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Neurally mediated syncope and cardiac beta-adrenergic receptor function.

S Boh-Oka1, H Ohmori, T Kawabe

  • 1Department of Medicine, Wakayama Medical University, Japan. boyan@mail.wakayama-med.ac.jp

Journal of Cardiovascular Pharmacology
|January 29, 2002
PubMed
Summary
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Neurally mediated syncope (NMS) involves altered autonomic nerve function, specifically increased beta-sensitivity and decreased beta-secretion. This may explain left ventricular hypercontraction in NMS patients.

Area of Science:

  • Cardiology
  • Neurology
  • Autonomic Neuroscience

Background:

  • Neurally mediated syncope (NMS) is a common condition with complex underlying mechanisms.
  • Understanding autonomic nerve function is crucial for elucidating NMS pathophysiology.

Purpose of the Study:

  • To investigate the mechanism of neurally mediated syncope (NMS) by evaluating basal autonomic nerve function.
  • To compare autonomic function in NMS patients with healthy controls using pharmacological testing and myocardial imaging.

Main Methods:

  • Utilized [123I]-metaiodobenzyl-guanidine (MIBG) single photon emission computed tomography (SPECT) to assess myocardial sympathetic innervation in nine NMS patients.
  • Administered pharmacological agents (atropine sulfate, isoproterenol, propranolol, phenylephrine, phentolamine) to assess autonomic function in five NMS patients and five controls.

Related Experiment Videos

  • Calculated various autonomic parameters including parasympathetic activity, beta- and alpha-sympathetic tone, sensitivity, and secretion.

    • Main Results:

    • Eight of nine NMS patients exhibited reduced myocardial [123I]-MIBG uptake on SPECT.
    • NMS patients showed significantly decreased beta-secretion (0.0027+/-0.0008 vs. 0.0060+/-0.0004 microg/kg/min/isp.; p < 0.05).
    • NMS patients demonstrated significantly increased beta-sensitivity (5850+/-947 vs. 3150+/-292 beats/microg/kg/min isp.; p < 0.05) compared to controls.

    Conclusions:

    • Increased beta-sensitivity in NMS patients may contribute to left ventricular hypercontraction.
    • These findings suggest a potential mechanism for neurally mediated syncope involving heightened cardiac beta-adrenergic responsiveness.