Comparison of Cardiac Pacing with Drug Therapy in the Treatment of Neurocardiogenic (Vasovagal) Syncope with Bradycardia or Asystole

Jasbir, S.; Jazayeri, Mohammad; Avitall, Boaz; Dhala, Anwer; Deshpande, Sanjay; Blanck, Zalmen; Akhtar, Masood

doi:10.1056/nejm199304153281504

Cited by 261 publications

(77 citation statements)

References 21 publications

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“…Finally, the presence of either reduced or increased MSNA in subjects with syncope may also explain the dissimilar therapeutic response observed in different populations (50,51). Conceivably, patients in whom syncope is associated with a blunted increase in sympathetic tone would benefit from ␣-adrenergic receptor agonists or from agents that increase sympathetic tone.…”

Section: Discussionmentioning

confidence: 99%

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

et al. 1997

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The pathophysiology of neurally mediated syncope is poorly understood. It has been widely assumed that excessive sympathetic activation in a setting of left ventricular hypovolemia stimulates ventricular afferents that trigger hypotension and bradycardia. We tested this hypothesis by determining if excessive sympathetic activation precedes development of neurally mediated syncope, and if this correlates with alterations in baroreflex function. We studied the changes in intraarterial blood pressure (BP), heart rate (HR), central venous pressure (CVP), muscle sympathetic nerve activity (MSNA), and plasma catecholamines evoked by upright tilt in recurrent neurally mediated syncope patients (SYN, 5 Ϯ 1 episodes/mo, n ϭ 14), age-and sex-matched controls (CON, n ϭ 23), and in healthy subjects who consistently experienced syncope during tilt (FS ϩ , n ϭ 20). Baroreflex responses were evaluated from changes in HR, BP, and MSNA that were obtained after infusions of phenylephrine and sodium nitroprusside. Compared to CON, patients with SYN had blunted increases in MSNA at low tilt levels, followed by a progressive decrease and ultimately complete disappearance of MSNA with syncope. SYN patients also had attenuation of norepinephrine increases and lower baroreflex slope sensitivity, both during tilt and after pharmacologic testing. FS ϩ subjects had the largest decrease in CVP with tilt and had significant increases in MSNA and heart rate baroreflex slopes. These data challenge the view that excessive generalized sympathetic activation is the precursor of the hemodynamic abnormality underlying recurrent neurally mediated syncope. ( J. Clin. Invest. 1997. 99:2736-2744.)

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Section: Discussionmentioning

confidence: 99%

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

et al. 1997

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“…In this regard, 2 recent publications claim success in treating humans for vasodepressor reactions with theophylline. 16,17 Earlier studies showed that the paradoxic bradycardia in this rat model depends on cardiac vagal afferents: it is blocked by cervical vagotomy or intrapericardial lidocaine but is independent of efferent vagal tone because it is unaffected by muscarinic receptor blockade with atropine. 6,7 Similarly, the paradoxic bradycardia response to inferior vena cava occlusion during isoproterenol and dipyridamole was not affected by pretreatment with atropine, but it was blocked by cervical vagotomy.…”

Section: Discussionmentioning

confidence: 85%

Role of Adenosine Receptors in the Paradoxic Bradycardia Response of Rats to Inferior Vena Cava Occlusion During an Infusion of Isoproterenol

Waxman

Asta

1998

Circulation

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Background-In susceptible humans, vasodepressor reactions are induced by restriction of venous return (upright tilting) and administration of isoproterenol. Because paradoxic bradycardia is a major manifestation of vasodepressor reactions, and allowing for extrapolation between paradoxic bradycardia in rats and vasodepressor reactions, we examined whether adenosine receptors mediate the paradoxic bradycardia reaction. Methods and Results-Paradoxic bradycardia was induced in rats by inferior vena cava occlusion during an isoproterenol infusion. We studied whether dipyridamole, an adenosine transport inhibitor, and aminophylline (nonselective) or DPCPX (selective) A 1 antagonists augmented or inhibited paradoxic bradycardia, respectively, during inferior vena cava occlusion. The maximum changes in R-R during 60 seconds of inferior vena cava occlusion were that (1) in control, the rate accelerated (⌬R-R, Ϫ9.7Ϯ0.8 ms, PϽ0.001); (2) during isoproterenol (0.8 g ⅐ min Ϫ1 ), paradoxic bradycardia occurred (⌬R-R, ϩ92.0Ϯ32.0 ms, PϽ0.001); (3) during isoproterenol but after dipyridamole, paradoxic bradycardia occurred at a much lower dose of isoproterenol (0.2 g ⅐ min Ϫ1 ), and the magnitude was increased at all doses (at 0.8 g ⅐ min Ϫ1 isoproterenol, ⌬R-R, ϩ195.6Ϯ27.6 ms, PϽ0.001 versus isoproterenol alone, ⌬R-R, ϩ92.0Ϯ32 ms); (4) during isoproterenol and dipyridamole, atropine did not block paradoxic bradycardia, but cervical vagotomy inhibited paradoxic bradycardia (⌬R-R, ϩ5.6Ϯ1.8 ms, PϽ0.001 compared with isoproterenol and dipyridamole alone); and (5) during isoproterenol alone, aminophylline or DPCPX blocked paradoxic bradycardia (⌬R-R, Ϫ5.4Ϯ1.0 ms, and ⌬R-R, Ϫ2.6Ϯ0.5 ms, respectively, each PϽ0.001 compared with isoproterenol alone). Conclusions-The adenosine A 1 receptor mediates the paradoxic bradycardia reflex during inferior vena cava occlusion in the face of isoproterenol via vagal afferents. (Circulation. 1998;98:1228-1235.)

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“…28 Sra et al studied 22 patients by tilting test with temporary pacing. 17 Although they concluded that artificial pacing at a rate 20% higher than the basic HR could not prevent vasovagal syncope, the reduction of arterial blood pressure was significantly less during the pacing study. Furthermore, only 5 patients developed syncopes during tilting test with pacing compared with 18 patients who fainted during baseline tilt test without pacing.…”

Section: Discussionmentioning

confidence: 96%

“…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

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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

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Comparison of Cardiac Pacing with Drug Therapy in the Treatment of Neurocardiogenic (Vasovagal) Syncope with Bradycardia or Asystole

Abstract: In patients with neurocardiogenic syncope associated with bradycardia or asystole, drug therapy is often effective in preventing syncope, whereas artificial pacing is not.

Cited by 261 publications

References 21 publications

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

Role of Adenosine Receptors in the Paradoxic Bradycardia Response of Rats to Inferior Vena Cava Occlusion During an Infusion of Isoproterenol

Hemodynamic significance of heart rate in neurally mediated syncope

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