vasovagal) syncope.

15 to 4 toxicities included neutropenia (34%), vasovagal syncope (10%), hypertension (7%), nausea/vomit

16 Most had vasovagal syncope (227 [35%]); other causes included car

17 ervational cohort study of 153 patients with vasovagal syncope, 52 of whom received beta-blockers.

18 ilt in 25 healthy subjects with tilt-induced vasovagal syncope and 25 age-matched nonsyncopal control

19 iated syncope beyond patients with recurrent vasovagal syncope and asystole documented by implantable

20 toxicity was reversible ataxia at 114 mg/m2, vasovagal syncope and motor neuropathy at 88 mg/m2, and

21 Vasovagal syncope appears to have a benign prognosis.

22 The triggering mechanisms of vasovagal syncope are complex.

23 Triggers of vasovagal syncope are likely to be protean, and many pot

24 The dynamic autonomic processes leading to vasovagal syncope are poorly understood.

25 es the proportion of patients with recurrent vasovagal syncope by at least 40%, representing a pre-sp

26 e objective was to investigate mechanisms of vasovagal syncope by identifying laboratory techniques t

27 at fludrocortisone reduced the likelihood of vasovagal syncope by the specified risk reduction of 40%

28 e >/=40 years with head-up tilt test-induced vasovagal syncope compared with sham pacing.

29 nomic dysregulation that predisposes them to vasovagal syncope during head-up tilt.

30 We determined whether beta-blockers prevent vasovagal syncope in an age-related fashion.

31 beta-blocker treatment may suppress vasovagal syncope in middle-aged patients aged >42 years

32 kers have little effectiveness in preventing vasovagal syncope in unselected populations, but they mi

33 ast 2 years and a positive cardioinhibitory (Vasovagal Syncope International Study types 2A and 2B) r

34 Vasovagal syncope is a common clinical syndrome that has

35 The population of patients with vasovagal syncope is highly heterogeneous.

36 Vasovagal syncope is preceded by a period of hyperpnea a

37 tients who have infrequent events or in whom vasovagal syncope is suspected.

38 Vasovagal syncope is the most common type of syncope and

39 ial of fludrocortisone for the prevention of vasovagal syncope; ISRCTN51802652; Prevention of Syncope

40 ntricular tachycardia to the adolescent with vasovagal syncope, new and effective therapies have evol

41 t assessed the effects of fludrocortisone in vasovagal syncope over a 1-year treatment period.

42 and the effects of three drugs used to treat vasovagal syncope (propranolol, clonidine, and paroxetin

43 ethods for risk stratification, treatment of vasovagal syncope, radiofrequency ablation for atrial fi

44 Pacing in vasovagal syncope remains controversial.

45 normal subjects and patients with recurrent vasovagal syncope (VVS) is unclear.

46 ) with those of 31 patients with established vasovagal syncope (VVS).

47 pontaneous recovery; the most common form is vasovagal syncope (VVS).

48 Vasovagal syncope was more common among the No-LQTS subs

49 diovascular control in the period leading to vasovagal syncope we monitored beat-to-beat blood pressu

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