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

• Authors: Brandon K. Fornwalt, Emory University; Rose M. Cummings, Emory University; Takeshi Arita, Emory University; Jana G. Delfino, Emory University; Derek Fyfe, Emory University; Robert M Campbell, Emory University; Margaret Strieper, Emory University; John Oshinski, Emory University; Patricio Frias, Emory University
• Journal Title: Journal of Cardiovascular Electrophysiology
• Volume: Volume 19, Number 5
• Publisher: Wiley: 12 months | 2008-05-01, Pages 483-488
• Type of Work: Article | Post-print: After Peer Review
• Publisher DOI: http://doi.org/10.1111/j.1540-8167.2007.01079.x
• Subjects: Health Sciences, Medicine and Surgery; Engineering, Biomedical
• 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

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.