Cardiac electrophysiologic and hemodynamic correlates of neurally mediated syncope

doi:10.1016/0002-9149(89)91077-1

The American Journal of Cardiology

Volume 63, Issue 1, 1 January 1989, Pages 66-72

https://doi.org/10.1016/0002-9149(89)91077-1 Get rights and content

Abstract

This study assessed the temporal relation of RR interval, AH interval and systemic blood pressure changes during induced symptomatic bradycardiahypotension episodes in 14 patients with recurrent syncope suspected of being neurally mediated. Upright tilt with isoproterenol reproduced symptoms in 9 of 14 patients (positive response) and was negative in 5 of 14 (negative response). Isoproterenol alone shortened supine RR intervals in all patients. With tilt, however, isoproterenol prolonged RR intervals in those with positive results (supine 519 ± 124 ms vs tilt 845 ±212 ms, p < 0.005) while further shortening RR intervals among negative responders (supine 436 ± 90 ms vs tilt 377 ± 82 ms, p < 0.05). Similarly, tilt with isoproterenol prolonged AH intervals in patients with positive responses despite RR prolongation, while shortening AH in negative responders. Additionally, with combined tilt and isoproterenol, systemic arterial pressure decreased significantly in patients with positive responses (systolic 99 ± 13 vs 57 ± 13 mm Hg, p < 0.001, diastolic 62 ± 17 vs 28 ± 9 mm Hg, p < 0.001) but not in patients with negative responses. Further, onset of hypotension (42 ± 14 seconds after tilt) preceded onset of RR interval prolongation (52 ± 23 seconds after tilt). Syncope (142 ± 72 seconds after tilt) coincided closely with nadir of systemic pressure (136 ± 74 seconds) and both tended to precede maximum RR prolongation (152 ± 87 seconds). Thus, the bradycardia and hypotension associated with neurally mediated syncope exhibit characteristic but distinctly different time courses, with arterial pressure changes developing earlier and coinciding more closely with symptom development.

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Cited by (87)

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2004, Cardiac Electrophysiology: From Cell to Bedside
Utility of a single-stage isoproterenol tilt table test in adults a randomized comparison with passive head-up tilt
1999, Journal of the American College of Cardiology
OBJECTIVES
This study was conducted to develop a time-efficient tilt table test.
BACKGROUND
Current protocols of tilt table testing are quite time-consuming. This study was designed to assess the diagnostic value, tolerance and procedural time of a single-stage isoproterenol tilt table protocol.
METHODS
A single-stage isoproterenol tilt table test was compared with the passive tilt table test. The study was prospectively designed in a randomized and crossover fashion.
RESULTS
The study population consisted of 111 patients with a history of syncope (mean age 55 ± 20 years). Of the total, 62 patients (56%; 95% confidence interval, 46% to 65%) had a positive vasovagal response during isoproterenol tilt table testing and 35 (32%; 23% to 41%) during passive tilt table testing (p = 0.002). The mean procedural times of the study population were 11.7 ± 3.6 min and 36.9 ± 13.3 min for isoproterenol and passive tilt table testing, respectively (p < 0.001). All patients tolerated single-stage isoproterenol testing. In the 23 control subjects (mean age 34 ± 11 years), the apparent specificities were 91% (72% to 99%) and 83% (61% to 99%) for passive and single-stage tilt table testing, respectively.
CONCLUSIONS
The single-stage isoproterenol tilt table test was more effective in inducing a positive vasovagal response in an adult population than the standard passive tilt table test, and it significantly reduced the procedural time. The increase in positive yield was associated with a moderate decrease in apparent specificity. These observations support the conclusion that single-stage tilt table testing could be a reasonable diagnostic option in patients undergoing syncope evaluation.
Abnormality of alpha-adrenergic vascular response in patients with neurally mediated syncope
1998, American Journal of Cardiology
Although diagnosis of neurally mediated syncope (NMS) using the head-up tilt (HUT) test has been established, the precise etiologic mechanism of NMS is still obscure. Previously, we reported the contribution of impaired α-adrenergic vascular response to syncope in patients with various arrhythmias. This study evaluates α-adrenergic vascular response in 21 NMS patients with syncope and a positive HUT test (80 degrees, 30 minutes, and low-dose isoproterenol, NMS group, mean age 31 ± 14 years) and 21 control subjects (C group, 33 ± 14 years) who had no evidence of syncope and no structural heart disease. After 30 minutes in a recumbent position, pharmacologic total autonomic blockade was attained using atropine and propranolol. Thereafter, increased systolic blood pressure with 0.4 μg/kg/min phenylephrine (designated as ΔBPphenyl) and decreased systolic blood pressure with 0.5 μg/kg/30 seconds of phentolamine (designated as ΔBPphent) were measured as indexes of α-adrenergic vascular sensitivity and activity, respectively. ΔBPphenyl in the NMS group (70.0 ± 37) was significantly less than that in C group (107 ± 38, p <0.005). ΔBPphent was significantly greater in the NMS group than in the C group (33.5 ± 10 vs 21.0 ± 14, p <0.005). Thus, decreased α-adrenergic vascular sensitivity and elevated α-adrenergic vascular tone were observed in patients with NMS. Although it is not known whether the mechanism causing NMS can be attributed to this abnormal α-adrenergic vascular response, the abnormality could at least contribute to augmenting the symptoms of NMS.

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^☆: This work was completed during Dr. Benditt's tenure as an Established Investigator of the American Heart Association, Dallas, Texas.

¹: Dr. Chen's present address: Fujian Provincial Research Institute for Medical Sciences, Wu-Shi Road, Fuzhou, Fujian, People's Republic of China.

³: Dr. Chen was supported in part by a grant-in-aid from the Education Ministry, People's Republic of China, and by the Minnesota Medical Foundation Electrophysiology Research Fund.

²: Dr. Almquist's present address: Cardiology Division, Marshfield Clinic, Marshfield, Wisconsin.

⁴: Dr. Almquist was supported in part by the Kenneth N. Rosen Fellowship of the North American Society for Pacing and Electrophysiology (NASPE).

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Cardiac electrophysiologic and hemodynamic correlates of neurally mediated syncope☆

Abstract

JACC

Hypotension and syncope

Isoproterenol-induced vasodepressor reactions in man (abstr)

Clin Invest Med

Vasovagal syncope. Vagal overtone or lack of sympathetic stimulation? (abstr)

Circulation

Provocation of bradycardia and hypotension by isoproterenol in patients with unexplained syncope (abstr)

Circulation

Prevention of neurally-mediated syncope by selective beta-1 adrenoceptor blockade (abstr)

Circulation

Head-up tilt: a useful test for investigating unexplained syncope

Lancet

Enhanced atrioventricular node conduction in man: electrophysiologic effects of pharmacologic autonomic blockade

Circulation

Carotid sinus hypersensitivity: evaluation of the vasodepressor component

Circulation