Changes in Cardiac Repolarization Following Short Periods of Ventricular Pacing

• Published in: Journal of cardiovascular electrophysiology 1998-03, Vol.9 (3), p.269-280
• Main Authors: GOYAL, RAJIVA, SYED, ZAFFER A., MUKHOPADHYAY, PARTHA S., SOUZA, JOSEPH, ZIVIN, ADAM, KNIGHT, BRADLEY P, MAN, K. CHING, STRICKBERGER, S. ADAM, MORADY, FRED
• Format: Article
• Language: English
• Subjects: Action Potentials - physiology; Adult; autonomic blockade; cardiac memory; Cardiac Pacing, Artificial; Catheter Ablation; Data Interpretation, Statistical; Electrocardiography; Female; Heart - physiology; Humans; Male; Middle Aged; monophasic action potential; Online Systems; Tachycardia, Supraventricular - physiopathology; Tachycardia, Supraventricular - therapy; Ventricular Function; ventricular pacing; ventricular repolarization
• ISSN: 1045-3873; 1540-8167
• DOI: 10.1111/j.1540-8167.1998.tb00912.x

Cardiac Memory. Introduction: “Cardiac memory” (primary T wave change) is thought to occur after 15 minutes to several hours of right ventricular (RV) pacing. The two components of the temporal change in repolarization are memory and accumulation. The purpose of this study was to examine quantitatively the effect of short periods of ventricular pacing on the human cardiac action potential, using monophasic action potential (MAP) recordings. Methods and Results: Thirty‐one patients (ages 43 ± 14 years) with structurally normal hearts undergoing a clinically indicated electrophysiologic procedure were enrolled. Catheters were placed in the right atrium (RA) and RV, and a MAP catheter was positioned at the RV septum. APD90 was calculated from digitized MAP recordings. MAP morphology comparisons were performed using the root mean square (RMS) of the difference between complexes. All pacing was at 500‐msec cycle length. There were four pacing protocols: (1) RA pacing was performed for approximately 15 minutes to evaluate temporal stability of the MAP recordings (5 pts); (2) to evaluate the memory phenomenon, four successive 1‐minute episodes of RV pacing were interspersed with 2 minutes of RA pacing (5 pts); (3) the accumulation phenomenon was evaluated by assessing the effects of 1, 5, 10, and 15 minutes of RV pacing on the MAP during RA pacing (16 pts); and (4) 20 minutes of RV pacing was followed by 10 minutes of RA pacing to correlate visually apparent T wave changes with changes in MAP recordings (5 pts). In the control patients, no changes in APD90 or RMS analysis were noted during 14.9 ± 1.4 minutes of RA pacing. In the second protocol, RMS of the difference between the baseline MAP complexes and the signal average of the first 50 beats following each of four 1‐minute RV pacing trains demonstrated progressively greater differences in morphology after successive episodes of RV pacing. In protocol 3, RMS analysis identified a progressively greater difference between the baseline MAP recording and the average of the first 50 beats after 1,5, 10, and 15 minutes of RV pacing. In protocol 4, visually apparent changes in T waves occurred in parallel with the RMS of the difference between the baseline MAP recordings and the average of the first 50 beats after 20 minutes of RV pacing. Similar changes also were demonstrated by APD90 analysis. Conclusion: This study is the first to demonstrate that episodes of abnormal ventricular activation as short as 1 minute in