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Sustained Suppression of Premature Ventricular Contractions by a Three-Month Pacing Adjustment
Henry Sackin1, David Campbell2, Julie Werth2
1Physiology, Rosalind Franklin University of Medicine and Science, North Chicago, USA.
Insights
Increasing pacemaker lower limit rate significantly reduced premature ventricular contractions (PVCs) in a patient. This noninvasive method offered sustained PVC reduction, suggesting a novel therapeutic approach for managing ventricular arrhythmias.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Pacing
Background:
- Premature ventricular contractions (PVCs) exceeding 15% of heartbeats can cause cardiomyopathy in systolic dysfunction patients.
- Cardiac ablation is a common but hazardous treatment for reducing PVCs.
- Pacemaker therapy is crucial for managing bradycardia and other cardiac conditions.
Observation:
- A patient with a pacemaker experienced a significant reduction in PVCs from 31% to 3% within seven days.
- The reduction was achieved by noninvasively increasing the pacemaker's lower limit pacing rate from 50 to 60 bpm.
- PVC levels remained below 5% even after the pacing rate was reverted to 50 bpm.
Findings:
- A temporary increase in pacemaker lower limit pacing rate led to a dramatic and sustained reduction in PVCs.
- The PVC suppression persisted for at least three months after the pacing rate was returned to the baseline.
- This suggests a potential for pacemaker programming to induce long-term suppression of ectopic activity.
Implications:
- Noninvasive pacemaker programming may offer a safer alternative to cardiac ablation for managing significant PVC burdens.
- The findings suggest that altering pacing parameters can induce beneficial ventricular remodeling and suppress arrhythmias.
- This approach could be explored further in patients with pacemaker dependency and high PVC loads.
Abstract:
Premature ventricular contractions (PVCs) that comprise more than 15% of total heartbeats can induce cardiomyopathy in patients with systolic dysfunction, and cardiac ablation is frequently used to reduce PVCs in this patient group. However, cardiac ablation is not entirely without hazards. We report a noninvasive method that dramatically reduced PVCs in a cardiac pacemaker patient from 31% to 3% in seven days by increasing the lower limit pacing rate from 50 beats per minute (bpm) to 60 bpm. Not only were our patient's PVCs reduced by the initial pacing elevation, but PVC levels were maintained below 5% even after the pacemaker's lower limit was returned to its original value of 50 bpm. This irreversible suppression of PVC activity following a three-month pacing elevation is a novel result that might be caused by ventricular remodeling of the original ectopic focus.
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