Author + information
- Received August 3, 1982
- Revision received December 28, 1982
- Accepted December 30, 1982
- Published online June 1, 1983.
- Paul A. Levine, MD, FACC*,*,
- S. Serge Barold, MB, FACC†,
- Ross D. Fletcher, MD, FACC‡ and
- Paul Talbot, MB§
- ↵*Address for reprints: Paul A. Levine, MD, University Hospital, 75 East Newton Street, Boston, Massachusetts 02118.
Six cases are presented in which a transient or chronic rise in the stimulation threshold of a permanently implanted unipolar pacemaker resulted in the loss of effective pacing after therapeutic defibrillation or cardioversion. Although damage to the pulse generator may still occur, leading to a loss of function as demonstrated in a seventh patient, improvements in the internal protection circuits of the present generation of pacemakers makes this less likely while possibly predisposing to endocardial burns and increased fibrosis at the electrode-endocardial interface. The theoretical explanations for this phenomenon are discussed, along with recommendations for the prospective and retrospective management of the pacemaker patient who requires defibrillation or cardioversion.
- Received August 3, 1982.
- Revision received December 28, 1982.
- Accepted December 30, 1982.
- American College of Cardiology Foundation