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

Area of Science:

• Cardiology
• Autonomic Neuroscience
• Physiology

Background:

• The exact cause of neurally mediated syncope (NMS) is unclear.
• A common theory suggests overactive sympathetic nervous system (SNS) triggers NMS.
• This study investigates the role of SNS activation in NMS pathophysiology.

Purpose of the Study:

• To test the hypothesis that excessive sympathetic activation precedes NMS.
• To examine the correlation between sympathetic activation and baroreflex function in NMS.
• To challenge the prevailing theory of generalized sympathetic overactivity in NMS.

Main Methods:

• Measured blood pressure, heart rate, central venous pressure, muscle sympathetic nerve activity (MSNA), and plasma catecholamines during upright tilt.
• Assessed baroreflex sensitivity using phenylephrine and sodium nitroprusside infusions.
• Compared NMS patients (SYN), controls (CON), and healthy subjects prone to syncope (FS+).

Main Results:

• SYN patients showed blunted MSNA increases and reduced norepinephrine levels compared to CON.
• MSNA progressively decreased, ultimately disappearing during syncope in SYN patients.
• NMS patients exhibited attenuated baroreflex sensitivity.
• FS+ subjects displayed significant MSNA and heart rate increases with tilt.

Conclusions:

• Recurrent NMS is not preceded by excessive generalized sympathetic activation.
• The findings challenge the established view of SNS overactivity as the cause of NMS.
• Altered sympathetic response and baroreflex dysfunction are implicated in NMS.