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Author Notes:

Address for correspondence: Brandon K. Fornwalt, B.S., Emory University School of Medicine, Department of Biomedical Engineering, 101 Woodruff Circle, Suite 2001, Atlanta, GA 30322, USA. Fax: 404-712-5948; E-mail: bfornwa@emory.edu

Emory University has applied for a patent on using cross-correlation to quantify dyssynchrony.

B.K. Fornwalt and Drs. Fyfe and Oshinski are coauthors on the patent.

Subjects:

Research Funding:

This work was supported by grants from the Wallace H. Coulter Foundation (Miami, Florida), the American Heart Association (Dallas, TX, Pre-doctoral Fellowship for BKF, Award 0615089B), and NIH MSTP grant T32 GM08169.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Cardiac & Cardiovascular Systems
  • Cardiovascular System & Cardiology
  • ventricular dyssynchrony
  • pacing
  • diastolic function
  • pediatrics
  • echocardiography
  • CARDIAC RESYNCHRONIZATION THERAPY
  • HEART-FAILURE
  • ATRIOVENTRICULAR-BLOCK
  • DILATED CARDIOMYOPATHY
  • RELAXATION
  • ASYNCHRONY
  • DYSFUNCTION
  • MUSCLE
  • MOTION
  • SITE

Acute pacing-induced dyssynchronous activation of the left ventricle creates systolic dyssynchrony with preserved diastolic synchrony

Tools:

Journal Title:

Journal of Cardiovascular Electrophysiology

Volume:

Volume 19, Number 5

Publisher:

, Pages 483-488

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Dyssynchrony During Acute RV Apex Pacing. Introduction: Patients with heart block have conventionally received a pacemaker that stimulates the right ventricular apex (RVA) to restore heart rate control. While RVA pacing has been shown to create systolic dyssynchrony acutely, dyssynchrony can also occur in diastole. The effects of acute RVA pacing on diastolic synchrony have not been investigated. RVA pacing acutely impairs diastolic function by increasing the time constant of relaxation, decreasing the peak lengthening rate and decreasing peak negative dP/dt. We therefore hypothesized that acute RVA pacing would cause diastolic dyssynchrony in addition to creating systolic dyssynchrony. Methods and Results: Fourteen patients (13 ± 4 years old) with non-preexcited supraventricular tachycardia underwent ablation therapy with subsequent testing to confirm elimination of the tachycardia substrate. Normal cardiac structure and function were then documented on two-dimensional echocardiography and 12-lead electrocardiography prior to enrollment. Tissue Doppler images were collected during normal sinus rhythm (NSR), right atrial appendage pacing (AAI), and VVI-RVA pacing during the postablation waiting interval. Systolic and diastolic dyssynchrony were quantified using cross-correlation analysis of tissue Doppler velocity curves. Systolic dyssynchrony increased 81% during RVA pacing relative to AAI and NSR (P < 0.01). Diastolic synchrony was not affected by the different pacing modes (P = 0.375). Conclusion: Acute dyssynchronous activation of the LV created by RVA pacing resulted in systolic dyssynchrony with preserved diastolic synchrony in pediatric patients following catheter ablation for treatment of supraventricular tachycardia. Our results suggest that systolic and diastolic dyssynchrony are not tightly coupled and may develop through separate mechanisms.

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© 2008 by Futura Publishing Company, Inc.

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