Faculty Advisor or Committee Member

Glenn R. Gaudette, Advisor

Faculty Advisor or Committee Member

Kristen L. Billiar, Committee Member

Faculty Advisor or Committee Member

Ki H. Chon, Department Head




Every year 400,000 - 600,000 people in the United States die from sudden cardiac death. Sudden cardiac death is often caused by irregular electrical impulses, or arrhythmias, in the heart. Arrhythmias can be corrected through pharmacological therapies, device therapies, or both. One type of device therapy, pacemakers, are inserted in the heart to correct arrhythmias. After a period of ventricular pacing, cardiac memory is defined by changes in the T-wave that are persistent upon return to normal activation pathways. During ventricular pacing, regional stroke work in areas closest to the pacing electrode is significantly decreased. We hypothesize that the mechanical function in the region around the pacing site will continue to have altered mechanical function after cession of pacing, in effect showing a mechanical cardiac memory. To test the hypothesis, nine canine models were implanted with pacing electrodes in both the atrium and ventricle. After a forty- minute stabilization period, baseline data were obtained during atrial pacing. Cardiac memory was induced in five canine models through a two-hour period of ventricular pacing followed immediately by atrial pacing. The remaining canine models served as controls, undergoing atrial pacing for two hours. High- density mapper (HDM) was used to determine mechanical function in a region centered approximately 1 cm away from the pacing electrode. No differences in global function (tau, developed pressure, dP/dtmax, dP/dtmin) were found after two hours of ventricular pacing upon return to normal activation pathways. There was a significant decrease in regional stroke work in an area close to the electrode between baseline (5.7 ± 2.6 %), during ventricular pacing (-3.8 ± 0.9 %)(p<0.05) and after two hours of ventricular pacing upon return to normal activation pathways (2.4 ± 1.6 %)(p<0.05). Further, systolic area contraction was also significantly different between baseline (5.0 ± 6.6 %) and after two hours of ventricular pacing upon return to normal activation pathways (0.2 ± 7.4 %)(p<0.05). Diastolic twist and diastolic twist rates showed no significant differences. Finally, contractile principal strain increased by inducing cardiac memory (-2.6 ± 0.3 %) as compared to baseline (-1.1 ± 0.5 %)(p<0.05). These findings suggest there is a mechanical correlation to electrical cardiac memory.


Worcester Polytechnic Institute

Degree Name



Biomedical Engineering

Project Type


Date Accepted





Cardiac Memory, HDM, Mechanical function