Unexplained Syncope Evaluated by Electrophysiologic Studies and Head-up Tilt Testing

Jasbir, S.; Anderson, Alfred J.; Sheikh, Shabbir Hussain; Avitall, Boaz; Tchou, Patrick; Troup, Paul J.; Gilbert, Carol J.; Akhtar, Masood; Jazayeri, Mohammad

doi:10.7326/0003-4819-114-12-1013

Cited by 205 publications

(54 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The pathophysiologic mechanism of N-M syncope is not fully understood. The postulated mechanism of N-M syncope is as follows 11,12) : an upright posture leads to pooling of blood in the lower limbs, resulting in decreased venous return. A normal compensatory response increases sympathetic tone presenting as reflex tachycardia, and more forceful contraction of the heart and peripheral vasoconstriction occur.…”

Section: Discussionmentioning

confidence: 99%

“…9,10) The cause of hypotension-bradycardia in patients with N-M syncope is not fully understood, but may be triggered by increased activity of ventricular mechanoreceptors secondary to enhanced sympathetic tone and empty left ventricular cavity. 11,12) Thus, we postulate that beta-blockers may be effective at preventing the occurrence of N-M syncope. Accordingly, we conducted this study to assess the efficacy of Atenolol (a beta-blocker) for the treatment of N-M syncope by repeating the HUT test in patients with unexplained syncope or pre-syncope who had a positive HUT test.…”

mentioning

confidence: 99%

See 1 more Smart Citation

<b>Usefulness of Head-up Tilt Test in the Evaluation and Management of Unexplained Syncope or Pre-syncope</b>

Fang

Kuo

2000

Jpn Heart J

View full text Add to dashboard Cite

SUMMARYThis study included 87 consecutive patients with unexplained syncope or pre-syncope who had undergone the head-up tilt (HUT) test with concomitant isoproterenol infusion. A positive response was defined as development of syncope or pre-syncope in association with substantial hypotension (decline of systolic blood pressure > 20 mmHg). Coronary artery spasm was suggested from the clinical symptoms and electrocardiographic findings in 1 patient (1 / 87 = 1.1%). Intolerance to isoproterenol infusion was noted in 8 cases (8 / 87 = 9%). Of the 78 patients who completed the study, 73 showed positive responses (73 / 78 = 94%). (baseline systolic blood pressure = 125 ± 23 mmHg vs endpoint systolic blood pressure = 76 ± 11 mmHg, p < 0.05; baseline heart rate = 73 ± 14 beats per minute vs endpoint HR = 80 ± 24 beats per minute, p < 0.05). In 73 patients who showed positive responses, the systolic blood pressure (SBP) and heart rate (HR) returned to a safe level at 2 minutes when the patients were returned to a supine position (post-study 2 minutes SBP = 124 ± 18 mmHg vs baseline SBP = 125 ± 23 mmHg, p = NS; post-study 2 minutes HR = 82 ± 18 beats per minute vs baseline HR = 73 ± 14 beats per minute, p < 0.05). All 73 patients with a positive HUT test received Atenolol therapy (50 mg daily). Only 35 of these 73 patients took Atenolol regularly and had a repeat HUT test. After atenolol therapy, persistent positive responses were observed in 19 cases (19 / 35 = 54%) and negative responses were noted in 16 cases (16 / 35 = 46%). The mean dosage of isoproterenol needed to provoke a positive HUT test in 19 patients who had received Atenolol therapy and had a positive repeat HUT test was 2.3 ± 1.2 µg / min at baseline and 3.5 ± 0.9 µg / min for post-Atenolol therapy (p < 0.001). Sixteen patients with a negative repeat HUT test were treated continuously with Atenolol and followed for a mean period of 13 ± 11 months (range, 1-34 months). All 16 patients were free of syncope or pre-syncope during the period of follow up. In conclusion, the HUT test is mostly well tolerated and safe, even though the test has a low rate of adverse effects. Atenolol is effective for the prevention of provoked or spontaneous recurrent syncope or pre-syncope. (Jpn Heart J 2000; 41: 623-631)

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

<b>Usefulness of Head-up Tilt Test in the Evaluation and Management of Unexplained Syncope or Pre-syncope</b>

Fang

Kuo

2000

Jpn Heart J

View full text Add to dashboard Cite

show abstract

“…Heart rate seems to play an important role in vasovagal syncope since anticholinergic agents [2][3][4][5][6][7] and pacemaker therapy 5,[8][9][10][11][12] have been shown to be effective in preventing recurrent symptoms. Increased vagal tone has been identified as a responsible factor in some patients with recurrent unexplained syncope.…”

Section: Introductionmentioning

confidence: 99%

“…14 On the other hand, HR was considered to play only a minor role in vasodepressor syncope because beta-adrenergic blocking drugs are found to be efficacious in treating patients with vasodepressor syncope. 5,6,15 It has been shown that vasovagal attacks could not be aborted by administration of atropine 15,16 or by artificial pacing. 16,17 Confronted with these diverse results, it appears appropriate to reassess the hemodynamic differences between patients who do and do not develop bradycardia during vasovagal/ vasodepressor syncope.…”

Section: Introductionmentioning

confidence: 99%

Hemodynamic significance of heart rate in neurally mediated syncope

Chan

Wang

et al. 2004

Clinical Cardiology

View full text Add to dashboard Cite

SummaryBackground: Vasovagal and vasodepressor syncope are used interchangeably in the literature to describe the common faint syndrome, now collectively named neurally mediated syncope. The significance of heart rate (HR) in these reflex-induced reactions remains unclear.Hypothesis: The study was undertaken to investigate the hemodynamic significance of HR in tilt-induced neurally mediated syncope.Methods: In all, 113 patients with syncope of unknown etiology were studied by head-up tilt test with invasive hemodynamic monitoring. Thirty-five patients (15 women, 20 men, age range 21 to 72 years) developed syncope and were enrolled for analysis. The hemodynamic data were compared between patients who developed bradycardia (vasovagal group, n = 15) and those without bradycardia (vasodepressor group, n = 20).Results: The baseline hemodynamic data (mean ± standard deviation) and the hemodynamic responses after 10-min headup tilt were similar between patients in the vasovagal and vasodepressor groups. During syncope, patients with vasovagal reaction developed hypotension and paradoxical bradycardia (HR = 52.4 ± 5.9 beats/min), while patients with vasodepressor reaction developed a precipitous drop in arterial blood pressure with inappropriate HR (105 ± 21 beats/min) compensation. Patients with vasovagal syncope manifested a significantly lower cardiac index and a significantly higher systemic

show abstract

“…14 Invasive electrophysiologic studies can be performed to clarify whether the syncope is caused by an arrhythmia such as ventricular tachycardia, supraventricular tachycardia, sinus node dysfunction, or intracardiac conduction delay. 15 If NMS is suspected in the absence of structural heart disease, a head-up tilt-table (HUTT) test is performed to confirm the diagnosis. 16 This is a provocative test in which the patient undergoes an orthostatic challenge designed to determine his or her susceptibility to syncope.…”

Section: Diagnosismentioning

confidence: 99%