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High-frequency ventricular ectopy can increase sympathetic neural activity in humans.

Michael L Smith¹, Mohamed H Hamdan, Stephen L Wasmund

¹Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas, USA. msmith@hsc.unt.edu

|February 27, 2010

Summary

Frequent ventricular ectopy increases sympathetic nerve activity (SNA), potentially leading to life-threatening arrhythmias. This study shows elevated SNA in both peripheral tissues and the heart due to high rates of ectopic beats.

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Area of Science:

Cardiology
Autonomic Nervous System Research
Electrophysiology

Background:

Sudden cardiac death is often caused by ventricular arrhythmias.
Ventricular ectopy frequently precedes these arrhythmias.
Ectopic beats are known to transiently increase sympathetic nerve activity (SNA).

Purpose of the Study:

To test the hypothesis that high rates of ventricular ectopy increase SNA.
To investigate if increased SNA creates a pro-arrhythmic environment.
To understand the link between ectopy, SNA, and ventricular tachycardia/fibrillation.

Main Methods:

Measured muscle SNA, coronary sinus catecholamine, and arterial pressure.
Inducted graded rates of ventricular ectopy (4:1 to 1:1 sinus to ectopic beat ratio).
Study included 21 patients undergoing electrophysiologic testing.

Main Results:

Muscle SNA and coronary sinus norepinephrine levels significantly increased with higher ectopy rates (P < .05).
The change in muscle SNA strongly correlated with changes in coronary sinus norepinephrine (r = .72, P < .001).

Conclusions:

High rates of ventricular ectopy evoke sympathoexcitation, elevating SNA.
This elevated SNA occurs in both peripheral tissues and the heart.
The altered autonomic state may increase susceptibility to life-threatening tachyarrhythmias.