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Tilt Testing with Combined Lower Body Negative Pressure: a "Gold Standard" for Measuring Orthostatic Tolerance

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Recurrent postural vasovagal syncope: sympathetic nervous system phenotypes.

Gautam Vaddadi¹, Ling Guo, Murray Esler

¹Human Neurotransmitter Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia. Gautam.vaddadi@bakeridi.edu.au

Circulation. Arrhythmia and Electrophysiology

|August 17, 2011

Summary

Vasovagal syncope patients have distinct sympathetic nervous system issues. Phenotyping by blood pressure reveals unique abnormalities, paving the way for targeted therapies.

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Published on: September 11, 2018

Area of Science:

Cardiovascular Physiology
Autonomic Nervous System Research
Neuroscience

Background:

Vasovagal syncope pathophysiology is unclear, with ineffective treatments.
Patients present with either normal or low supine systolic blood pressure.
Distinct neural circulatory control mechanisms may exist between these phenotypes.

Purpose of the Study:

To investigate neural circulatory control in vasovagal syncope patients.
To differentiate sympathetic nervous system responses based on blood pressure phenotype.
To identify specific mechanisms underlying treatment resistance.

Main Methods:

Assessed sympathetic nervous system activity via microneurography, norepinephrine spillover, and Western blot.
Tested 36 vasovagal syncope patients (15 low BP, 21 normal BP) and 18 controls.
Utilized head-up tilt (HUT) to simulate orthostatic stress.

Main Results:

Healthy subjects showed increased nerve firing and norepinephrine spillover during HUT.
Vasovagal syncope patients exhibited subnormal norepinephrine spillover despite normal or increased nerve firing.
Low BP phenotype linked to reduced tyrosine hydroxylase; normal BP phenotype to increased norepinephrine transporter.

Conclusions:

Recurrent vasovagal syncope patients display unique sympathetic nervous system abnormalities when phenotyped.
These abnormalities involve a disjunction between sympathetic nerve activity and neurotransmitter release.
Targeting identified mechanisms may lead to more effective vasovagal syncope treatments.