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

Michael L. Smith, Mohamed H. Hamdan, Stephen L. Wasmund, Christina F. Kneip, Jose A. Joglar, Richard L. Page

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


Background: Sudden cardiac death is usually caused by ventricular arrhythmias and in many cases, is preceded by frequent ventricular ectopy. It is known that ectopic beats cause transient increases in sympathetic nerve activity (SNA). Objective: Because high SNA is known to be arrhythmogenic, we hypothesized that high rates of ectopy increase SNA, thereby creating a milieu that favors development of ventricular tachycardia and/or fibrillation. Methods: This study measured muscle SNA, coronary sinus catecholamine, and arterial pressure during graded rates of ventricular ectopy (from 4:1 to 1:1, sinus to ectopic beat ratio) in a total of 21 patients referred for electrophysiologic testing. Results: Both muscle SNA and coronary sinus norepinephrine increased significantly with increased ectopy frequency (P < .05). Moreover, the change in muscle SNA correlated significantly with the change in coronary sinus norepinephrine levels (r = .72, P < .001). Conclusion: These data demonstrate that sympathoexcitation evoked by high rates of ventricular ectopy can contribute to a state of elevated SNA both in peripheral tissues and within the heart. This altered autonomic state may contribute to an increased susceptibility to life-threatening tachyarrhythmias in patients with high rates of ectopy.

Original languageEnglish (US)
Pages (from-to)497-503
Number of pages7
JournalHeart Rhythm
Issue number4
StatePublished - Apr 2010


  • Arrhythmia
  • Baroreflex
  • Sudden cardiac death
  • Sympathetic nerve activity
  • Ventricular Tachycardia

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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